# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks licensees for human T-cell lines, C8166 and C8166-45, transformed by HTLV-1. C8166-45, a subclone of C8166, contains three transcriptionally active proviruses useful for testing biological activities involved in T-cell immortalization and growth.

Description of Technology:

Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus reported and is recognized as an etiological agent of adult T-cell leukemia (ATL). However, only a small percentage of individuals develop symptomatic ATL which carries a poor prognosis. The latency period can last for decades and universal screening for HTLV-1 infection has ceased. Thus, the C8166-45 and C8166 cell lines are  necessary components for understanding the mechanisms of HTLV-1 infection and improving clinical outcomes.

NCI researchers derived C8166-45 by cocultivation or fusion of umbilical cord blood lymphocyte with T-cells cultures from leukemia-lymphoma patients. It is highly permissive to HIV-1 infection and characterized for its suitability in replication-competent lentiviral (RCL) assays to assess its safety for gene therapy products, such as lentiviral vectors. Both cell lines are highly useful in studying viral protein interactions, immortalization of human T-cells, and HIV replication.

NCI is seeking parties to non-exclusively license the C8166-45 and C8166 cell lines.

Potential Commercial Applications:

Investigation of HTLV pathogenesis and replication

Studies of virus-induced T-cell transformation

Studies of HTLV expression regulation by human T-cells

Studies of HIV replication

Competitive Advantages:

Contains a low amount of viral proteins

Does not release detectable virus particles

Suitable for testing RCL assay sensitivity

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks licensees for human T-cell lines, C8166 and C8166-45, transformed by HTLV-1. C8166-45, a subclone of C8166, contains three transcriptionally active proviruses useful for testing biological activities involved in T-cell immortalization and growth.

Description of Technology:

Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus reported and is recognized as an etiological agent of adult T-cell leukemia (ATL). However, only a small percentage of individuals develop symptomatic ATL which carries a poor prognosis. The latency period can last for decades and universal screening for HTLV-1 infection has ceased. Thus, the C8166-45 and C8166 cell lines are  necessary components for understanding the mechanisms of HTLV-1 infection and improving clinical outcomes.

NCI researchers derived C8166-45 by cocultivation or fusion of umbilical cord blood lymphocyte with T-cells cultures from leukemia-lymphoma patients. It is highly permissive to HIV-1 infection and characterized for its suitability in replication-competent lentiviral (RCL) assays to assess its safety for gene therapy products, such as lentiviral vectors. Both cell lines are highly useful in studying viral protein interactions, immortalization of human T-cells, and HIV replication.

NCI is seeking parties to non-exclusively license the C8166-45 and C8166 cell lines.

Potential Commercial Applications:

Investigation of HTLV pathogenesis and replication

Studies of virus-induced T-cell transformation

Studies of HTLV expression regulation by human T-cells

Studies of HIV replication

Competitive Advantages:

Contains a low amount of viral proteins

Does not release detectable virus particles

Suitable for testing RCL assay sensitivity

# data[].attributes.field_collaboration_description.value
The NCI seeks licensing for the C8166-45 and C8166 cell lines.

# data[].attributes.field_collaboration_description.processed
The NCI seeks licensing for the C8166-45 and C8166 cell lines.

# data[].attributes.field_licensingcontact_htmls[]
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts[].value
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_publications[].value
DeBoer J, et al. Alterations in the nuclear proteome of HIV-1 infected T-cells. (PMID 25240327)

# data[].attributes.field_publications[].processed
DeBoer J, et al. Alterations in the nuclear proteome of HIV-1 infected T-cells. (PMID 25240327)

# data[].attributes.field_publications[].value
Salahuddin SZ, et al. Restricted expression of human T-cell leukemia-lymphoma virus (HTLV) in transformed human umbilical cord blood lymphocytes. (PMID 6412453)

# data[].attributes.field_publications[].processed
Salahuddin SZ, et al. Restricted expression of human T-cell leukemia-lymphoma virus (HTLV) in transformed human umbilical cord blood lymphocytes. (PMID 6412453)

# data[].attributes.field_publications[].value
Cornetta K, et al. Absence of replication-competent lentivirus in the clinic: analysis of infused T cell products. (PMID 28970045)

# data[].attributes.field_publications[].processed
Cornetta K, et al. Absence of replication-competent lentivirus in the clinic: analysis of infused T cell products. (PMID 28970045)

# data[].attributes.field_technology_names[]
C8166-45 Cell Line (NIH AIDS Reagent Repository Catalog No. 404) and C8166 cell line

# data[].attributes.title
Use of Antihistamine Compounds for the Treatment of Hepatitis C Virus

# data[].attributes.body.value
The vast majority of people infected with Hepatitis C Virus (HCV) will have chronic infection. Over decades, this can lead to liver disease and liver cancer. In fact, HCV infection is the leading cause of liver transplants in the U.S. Several new drugs have recently come into the market that will likely change the HCV treatment paradigm. However, the effectiveness of these new drugs can vary depending on the HCV genotype. Thus, there is still the need for additional new therapeutics against HCV.

The subject technology are small molecule compounds identified using a novel cell-based high throughput assay of HCV infection. The compounds are antihistamines that show potent antiviral properties against HCV. One advantage of these compounds is that they are already on the market for the treatment of allergic reactions and, thus, have been used extensively in humans and have excellent safety profiles with known pharmaceutical properties. The subject technology can also potentially be used in combination with other HCV therapeutics.

# data[].attributes.body.processed
The vast majority of people infected with Hepatitis C Virus (HCV) will have chronic infection. Over decades, this can lead to liver disease and liver cancer. In fact, HCV infection is the leading cause of liver transplants in the U.S. Several new drugs have recently come into the market that will likely change the HCV treatment paradigm. However, the effectiveness of these new drugs can vary depending on the HCV genotype. Thus, there is still the need for additional new therapeutics against HCV.

The subject technology are small molecule compounds identified using a novel cell-based high throughput assay of HCV infection. The compounds are antihistamines that show potent antiviral properties against HCV. One advantage of these compounds is that they are already on the market for the treatment of allergic reactions and, thus, have been used extensively in humans and have excellent safety profiles with known pharmaceutical properties. The subject technology can also potentially be used in combination with other HCV therapeutics.

# data[].attributes.field_commercial_applications.value
Prevention or treatment of HCV infection.

# data[].attributes.field_commercial_applications.processed
Prevention or treatment of HCV infection.

# data[].attributes.field_competitive_advantages.value
These compounds are already on the market and, thus, have known safety profiles and pharmaceutical properties.

# data[].attributes.field_competitive_advantages.processed
These compounds are already on the market and, thus, have known safety profiles and pharmaceutical properties.

# data[].attributes.field_development_status.value
Early-stage

In vitro data available

# data[].attributes.field_development_status.processed
Early-stage

In vitro data available

# data[].attributes.field_inventor_companies[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

# data[].attributes.field_inventor_companies[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

# data[].attributes.field_inventor_companies[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

# data[].attributes.field_licensingcontact_hrefs[]
carolyn.buller@nih.gov?subject=Web Inquiry on [TAB-2808] Use of Antihistamine Compounds for the Treatment of Hepatitis C Virus&body=Please send me information about technology [TAB-2808] Use of Antihistamine Compounds for the Treatment of Hepatitis C Virus.

# data[].attributes.field_licensingcontact_htmls[]
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts[].value
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
carolyn.buller@nih.gov?subject=Web Inquiry on [TAB-2808] Use of Antihistamine Compounds for the Treatment of Hepatitis C Virus&body=Please send me information about technology [TAB-2808] Use of Antihistamine Compounds for the Treatment of Hepatitis C Virus.

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2014/066680
Filed on 2014-11-20
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2014/066680
Filed on 2014-11-20
Status: Expired

# data[].attributes.field_patents[].value
US
National Stage 15/039,781
Filed on 2016-05-26
Status: Abandoned

# data[].attributes.field_patents[].processed
US
National Stage 15/039,781
Filed on 2016-05-26
Status: Abandoned

# data[].attributes.field_patents[].value
US
Provisional (PRV) 61/909,414
Filed on 2013-11-27
Status: Abandoned

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 61/909,414
Filed on 2013-11-27
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2014/066680
Filed on 2014-11-20
Status: Expired

# data[].attributes.field_patent_htmls[]
US
National Stage 15/039,781
Filed on 2016-05-26
Status: Abandoned

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 61/909,414
Filed on 2013-11-27
Status: Abandoned

# data[].attributes.field_patent_titles[]
Heterocyclic Compounds and Methods of Use Thereof

# data[].attributes.field_patent_titles[]
Piperidine and Piperazine Derivatives and Their Use in Treating Viral Infections and Cancer

# data[].attributes.field_patent_titles[]
Heterocyclic Compounds and Methods of Use Thereof

# data[].attributes.field_technology_names[]
Use Of Chlorcyclizine And Its Related Analogs In Treatment Of Hepatitis C

# data[].attributes.field_technology_owners[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NCATS - NCGC

# data[].attributes.title
Alb-tTA (Tg(Alb1-tTA)3123Lng) Mouse Model for Liver Function Studies

# data[].attributes.body.value
Tetracycline-responsive transcriptional activator driven by the liver-specific mouse albumin promoter (Alb-tTA).

The E. Coli tetracycline operon regulatory system was used to generate a liver-specific transcription activation system that was inhibited by tetracycline. The transcription activator was a fused protein consisting of a tetracycline repressor gene (tetR) that was only active in the presence of tetracycline and a herpes simplex virus protein (VP-16) transcription activating domain. Transcription was induced only in the absence of tetracycline (Tet-Off). A liver-specific promoter such as mouse albumin determined that the tetracycline-regulated transcriptional activator (tTA) would be expressed specifically in liver. To study the effect of the transcription activator on a target gene (for example, Simian Virus 40 (SV4) large tumor (T) antigen (TAg)) specifically in liver, Alb-tTA mice were mated with transgenic mice in which the Target gene (TAg) was controlled by the E.Coli Tetracycline Operator (Tet-O). In this example, TAg was expressed in hepatocytes in the absence of Tetracycline, leading to hepatoma formation. When the mice were treated with tetracycline, TAg was not expressed and hepatomas did not form.

# data[].attributes.body.processed
Tetracycline-responsive transcriptional activator driven by the liver-specific mouse albumin promoter (Alb-tTA).

The E. Coli tetracycline operon regulatory system was used to generate a liver-specific transcription activation system that was inhibited by tetracycline. The transcription activator was a fused protein consisting of a tetracycline repressor gene (tetR) that was only active in the presence of tetracycline and a herpes simplex virus protein (VP-16) transcription activating domain. Transcription was induced only in the absence of tetracycline (Tet-Off). A liver-specific promoter such as mouse albumin determined that the tetracycline-regulated transcriptional activator (tTA) would be expressed specifically in liver. To study the effect of the transcription activator on a target gene (for example, Simian Virus 40 (SV4) large tumor (T) antigen (TAg)) specifically in liver, Alb-tTA mice were mated with transgenic mice in which the Target gene (TAg) was controlled by the E.Coli Tetracycline Operator (Tet-O). In this example, TAg was expressed in hepatocytes in the absence of Tetracycline, leading to hepatoma formation. When the mice were treated with tetracycline, TAg was not expressed and hepatomas did not form.

# data[].attributes.field_inventor_companies[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

# data[].attributes.field_licensingcontact_hrefs[]
carolyn.buller@nih.gov?subject=Web Inquiry on [TAB-2420] Alb-tTA (Tg(Alb1-tTA)3123Lng) Mouse Model for Liver Function Studies&body=Please send me information about technology [TAB-2420] Alb-tTA (Tg(Alb1-tTA)3123Lng) Mouse Model for Liver Function Studies.

# data[].attributes.field_licensingcontact_htmls[]
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts[].value
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
carolyn.buller@nih.gov?subject=Web Inquiry on [TAB-2420] Alb-tTA (Tg(Alb1-tTA)3123Lng) Mouse Model for Liver Function Studies&body=Please send me information about technology [TAB-2420] Alb-tTA (Tg(Alb1-tTA)3123Lng) Mouse Model for Liver Function Studies.

# data[].attributes.field_publications[].value
Manickan E, et al.

# data[].attributes.field_publications[].processed
Manickan E, et al.

# data[].attributes.field_technology_owners[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

# data[].attributes.title
MUP-tTA Mouse Model for Liver Function Studies

# data[].attributes.body.value
Tetracycline-responsive transcriptional activator driven by the liver-specific mouse major urinary protein promoter (MUP-tTA).

The E. Coli tetracycline operon regulatory system was used to generate a liver-specific transcription activation system that was inhibited by tetracycline. The transcription activator was a fused protein consisting of a tetracycline repressor gene (tetR) that was only active in the presence of tetracycline and a herpes simplex virus protein (VP-16) transcription activating domain (Tet-Off). Transcription was induced only in the absence of tetracycline (Tet-Off). A liver-specific promoter such as the mouse major urinary protein (MUP) promoter determined that the tetracycline-regulated transcriptional activator (tTA) would be expressed specifically in liver. To study the effect of the transcription activator on a target gene (for example, beta-galactosidase, LacZ) specifically in liver, MUP-tTA mice would be mated with transgenic mice in which the TAg Target gene was controlled by the E.Coli Tetracycline Operator (Tet-O). The Tet technology may require a separate license.

# data[].attributes.body.processed
Tetracycline-responsive transcriptional activator driven by the liver-specific mouse major urinary protein promoter (MUP-tTA).

The E. Coli tetracycline operon regulatory system was used to generate a liver-specific transcription activation system that was inhibited by tetracycline. The transcription activator was a fused protein consisting of a tetracycline repressor gene (tetR) that was only active in the presence of tetracycline and a herpes simplex virus protein (VP-16) transcription activating domain (Tet-Off). Transcription was induced only in the absence of tetracycline (Tet-Off). A liver-specific promoter such as the mouse major urinary protein (MUP) promoter determined that the tetracycline-regulated transcriptional activator (tTA) would be expressed specifically in liver. To study the effect of the transcription activator on a target gene (for example, beta-galactosidase, LacZ) specifically in liver, MUP-tTA mice would be mated with transgenic mice in which the TAg Target gene was controlled by the E.Coli Tetracycline Operator (Tet-O). The Tet technology may require a separate license.

# data[].attributes.field_inventor_companies[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

# data[].attributes.field_licensingcontact_hrefs[]
carolyn.buller@nih.gov?subject=Web Inquiry on [TAB-2421] MUP-tTA Mouse Model for Liver Function Studies&body=Please send me information about technology [TAB-2421] MUP-tTA Mouse Model for Liver Function Studies.

# data[].attributes.field_licensingcontact_htmls[]
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts[].value
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Buller, Carolyn
carolyn.buller@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
carolyn.buller@nih.gov?subject=Web Inquiry on [TAB-2421] MUP-tTA Mouse Model for Liver Function Studies&body=Please send me information about technology [TAB-2421] MUP-tTA Mouse Model for Liver Function Studies.

# data[].attributes.field_publications[].value
Manickan E, et al.

# data[].attributes.field_publications[].processed
Manickan E, et al.

# data[].attributes.field_technology_owners[]
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

# data[].attributes.title
Small Molecule Activators of Human Pyruvate Kinase for Treatment of Cancer and Enzyme-Deficient Hemolytic Anemia

# data[].attributes.body.value
NIH investigators have discovered a series of small compounds with the potential to treat a variety of cancers as well as hemolytic anemia. Contrary to most cancer medications, these molecules can be non-toxic to normal cells because they target a protein specific to the metabolic pathways in tumors, thus representing a significant clinical advantage over less-specific chemotherapeutics.

The invention described here is a series of small molecules that activate pyruvate kinase (PK) isoform M2. PK-M2 is a critical metabolic enzyme that is affected in all forms of cancer. Inactivation of PK-M2 leads to a buildup of metabolic intermediates inside the cell. Tumor cells require a buildup of metabolic intermediates in order to undergo rapid cell growth and proliferation. Hence, activation of PK-M2 in tumor cells may prevent the buildup of metabolic intermediates and thereby stall tumor cell proliferation or destroy the tumor cells. Further, while in normal adult cells only PK isoforms R, L, or M1 are active, in all tumors only PK-M2 is active. Therefore, PK-M2 activation would affect only tumor cells, and small-molecule PK-M2 activators are not expected to be toxic to healthy cells.

In addition, in patients with PK-R deficiency the buildup of metabolic intermediates in red blood cells ultimately leads to the loss of water from the cells and cell death. Small-molecule induced activation of PK-R in PK-deficient red blood cells may enhance vitality of these cells and decrease or eliminate enzyme-deficient hemolytic anemia in a patient.

# data[].attributes.body.processed
NIH investigators have discovered a series of small compounds with the potential to treat a variety of cancers as well as hemolytic anemia. Contrary to most cancer medications, these molecules can be non-toxic to normal cells because they target a protein specific to the metabolic pathways in tumors, thus representing a significant clinical advantage over less-specific chemotherapeutics.

The invention described here is a series of small molecules that activate pyruvate kinase (PK) isoform M2. PK-M2 is a critical metabolic enzyme that is affected in all forms of cancer. Inactivation of PK-M2 leads to a buildup of metabolic intermediates inside the cell. Tumor cells require a buildup of metabolic intermediates in order to undergo rapid cell growth and proliferation. Hence, activation of PK-M2 in tumor cells may prevent the buildup of metabolic intermediates and thereby stall tumor cell proliferation or destroy the tumor cells. Further, while in normal adult cells only PK isoforms R, L, or M1 are active, in all tumors only PK-M2 is active. Therefore, PK-M2 activation would affect only tumor cells, and small-molecule PK-M2 activators are not expected to be toxic to healthy cells.

In addition, in patients with PK-R deficiency the buildup of metabolic intermediates in red blood cells ultimately leads to the loss of water from the cells and cell death. Small-molecule induced activation of PK-R in PK-deficient red blood cells may enhance vitality of these cells and decrease or eliminate enzyme-deficient hemolytic anemia in a patient.

# data[].attributes.field_collaboration_description.value
The NIH Chemical Genomics Center is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize appropriate lead compounds described in U.S. Provisional Application No. 61/199,763. Please contact Dr. Craig J. Thomas via e-mail (craigt@nhgri.nih.gov) for more information.

# data[].attributes.field_collaboration_description.processed
The NIH Chemical Genomics Center is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize appropriate lead compounds described in U.S. Provisional Application No. 61/199,763. Please contact Dr. Craig J. Thomas via e-mail (craigt@nhgri.nih.gov) for more information.

# data[].attributes.field_commercial_applications.value
Therapeutic for cancer

Therapeutic for enzyme-deficient hemolytic anemia

# data[].attributes.field_commercial_applications.processed
Therapeutic for cancer

Therapeutic for enzyme-deficient hemolytic anemia

# data[].attributes.field_inventor_companies[]
National Human Genome Research Institute (NHGRI)

# data[].attributes.field_licensingcontact_hrefs[]
rebecca.erwin-cohen@nih.gov?subject=Web Inquiry on [TAB-1930] Small Molecule Activators of Human Pyruvate Kinase for Treatment of Cancer and Enzyme-Deficient Hemolytic Anemia&body=Please send me information about technology [TAB-1930] Small Molecule Activators of Human Pyruvate Kinase for Treatment of Cancer and Enzyme-Deficient Hemolytic Anemia.

# data[].attributes.field_licensingcontact_htmls[]
Erwin-Cohen, Rebecca
rebecca.erwin-cohen@nih.gov

# data[].attributes.field_licensing_contacts[].value
Erwin-Cohen, Rebecca
rebecca.erwin-cohen@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Erwin-Cohen, Rebecca
rebecca.erwin-cohen@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
rebecca.erwin-cohen@nih.gov?subject=Web Inquiry on [TAB-1930] Small Molecule Activators of Human Pyruvate Kinase for Treatment of Cancer and Enzyme-Deficient Hemolytic Anemia&body=Please send me information about technology [TAB-1930] Small Molecule Activators of Human Pyruvate Kinase for Treatment of Cancer and Enzyme-Deficient Hemolytic Anemia.

# data[].attributes.field_patents[].value
US
Provisional (PRV) 61/104,091
Filed on 2008-10-09
Status: Abandoned

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 61/104,091
Filed on 2008-10-09
Status: Abandoned

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2009/060237
Filed on 2009-10-09
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2009/060237
Filed on 2009-10-09
Status: Expired

# data[].attributes.field_patents[].value
US Patent 8,841,305
Filed on 2011-04-25
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 8,841,305
Filed on 2011-04-25
Status: Issued

# data[].attributes.field_patents[].value
US Patent 8,937,067
Filed on 2012-03-29
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 8,937,067
Filed on 2012-03-29
Status: Issued

# data[].attributes.field_patents[].value
US Patent 9,707,230
Filed on 2016-03-21
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 9,707,230
Filed on 2016-03-21
Status: Issued

# data[].attributes.field_patents[].value
US Patent 9,290,512
Filed on 2014-12-19
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 9,290,512
Filed on 2014-12-19
Status: Issued

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 61/104,091
Filed on 2008-10-09
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2009/060237
Filed on 2009-10-09
Status: Expired

# data[].attributes.field_patent_htmls[]
US Patent 8,841,305
Filed on 2011-04-25
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 8,937,067
Filed on 2012-03-29
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 9,707,230
Filed on 2016-03-21
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 9,290,512
Filed on 2014-12-19
Status: Issued

# data[].attributes.field_patent_titles[]
Activators Of Human Pyruvate Kinase M2 Receptor

# data[].attributes.field_technology_names[]
Small Molecule Activators Of Human Pyruvate Kinase

# data[].attributes.title
Pyruvate Kinase M2 Activators for the Treatment of Cancer

# data[].attributes.body.value
NIH investigators have discovered a series of small compounds with the potential to treat a variety of cancers as well as hemolytic anemia. Contrary to most cancer medications, these molecules can be non-toxic to normal cells because they target a protein specific to the metabolic pathways in tumors, thus representing a significant clinical advantage over less-specific chemotherapeutics.

The invention described here is a series of small molecules that activate pyruvate kinase (PK) isoform M2. PK-M2 is a critical metabolic enzyme that is affected in all forms of cancer. Inactivation of PK-M2 leads to a buildup of metabolic intermediates inside the cell. Tumor cells require a buildup of metabolic intermediates in order to undergo rapid cell growth and proliferation. Hence, activation of PK-M2 in tumor cells may prevent the buildup of metabolic intermediates and thereby stall tumor cell proliferation or destroy the tumor cells. Further, while in normal post-embryonic cells only PK isoforms R, L, or M1 are active, in all tumors only PK-M2 is active. So, PK-M2 activation would affect only tumor cells, and small-molecule PK-M2 activators may not be toxic to healthy cells.

This invention discloses the use of two new small molecule pharmacophores that can activate PKM2 through the allosteric site: 3-oxo-3,4-dihydro-2H-benzo [b] [1,4] oxazine-7-sulfonamides, and 2-oxo-1,2,3,4-tetrahydroquinoline-6-sulfonamides.

# data[].attributes.body.processed
NIH investigators have discovered a series of small compounds with the potential to treat a variety of cancers as well as hemolytic anemia. Contrary to most cancer medications, these molecules can be non-toxic to normal cells because they target a protein specific to the metabolic pathways in tumors, thus representing a significant clinical advantage over less-specific chemotherapeutics.

The invention described here is a series of small molecules that activate pyruvate kinase (PK) isoform M2. PK-M2 is a critical metabolic enzyme that is affected in all forms of cancer. Inactivation of PK-M2 leads to a buildup of metabolic intermediates inside the cell. Tumor cells require a buildup of metabolic intermediates in order to undergo rapid cell growth and proliferation. Hence, activation of PK-M2 in tumor cells may prevent the buildup of metabolic intermediates and thereby stall tumor cell proliferation or destroy the tumor cells. Further, while in normal post-embryonic cells only PK isoforms R, L, or M1 are active, in all tumors only PK-M2 is active. So, PK-M2 activation would affect only tumor cells, and small-molecule PK-M2 activators may not be toxic to healthy cells.

This invention discloses the use of two new small molecule pharmacophores that can activate PKM2 through the allosteric site: 3-oxo-3,4-dihydro-2H-benzo [b] [1,4] oxazine-7-sulfonamides, and 2-oxo-1,2,3,4-tetrahydroquinoline-6-sulfonamides.

# data[].attributes.field_collaboration_description.value
The National Center for Advancing Translational Sciences is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize these pyruvate kinase M2 activators. Please contact Dr. Matthew Boxer at boxerm@mail.nih.gov for more information.

# data[].attributes.field_collaboration_description.processed
The National Center for Advancing Translational Sciences is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize these pyruvate kinase M2 activators. Please contact Dr. Matthew Boxer at boxerm@mail.nih.gov for more information.

# data[].attributes.field_commercial_applications.value
Therapeutic developments for various cancers

Diagnostic assays for various cancers

Regulation of embryonic stem cell proliferation

# data[].attributes.field_commercial_applications.processed
Therapeutic developments for various cancers

Diagnostic assays for various cancers

Regulation of embryonic stem cell proliferation

# data[].attributes.field_competitive_advantages.value
Small molecule (series of analogs can be derived in search of improved performance)

Target a select group of cells (Cancerous cells)

# data[].attributes.field_competitive_advantages.processed
Small molecule (series of analogs can be derived in search of improved performance)

Target a select group of cells (Cancerous cells)

# data[].attributes.field_development_status.value
Early-stage

In vitro data available

# data[].attributes.field_development_status.processed
Early-stage

In vitro data available

# data[].attributes.field_inventor_companies[]
National Human Genome Research Institute (NHGRI)

# data[].attributes.field_inventor_companies[]
National Human Genome Research Institute (NHGRI)

# data[].attributes.field_inventor_companies[]
National Human Genome Research Institute (NHGRI)

# data[].attributes.field_inventor_companies[]
National Human Genome Research Institute (NHGRI)

# data[].attributes.field_licensingcontact_hrefs[]
rebecca.erwin-cohen@nih.gov?subject=Web Inquiry on [TAB-2202] Pyruvate Kinase M2 Activators for the Treatment of Cancer&body=Please send me information about technology [TAB-2202] Pyruvate Kinase M2 Activators for the Treatment of Cancer.

# data[].attributes.field_licensingcontact_htmls[]
Erwin-Cohen, Rebecca
rebecca.erwin-cohen@nih.gov

# data[].attributes.field_licensing_contacts[].value
Erwin-Cohen, Rebecca
rebecca.erwin-cohen@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Erwin-Cohen, Rebecca
rebecca.erwin-cohen@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
rebecca.erwin-cohen@nih.gov?subject=Web Inquiry on [TAB-2202] Pyruvate Kinase M2 Activators for the Treatment of Cancer&body=Please send me information about technology [TAB-2202] Pyruvate Kinase M2 Activators for the Treatment of Cancer.

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2011/033852
Filed on 2011-04-26
Status: Expired

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Patent Cooperation Treaty
(PCT) PCT/US2011/033852
Filed on 2011-04-26
Status: Expired

# data[].attributes.field_patents[].value
US
National Stage 13/643,594
Filed on 2012-10-26
Status: Abandoned

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US
National Stage 13/643,594
Filed on 2012-10-26
Status: Abandoned

# data[].attributes.field_patents[].value
US
Provisional (PRV) 61/329,158
Filed on 2010-04-29
Status: Abandoned

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US
Provisional (PRV) 61/329,158
Filed on 2010-04-29
Status: Abandoned

# data[].attributes.field_patents[].value
US Patent 9,708,267
Filed on 2015-03-10
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 9,708,267
Filed on 2015-03-10
Status: Issued

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2011/033852
Filed on 2011-04-26
Status: Expired

# data[].attributes.field_patent_htmls[]
US
National Stage 13/643,594
Filed on 2012-10-26
Status: Abandoned

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 61/329,158
Filed on 2010-04-29
Status: Abandoned

# data[].attributes.field_patent_htmls[]
US Patent 9,708,267
Filed on 2015-03-10
Status: Issued

# data[].attributes.field_publications[].value
Jiang JK, et al.

# data[].attributes.field_publications[].processed
Jiang JK, et al.

# data[].attributes.field_publications[].value
Boxer MB, et al.

# data[].attributes.field_publications[].processed
Boxer MB, et al.

# data[].attributes.title
Use of Acetalax for Treatment of Triple Negative Breast Cancer

# data[].attributes.body.value
Summary:

NCI seeks research co-development and/or potential licensees for a potential novel treatment for triple-negative breast cancer (TNBC) with acetalax (oxyphenisatin acetate).

Description of Technology:

Triple negative (progesterone receptor (PR)-, estrogen receptor (ER)-, human epidermal growth receptor 2 (HER2)-) breast cancer (TNBC) is an aggressive subtype that affects 15-20% of the 1.7 million cases of breast cancer occurring annually.  Currently, standard treatments of TNBC include cytotoxic chemotherapies, surgery, and radiation. However, TNBC readily becomes resistant to chemotherapy, and those with TNBC are more likely to have a recurrence or die within five years compared to those with other breast cancer types. Therefore, there is a need for safer and more effective TNBC treatments to improve patient outcomes.

Investigators from the National Cancer Institute (NCI) and collaborating institutions have identified the compound acetalax (oxyphenisatin acetate) as a promising potential therapy for TNBC. Strikingly, acetalax’s cytotoxic effect checked first against ~178 FDA-approved or clinical trial oncology drugs on the three TNBC against the NCI-60 panel of cancer cell lines – subsequently followed up using the 22 different TNBC cell lines checked against 15 oncology drugs – were significantly most cytotoxic.
Acetalax’s efficacy in vivo has been investigated using a TNBC patient-derived xenograft (PDX) mouse model. Untreated PDX mice exhibited a tumor volume doubling rate of approximately 7-8 days whereas acetalax-treated mice tumor volumes decreased to undetectable levels in approximately 13 days.

Potential Commercial Applications:

A therapeutic for Triple Negative Breast Cancer

Potential therapeutic for recalcitrant or estrogen-dependent cancers

Potential applicability to breast (non-Triple Negative), ovarian, pancreatic, sarcoma, and uterine cancers

Competitive Advantages:

Repurposed, previously approved FDA drug for a novel use as a therapeutic for TNBC and other cancers

Repurposed, previously approved drugs can have an expedited approval process due in part to pre-existing safety data

# data[].attributes.body.processed
Summary:

NCI seeks research co-development and/or potential licensees for a potential novel treatment for triple-negative breast cancer (TNBC) with acetalax (oxyphenisatin acetate).

Description of Technology:

Triple negative (progesterone receptor (PR)-, estrogen receptor (ER)-, human epidermal growth receptor 2 (HER2)-) breast cancer (TNBC) is an aggressive subtype that affects 15-20% of the 1.7 million cases of breast cancer occurring annually.  Currently, standard treatments of TNBC include cytotoxic chemotherapies, surgery, and radiation. However, TNBC readily becomes resistant to chemotherapy, and those with TNBC are more likely to have a recurrence or die within five years compared to those with other breast cancer types. Therefore, there is a need for safer and more effective TNBC treatments to improve patient outcomes.

Investigators from the National Cancer Institute (NCI) and collaborating institutions have identified the compound acetalax (oxyphenisatin acetate) as a promising potential therapy for TNBC. Strikingly, acetalax’s cytotoxic effect checked first against ~178 FDA-approved or clinical trial oncology drugs on the three TNBC against the NCI-60 panel of cancer cell lines – subsequently followed up using the 22 different TNBC cell lines checked against 15 oncology drugs – were significantly most cytotoxic.
Acetalax’s efficacy in vivo has been investigated using a TNBC patient-derived xenograft (PDX) mouse model. Untreated PDX mice exhibited a tumor volume doubling rate of approximately 7-8 days whereas acetalax-treated mice tumor volumes decreased to undetectable levels in approximately 13 days.

Potential Commercial Applications:

A therapeutic for Triple Negative Breast Cancer

Potential therapeutic for recalcitrant or estrogen-dependent cancers

Potential applicability to breast (non-Triple Negative), ovarian, pancreatic, sarcoma, and uterine cancers

Competitive Advantages:

Repurposed, previously approved FDA drug for a novel use as a therapeutic for TNBC and other cancers

Repurposed, previously approved drugs can have an expedited approval process due in part to pre-existing safety data

# data[].attributes.field_licensingcontact_hrefs[]
michaela.mccrary@nih.gov?subject=Web Inquiry on [TAB-4020] Use of Acetalax for Treatment of Triple Negative Breast Cancer&body=Please send me information about technology [TAB-4020] Use of Acetalax for Treatment of Triple Negative Breast Cancer.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
McCrary, Michaela
michaela.mccrary@nih.gov

# data[].attributes.field_licensing_contacts[].value
McCrary, Michaela
michaela.mccrary@nih.gov

# data[].attributes.field_licensing_contacts[].processed
McCrary, Michaela
michaela.mccrary@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
michaela.mccrary@nih.gov?subject=Web Inquiry on [TAB-4020] Use of Acetalax for Treatment of Triple Negative Breast Cancer&body=Please send me information about technology [TAB-4020] Use of Acetalax for Treatment of Triple Negative Breast Cancer.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 62/627,926
Filed on 2018-02-08
Status: Abandoned

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 62/627,926
Filed on 2018-02-08
Status: Abandoned

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2019/017239
Filed on 2019-02-08
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2019/017239
Filed on 2019-02-08
Status: Expired

# data[].attributes.field_patents[].value
European Patent
National Stage 19707221.8
Filed on 2019-02-08
Status: Issued

# data[].attributes.field_patents[].processed
European Patent
National Stage 19707221.8
Filed on 2019-02-08
Status: Issued

# data[].attributes.field_patents[].value
US
National Stage 16/967,472
Filed on 2020-08-05
Status: Pending

# data[].attributes.field_patents[].processed
US
National Stage 16/967,472
Filed on 2020-08-05
Status: Pending

# data[].attributes.field_patents[].value
US
Continuation (CON) None
Filed on None
Status: In Preparation

# data[].attributes.field_patents[].processed
US
Continuation (CON) None
Filed on None
Status: In Preparation

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 62/627,926
Filed on 2018-02-08
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2019/017239
Filed on 2019-02-08
Status: Expired

# data[].attributes.field_patent_htmls[]
European Patent
National Stage 19707221.8
Filed on 2019-02-08
Status: Issued

# data[].attributes.field_patent_htmls[]
US
National Stage 16/967,472
Filed on 2020-08-05
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Continuation (CON) None
Filed on None
Status: In Preparation

# data[].attributes.field_patent_titles[]
A METHOD OF TREATING TRIPLE-NEGATIVE BREAST CANCER

# data[].attributes.field_patent_titles[]
A METHOD OF TREATING TRIPLE-NEGATIVE BREAST CANCER

# data[].attributes.field_patent_titles[]
A METHOD OF TREATING TRIPLE-NEGATIVE BREAST CANCER

# data[].attributes.field_patent_titles[]
A METHOD OF TREATING TRIPLE-NEGATIVE BREAST CANCER

# data[].attributes.field_patent_titles[]
A METHOD OF TREATING TRIPLE-NEGATIVE BREAST CANCER

# data[].attributes.field_publications[].value
Rajapakse VN, et al. CellMinerCDB for Integrative Cross-Database Genomics and Pharmacogenomics Analyses of Cancer Cell Lines.

# data[].attributes.field_publications[].processed
Rajapakse VN, et al. CellMinerCDB for Integrative Cross-Database Genomics and Pharmacogenomics Analyses of Cancer Cell Lines.

# data[].attributes.field_technology_names[]
Use Of Acetalax For Treatment Of Triple Negative Breast Cancer.

# data[].attributes.field_technology_owners[]
Harvard Medical School, NCI, The Wellcome Trust Sanger Institute

# data[].attributes.title
Electrochemical Impedance Spectroscopy (EIS) Device to Resolve Individual Membrane Electrical Properties of Epithelial and Endothelial Tissues

# data[].attributes.body.value
Understanding the electrical properties of barrier tissues is crucial for deciphering their physiological functions and pathological conditions. These tissues, such as epithelial and endothelial layers, play critical roles in regulating the transport of ions, nutrients, and signaling molecules. By quantifying membrane-specific resistances, capacitances, and potentials, researchers gain valuable insights into epithelial development, barrier integrity, and disease progression.

However, current commercial setups fall short in providing comprehensive data, often oversimplifying complex electrical properties into a few parameters like trans-epithelial resistance (TER) and trans-epithelial potential (TEP). While some academic techniques exist for evaluating membrane-specific properties, they tend to be invasive or depend on chemical compound intervention. Additionally, these methods are often low-throughput and demand highly trained operators. These limitations hamper researchers' capability to obtain high-quality data for assessing epithelial cell health, maturation, and drug response.

Scientists at the NEI have developed a novel device to overcome these challenges by offering membrane-specific measurements in a non-invasive, high-throughput manner, rendering it a superior choice for researchers and clinicians. Utilizing Electrochemical Impedance Spectroscopy (EIS) measurements, they introduced a new technique to assess apical and basolateral electrical responses to stimuli, providing great insights into cell quality and function compared to existing commercial and academic approaches.

Advantages of Invention

Enables a non-invasive measurement into the electrical properties of barrier tissue membranes without using additional chemical perturbations.

Can be performed using low-cost hardware and software.

Does not require extensive training.

Potential Application

Assessment of electrical properties of epithelial tissue

Assessment of electrical properties of endothelial tissue

High-throughput drug screening assays

Long-term evaluation of epithelial or endothelial barrier development

# data[].attributes.body.processed
Understanding the electrical properties of barrier tissues is crucial for deciphering their physiological functions and pathological conditions. These tissues, such as epithelial and endothelial layers, play critical roles in regulating the transport of ions, nutrients, and signaling molecules. By quantifying membrane-specific resistances, capacitances, and potentials, researchers gain valuable insights into epithelial development, barrier integrity, and disease progression.

However, current commercial setups fall short in providing comprehensive data, often oversimplifying complex electrical properties into a few parameters like trans-epithelial resistance (TER) and trans-epithelial potential (TEP). While some academic techniques exist for evaluating membrane-specific properties, they tend to be invasive or depend on chemical compound intervention. Additionally, these methods are often low-throughput and demand highly trained operators. These limitations hamper researchers' capability to obtain high-quality data for assessing epithelial cell health, maturation, and drug response.

Scientists at the NEI have developed a novel device to overcome these challenges by offering membrane-specific measurements in a non-invasive, high-throughput manner, rendering it a superior choice for researchers and clinicians. Utilizing Electrochemical Impedance Spectroscopy (EIS) measurements, they introduced a new technique to assess apical and basolateral electrical responses to stimuli, providing great insights into cell quality and function compared to existing commercial and academic approaches.

Advantages of Invention

Enables a non-invasive measurement into the electrical properties of barrier tissue membranes without using additional chemical perturbations.

Can be performed using low-cost hardware and software.

Does not require extensive training.

Potential Application

Assessment of electrical properties of epithelial tissue

Assessment of electrical properties of endothelial tissue

High-throughput drug screening assays

Long-term evaluation of epithelial or endothelial barrier development

# data[].attributes.field_licensingcontact_hrefs[]
tedd.fenn@nih.gov?subject=Web Inquiry on [TAB-5142] Electrochemical Impedance Spectroscopy (EIS) Device to Resolve Individual Membrane Electrical Properties of Epithelial and Endothelial Tissues&body=Please send me information about technology [TAB-5142] Electrochemical Impedance Spectroscopy (EIS) Device to Resolve Individual Membrane Electrical Properties of Epithelial and Endothelial Tissues.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Fenn, Edward (Tedd)
tedd.fenn@nih.gov

# data[].attributes.field_licensing_contacts[].value
Fenn, Edward (Tedd)
tedd.fenn@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Fenn, Edward (Tedd)
tedd.fenn@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
tedd.fenn@nih.gov?subject=Web Inquiry on [TAB-5142] Electrochemical Impedance Spectroscopy (EIS) Device to Resolve Individual Membrane Electrical Properties of Epithelial and Endothelial Tissues&body=Please send me information about technology [TAB-5142] Electrochemical Impedance Spectroscopy (EIS) Device to Resolve Individual Membrane Electrical Properties of Epithelial and Endothelial Tissues.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/708,904
Filed on 2024-10-18
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/708,904
Filed on 2024-10-18
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/050192
Filed on 2025-10-09
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/050192
Filed on 2025-10-09
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/708,904
Filed on 2024-10-18
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/050192
Filed on 2025-10-09
Status: Pending

# data[].attributes.field_patent_titles[]
ELECTROCHEMICAL IMPEDANCE SPECTROSCOPY (EIS) DEVICE TO RESOLVE INDIVIDUAL MEMBRANE ELECTRICAL PROPERTIES OF EPITHELIAL AND ENDOTHELIAL TISSUES

# data[].attributes.field_patent_titles[]
ELECTROCHEMICAL IMPEDANCE SPECTROSCOPY (EIS) DEVICE TO RESOLVE INDIVIDUAL MEMBRANE ELECTRICAL PROPERTIES OF EPITHELIAL AND ENDOTHELIAL TISSUES

# data[].attributes.field_publications[].value
Lewallen CF, et al. A biologically validated mathematical model for decoding epithelial apical, basolateral, and paracellular electrical properties. (PMID: 37899750)

# data[].attributes.field_publications[].processed
Lewallen CF, et al. A biologically validated mathematical model for decoding epithelial apical, basolateral, and paracellular electrical properties. (PMID: 37899750)

# data[].attributes.field_technology_names[]
Electrochemical impedance spectroscopy (EIS) device to resolve individual membrane electrical properties of
epithelial/endothelial tissues

# data[].attributes.title
Electrochemical Impedance Spectroscopy (EIS) for Non-Destructive Assessment of Epithelial Integrity

# data[].attributes.body.value
This technology includes a novel apparatus and method that utilizes Electrochemical Impedance Spectroscopy (EIS) to assess the integrity of epithelial cell membranes non-destructively. By applying frequency-modulated voltage signals and facilitating fluid exchange on both sides of the epithelial tissue, this technology allows researchers to characterize membrane-specific responses with unprecedented accuracy. This advancement opens new avenues for drug discovery and evaluation of stem cell therapies, making it a vital tool for both academic and commercial research.

Potential Commercial Applications

Assessment of drug effects on epithelial cells in pharmaceutical research.

Standardized evaluation of stem cell therapies targeting epithelial tissues.

Research into epithelial physiology and pathology in various medical fields.

Competitive Advantages

Non-invasive technique that preserves tissue integrity, allowing for repeated measurements.

High-throughput capability enables faster drug discovery and evaluation processes.

Reduces reliance on traditional invasive methods, making it accessible to a broader range of researchers.

# data[].attributes.body.processed
This technology includes a novel apparatus and method that utilizes Electrochemical Impedance Spectroscopy (EIS) to assess the integrity of epithelial cell membranes non-destructively. By applying frequency-modulated voltage signals and facilitating fluid exchange on both sides of the epithelial tissue, this technology allows researchers to characterize membrane-specific responses with unprecedented accuracy. This advancement opens new avenues for drug discovery and evaluation of stem cell therapies, making it a vital tool for both academic and commercial research.

Potential Commercial Applications

Assessment of drug effects on epithelial cells in pharmaceutical research.

Standardized evaluation of stem cell therapies targeting epithelial tissues.

Research into epithelial physiology and pathology in various medical fields.

Competitive Advantages

Non-invasive technique that preserves tissue integrity, allowing for repeated measurements.

High-throughput capability enables faster drug discovery and evaluation processes.

Reduces reliance on traditional invasive methods, making it accessible to a broader range of researchers.

# data[].attributes.field_licensingcontact_htmls[]
Fenn, Edward (Tedd)
tedd.fenn@nih.gov

# data[].attributes.field_licensing_contacts[].value
Fenn, Edward (Tedd)
tedd.fenn@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Fenn, Edward (Tedd)
tedd.fenn@nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/479,798
Filed on 2023-01-13
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/479,798
Filed on 2023-01-13
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2024/011553
Filed on 2024-01-15
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2024/011553
Filed on 2024-01-15
Status: Expired

# data[].attributes.field_patents[].value
Canada
National Stage 3279965
Filed on 2025-07-14
Status: Pending

# data[].attributes.field_patents[].processed
Canada
National Stage 3279965
Filed on 2025-07-14
Status: Pending

# data[].attributes.field_patents[].value
United Kingdom
National Stage 2513195.4
Filed on 2025-08-13
Status: Pending

# data[].attributes.field_patents[].processed
United Kingdom
National Stage 2513195.4
Filed on 2025-08-13
Status: Pending

# data[].attributes.field_patents[].value
European Patent
National Stage 24705896.9
Filed on 2025-08-13
Status: Pending

# data[].attributes.field_patents[].processed
European Patent
National Stage 24705896.9
Filed on 2025-08-13
Status: Pending

# data[].attributes.field_patents[].value
US
Ordinary Patent (ORD) 18/412,842
Filed on 2024-01-15
Status: Pending

# data[].attributes.field_patents[].processed
US
Ordinary Patent (ORD) 18/412,842
Filed on 2024-01-15
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/479,798
Filed on 2023-01-13
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2024/011553
Filed on 2024-01-15
Status: Expired

# data[].attributes.field_patent_htmls[]
Canada
National Stage 3279965
Filed on 2025-07-14
Status: Pending

# data[].attributes.field_patent_htmls[]
United Kingdom
National Stage 2513195.4
Filed on 2025-08-13
Status: Pending

# data[].attributes.field_patent_htmls[]
European Patent
National Stage 24705896.9
Filed on 2025-08-13
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Ordinary Patent (ORD) 18/412,842
Filed on 2024-01-15
Status: Pending

# data[].attributes.field_patent_titles[]
APPARATUS AND METHOD FOR EXTRACELLULAR IMPEDANCE SPECTROSCOPY OF EPITHELIA

# data[].attributes.field_patent_titles[]
APPARATUS AND METHOD FOR EXTRACELLULAR IMPEDANCE SPECTROSCOPY OF EPITHELIA

# data[].attributes.field_patent_titles[]
APPARATUS AND METHOD FOR EXTRACELLULAR IMPEDANCE SPECTROSCOPY OF EPITHELIA

# data[].attributes.field_patent_titles[]
APPARATUS AND METHOD FOR EXTRACELLULAR IMPEDANCE SPECTROSCOPY OF EPITHELIA

# data[].attributes.field_patent_titles[]
APPARATUS AND METHOD FOR EXTRACELLULAR IMPEDANCE SPECTROSCOPY OF EPITHELIA

# data[].attributes.field_patent_titles[]
APPARATUS AND METHOD FOR EXTRACELLULAR IMPEDANCE SPECTROSCOPY OF EPITHELIA

# data[].attributes.field_technology_names[]
Using Electrochemical Impedance Spectroscopy (EIS) to determine epithelial integrity and cell membranes functional state

# data[].attributes.field_technology_owners[]
Georgia Institute of Technology, National Eye Institute (NEI), NIH - NEI

# data[].attributes.title
T Cell Receptors Targeting HPV 6 or HPV 11

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a collection of T cell receptors (TCRs) that specifically target HPV 6 or HPV 11 antigens.

Description of Technology:

Recurrent Respiratory Papillomatosis (RRP) and anogenital condyloma arise from chronic infection with human papillomavirus (HPV) 6 or 11. They can cause significant morbidity due to persistent papillomatous growths in the upper aerodigestive or anogenital tract. In RRP, lesions may obstruct the airway; leading to dysphonia, dyspnea, recurrent pneumonia, or pulmonary failure. In rare cases, it may progress to malignancy. Current treatment options for RRP include zopapogene imadenovec (Papzimeos), systemic bevacizumab, and repeated surgical debulking. Papzimeos can lead to durable responses in some patients but remains ineffective against pulmonary disease. Systemic bevacizumab can control disease, but prolonged use can lead to intolerable toxicities. Repeat surgical debulking causes cumulative surgical and anesthetic risks. Therefore, there remains a critical unmet need for safe and effective therapies for patients with aggressive or pulmonary RRP refractive to standard‑of‑care treatments.

Researchers at the National Cancer Institute (NCI) identified several T cell receptors (TCRs) with potential utility in adoptive cell therapy and other TCR-based approaches to treat HPV 6- or HPV 11-associated diseases, including RRP. These TCRs used engineered T cells derived from peripheral blood mononuclear cells (PBMCs), an easily accessible source of human immune cells. The engineered T cells demonstrated reproducible, antigen-specific recognition of multiple HPV 6 and HPV 11 proteins presented by diverse HLA class I subtypes. The inventors further showed that these TCR-engineered T cells effectively eliminated HPV 6/11-infected target cells. The results support the therapeutic potential of these TCRs for HPV-associated disease.

The NCI seeks research co-development partners and/or licensees to advance TCRs that specifically target HPV 6 or HPV 11 antigens. These TCRs have potential applications in the development of experimental cell-based immunotherapies and other TCR-based therapeutic platforms. Additional markets include diagnostics and research settings.

Potential Commercial Applications:

Treatment and diagnosis of recurrent respiratory papillomatosis (RRP) and other premalignant and nonmalignant conditions

Adoptive cell therapy

TCR-based therapy

Combination therapy

Treatment and diagnosis of additional HPV 6- or HPV 11-associated diseases and chronic infections

Adoptive cell therapy

TCR-based therapy

Combination therapy

Competitive Advantages:

Novel adoptive cell therapies, either as monotherapies or in combination with other therapeutic modalities

Promising freedom to practice as part of a comprehensive intellectual property portfolio for RRP therapeutics and diagnostics

Established FDA regulatory precedent for TCR-based therapeutics

Opportunity to qualify for regulatory incentives for rare diseases, including: orphan drug designation, priority review, and breakthrough therapy designation

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a collection of T cell receptors (TCRs) that specifically target HPV 6 or HPV 11 antigens.

Description of Technology:

Recurrent Respiratory Papillomatosis (RRP) and anogenital condyloma arise from chronic infection with human papillomavirus (HPV) 6 or 11. They can cause significant morbidity due to persistent papillomatous growths in the upper aerodigestive or anogenital tract. In RRP, lesions may obstruct the airway; leading to dysphonia, dyspnea, recurrent pneumonia, or pulmonary failure. In rare cases, it may progress to malignancy. Current treatment options for RRP include zopapogene imadenovec (Papzimeos), systemic bevacizumab, and repeated surgical debulking. Papzimeos can lead to durable responses in some patients but remains ineffective against pulmonary disease. Systemic bevacizumab can control disease, but prolonged use can lead to intolerable toxicities. Repeat surgical debulking causes cumulative surgical and anesthetic risks. Therefore, there remains a critical unmet need for safe and effective therapies for patients with aggressive or pulmonary RRP refractive to standard‑of‑care treatments.

Researchers at the National Cancer Institute (NCI) identified several T cell receptors (TCRs) with potential utility in adoptive cell therapy and other TCR-based approaches to treat HPV 6- or HPV 11-associated diseases, including RRP. These TCRs used engineered T cells derived from peripheral blood mononuclear cells (PBMCs), an easily accessible source of human immune cells. The engineered T cells demonstrated reproducible, antigen-specific recognition of multiple HPV 6 and HPV 11 proteins presented by diverse HLA class I subtypes. The inventors further showed that these TCR-engineered T cells effectively eliminated HPV 6/11-infected target cells. The results support the therapeutic potential of these TCRs for HPV-associated disease.

The NCI seeks research co-development partners and/or licensees to advance TCRs that specifically target HPV 6 or HPV 11 antigens. These TCRs have potential applications in the development of experimental cell-based immunotherapies and other TCR-based therapeutic platforms. Additional markets include diagnostics and research settings.

Potential Commercial Applications:

Treatment and diagnosis of recurrent respiratory papillomatosis (RRP) and other premalignant and nonmalignant conditions

Adoptive cell therapy

TCR-based therapy

Combination therapy

Treatment and diagnosis of additional HPV 6- or HPV 11-associated diseases and chronic infections

Adoptive cell therapy

TCR-based therapy

Combination therapy

Competitive Advantages:

Novel adoptive cell therapies, either as monotherapies or in combination with other therapeutic modalities

Promising freedom to practice as part of a comprehensive intellectual property portfolio for RRP therapeutics and diagnostics

Established FDA regulatory precedent for TCR-based therapeutics

Opportunity to qualify for regulatory incentives for rare diseases, including: orphan drug designation, priority review, and breakthrough therapy designation

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for a collection of T-cell receptors (TCRs) that specifically target HPV 6 or HPV 11 antigens.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for a collection of T-cell receptors (TCRs) that specifically target HPV 6 or HPV 11 antigens.

# data[].attributes.field_licensingcontact_hrefs[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5143] T Cell Receptors Targeting HPV 6 or HPV 11&body=Please send me information about technology [TAB-5143] T Cell Receptors Targeting HPV 6 or HPV 11.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].value
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5143] T Cell Receptors Targeting HPV 6 or HPV 11&body=Please send me information about technology [TAB-5143] T Cell Receptors Targeting HPV 6 or HPV 11.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 64/026,093
Filed on 2026-04-02
Status: Pending

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US
Provisional (PRV) 64/026,093
Filed on 2026-04-02
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 64/026,093
Filed on 2026-04-02
Status: Pending

# data[].attributes.field_patent_titles[]
T CELL RECEPTORS TARGETING HPV 6 OR HPV 11

# data[].attributes.field_related_inventions[].processed
E-143-2024-0

# data[].attributes.field_related_inventions[].processed
E-019-2025-0

# data[].attributes.field_technology_names[]
Discovery of a library of TCRs specific for T cell antigens from HPV 6 or 11

# data[].attributes.field_technology_owners[]
Center for Immuno-Oncology, National Institute on Deafness and Other Communication Disorders (NIDCD), NIH - NCI, Surgical Oncology Program

# data[].attributes.title
Matched Patient-Derived 3D Isocitrate Dehydrogenase (IDH)-Mutant Glioma Cell Lines for Modeling Malignant Transformation

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks licensees for matched patient-derived 3D Isocitrate Dehydrogenase (IDH)-mutant glioma cell lines, 403L and 403H, generated from the same patient before and after malignant transformation from WHO grade 2 to WHO grade 4 disease. This research material provides an opportunity to study IDH-mutant glioma progression, temozolomide-associated hypermutation, invasion, metabolism, and treatment resistance.

Description of Technology:

IDH-mutant gliomas often begin as lower-grade tumors but remain incurable and frequently progress to higher-grade disease through malignant transformation. This is clinically important but difficult to study because matched low-grade and high-grade tumor materials from the same patient are rare. Further, fixed tumor specimens are limited for repeated mechanistic or drug-response experiments.

Researchers at the National Cancer Institute (NCI) developed a matched pair of patient-derived cell models, 403L and 403H, from the same patient before and after malignant transformation. 403L was established from a WHO grade 2 IDH-mutant astrocytoma. 403H was derived from the recurrent WHO grade 4 tumor following radiation and temozolomide treatment. Both cell lines: (1) grow as 3D spheroids, (2) retain endogenous IDH1 R132H expression, and (3) were authenticated to the patient's germline by short tandem repeat (STR) profiling (100% match for 403L; 93.33% match for 403H).

The high-grade 403H line shows increased invasive behavior, temozolomide-associated hypermutation (tumor mutational burden of 70.07/Mb vs. 3.96/Mb in 403L), upregulated epithelial-mesenchymal transition (EMT) signaling (whereas Notch signaling is enriched in 403L), and changes in glioma-associated metabolism, including 2-hydroxyglutarate (2-HG), glutamine, fatty acid metabolism, and lactate/pyruvate flux. Furthermore, 403H showed significantly greater 3D invasion than 403L (p<0.0001). 403H formed infiltrative high-grade glioma in 4 of 5 orthotopically xenografted NSG mice. In contrast, 403L did not form tumors within 18 months.

Researchers at NCI seek licensees interested in using these cell lines as research tools for neuro-oncology studies. The models may be useful for studying IDH-mutant glioma progression, malignant transformation, tumor recurrence, treatment resistance, and preclinical response to IDH-targeted, DNA damage response, metabolic, or combination therapies.

Potential Commercial Applications:

Development of cancer therapeutics targeting IDH-mutant gliomas, including:

IDH inhibitors

DNA damage response agents

Metabolic drugs

Modeling of tumor evolution, recurrence, and temozolomide-associated hypermutation

Development of novel assays for glioma invasion, metabolism, and drug screening

Preclinical screening tool for IDH-targeted, DNA damage response, metabolic, or combination therapies

Comparative profiling of molecular, epigenetic, and metabolomic differences between low-grade and transformed gliomas

Competitive Advantages:

Minimized genetic background variability

Unique clinical model of the temozolomide-associated hypermutator phenotype and acquired treatment resistance

Stable 3D tumor spheroids provide a unique model retaining endogenous IDH1 R132H expression and grade-specific stem and lineage markers (SOX2, NESTIN, GFAP, OLIG2, beta 3-Tubulin)

Distinct functional models permitting the comparative interrogation of in vitro invasion and in vivo tumorigenicity

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks licensees for matched patient-derived 3D Isocitrate Dehydrogenase (IDH)-mutant glioma cell lines, 403L and 403H, generated from the same patient before and after malignant transformation from WHO grade 2 to WHO grade 4 disease. This research material provides an opportunity to study IDH-mutant glioma progression, temozolomide-associated hypermutation, invasion, metabolism, and treatment resistance.

Description of Technology:

IDH-mutant gliomas often begin as lower-grade tumors but remain incurable and frequently progress to higher-grade disease through malignant transformation. This is clinically important but difficult to study because matched low-grade and high-grade tumor materials from the same patient are rare. Further, fixed tumor specimens are limited for repeated mechanistic or drug-response experiments.

Researchers at the National Cancer Institute (NCI) developed a matched pair of patient-derived cell models, 403L and 403H, from the same patient before and after malignant transformation. 403L was established from a WHO grade 2 IDH-mutant astrocytoma. 403H was derived from the recurrent WHO grade 4 tumor following radiation and temozolomide treatment. Both cell lines: (1) grow as 3D spheroids, (2) retain endogenous IDH1 R132H expression, and (3) were authenticated to the patient's germline by short tandem repeat (STR) profiling (100% match for 403L; 93.33% match for 403H).

The high-grade 403H line shows increased invasive behavior, temozolomide-associated hypermutation (tumor mutational burden of 70.07/Mb vs. 3.96/Mb in 403L), upregulated epithelial-mesenchymal transition (EMT) signaling (whereas Notch signaling is enriched in 403L), and changes in glioma-associated metabolism, including 2-hydroxyglutarate (2-HG), glutamine, fatty acid metabolism, and lactate/pyruvate flux. Furthermore, 403H showed significantly greater 3D invasion than 403L (p<0.0001). 403H formed infiltrative high-grade glioma in 4 of 5 orthotopically xenografted NSG mice. In contrast, 403L did not form tumors within 18 months.

Researchers at NCI seek licensees interested in using these cell lines as research tools for neuro-oncology studies. The models may be useful for studying IDH-mutant glioma progression, malignant transformation, tumor recurrence, treatment resistance, and preclinical response to IDH-targeted, DNA damage response, metabolic, or combination therapies.

Potential Commercial Applications:

Development of cancer therapeutics targeting IDH-mutant gliomas, including:

IDH inhibitors

DNA damage response agents

Metabolic drugs

Modeling of tumor evolution, recurrence, and temozolomide-associated hypermutation

Development of novel assays for glioma invasion, metabolism, and drug screening

Preclinical screening tool for IDH-targeted, DNA damage response, metabolic, or combination therapies

Comparative profiling of molecular, epigenetic, and metabolomic differences between low-grade and transformed gliomas

Competitive Advantages:

Minimized genetic background variability

Unique clinical model of the temozolomide-associated hypermutator phenotype and acquired treatment resistance

Stable 3D tumor spheroids provide a unique model retaining endogenous IDH1 R132H expression and grade-specific stem and lineage markers (SOX2, NESTIN, GFAP, OLIG2, beta 3-Tubulin)

Distinct functional models permitting the comparative interrogation of in vitro invasion and in vivo tumorigenicity

# data[].attributes.field_collaboration_description.value
Researchers at NCI seek licensees interested in using these cell lines as research tools for neuro-oncology studies.

# data[].attributes.field_collaboration_description.processed
Researchers at NCI seek licensees interested in using these cell lines as research tools for neuro-oncology studies.

# data[].attributes.field_licensingcontact_hrefs[]
michael.pollack@nih.gov?subject=Web Inquiry on [TAB-5144] Matched Patient-Derived 3D Isocitrate Dehydrogenase (IDH)-Mutant Glioma Cell Lines for Modeling Malignant Transformation&body=Please send me information about technology [TAB-5144] Matched Patient-Derived 3D Isocitrate Dehydrogenase (IDH)-Mutant Glioma Cell Lines for Modeling Malignant Transformation.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Pollack, Michael
michael.pollack@nih.gov

# data[].attributes.field_licensing_contacts[].value
Pollack, Michael
michael.pollack@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Pollack, Michael
michael.pollack@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
michael.pollack@nih.gov?subject=Web Inquiry on [TAB-5144] Matched Patient-Derived 3D Isocitrate Dehydrogenase (IDH)-Mutant Glioma Cell Lines for Modeling Malignant Transformation&body=Please send me information about technology [TAB-5144] Matched Patient-Derived 3D Isocitrate Dehydrogenase (IDH)-Mutant Glioma Cell Lines for Modeling Malignant Transformation.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_publications[].value
Kim O, et al. A patient-derived cell model for malignant transformation in IDH-mutant glioma. (PMID: 39256867).

# data[].attributes.field_publications[].processed
Kim O, et al. A patient-derived cell model for malignant transformation in IDH-mutant glioma. (PMID: 39256867).

# data[].attributes.field_technology_names[]
403L and 403H, Patient-Derived 3D IDH-Mutant Glioma Cell Lines for Studying Malignant Transformation

# data[].attributes.title
Selective Expansion of Engineered TCR-T Cells for Use in Adoptive Cell Immunotherapy

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks capable licensees interested in commercializing T cell receptor (TCR)-engineered T cells expressing murine/human hybrid receptors.

Description of Technology:

TCR-T therapies, particularly those targeting patient-specific neoantigens, remain a promising approach to the treatment metastatic cancers. Contemporary gene engineering techniques permit both the targeted integration of the exogenous receptor(s) and further genetic manipulation of the host cells to enhance persistence and performance following adoptive transfer (e.g., through disruption of immune checkpoints such as CISH or PD1). However, these techniques often suffer from low transduction efficiencies and may result in the generation of infusion products with sub-optimal percentages of targeted cells.

NCI scientists designed a new method that enables the selective expansion of T lymphocytes, under GMP conditions, that have been engineered to stably express a murine-human hybrid TCR. These hybrid TCRs consist of human variable regions and murine constant regions. The inventive approach uses irradiated feeder cells and an anti-mouse TCR beta constant region antibody (e.g., H57) to provide stimulation, enabling the specific activation and expansion of T cells transduced with the hybrid TCRs. Critically, replacement of the OKT3 activating antibody from the standard rapid expansion protocol with one specific for the TCR murine constant region prevents the outgrowth of non-transduced cells. Consequently, the new method produces a cell population highly enriched for the desired engineered cells.

NCI seeks to market this method, which is analogous to an antigen-specific stimulation of the T cell, to companies interested in developing personalized ACT.

Potential Commercial Applications:

Enables the GMP production of personalized T cell therapy products targeting tumor specific mutations with a high percentage of engineered cells

Competitive Advantages:

Increased therapeutic benefit due to enhanced persistence and performance following adoptive T cell transfer

Increased therapeutic benefit due to improved surface expression of the therapeutic TCR αβ

TCR alpha/beta chains substantially eliminate the risk of mis-pairing with the endogenous alpha/beta chain sequences expressed by the host cell

Improved manufacturing since the population is highly enriched for the desired engineered cells

Greatly increases the frequency of tumor-specific T cells following expansion, exceeding what is achieved using alternative methods to generate mutation- or tumor-specific T cells

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks capable licensees interested in commercializing T cell receptor (TCR)-engineered T cells expressing murine/human hybrid receptors.

Description of Technology:

TCR-T therapies, particularly those targeting patient-specific neoantigens, remain a promising approach to the treatment metastatic cancers. Contemporary gene engineering techniques permit both the targeted integration of the exogenous receptor(s) and further genetic manipulation of the host cells to enhance persistence and performance following adoptive transfer (e.g., through disruption of immune checkpoints such as CISH or PD1). However, these techniques often suffer from low transduction efficiencies and may result in the generation of infusion products with sub-optimal percentages of targeted cells.

NCI scientists designed a new method that enables the selective expansion of T lymphocytes, under GMP conditions, that have been engineered to stably express a murine-human hybrid TCR. These hybrid TCRs consist of human variable regions and murine constant regions. The inventive approach uses irradiated feeder cells and an anti-mouse TCR beta constant region antibody (e.g., H57) to provide stimulation, enabling the specific activation and expansion of T cells transduced with the hybrid TCRs. Critically, replacement of the OKT3 activating antibody from the standard rapid expansion protocol with one specific for the TCR murine constant region prevents the outgrowth of non-transduced cells. Consequently, the new method produces a cell population highly enriched for the desired engineered cells.

NCI seeks to market this method, which is analogous to an antigen-specific stimulation of the T cell, to companies interested in developing personalized ACT.

Potential Commercial Applications:

Enables the GMP production of personalized T cell therapy products targeting tumor specific mutations with a high percentage of engineered cells

Competitive Advantages:

Increased therapeutic benefit due to enhanced persistence and performance following adoptive T cell transfer

Increased therapeutic benefit due to improved surface expression of the therapeutic TCR αβ

TCR alpha/beta chains substantially eliminate the risk of mis-pairing with the endogenous alpha/beta chain sequences expressed by the host cell

Improved manufacturing since the population is highly enriched for the desired engineered cells

Greatly increases the frequency of tumor-specific T cells following expansion, exceeding what is achieved using alternative methods to generate mutation- or tumor-specific T cells

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing for TCR-engineered T cells that will facilitate the ACT process.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing for TCR-engineered T cells that will facilitate the ACT process.

# data[].attributes.field_licensingcontact_hrefs[]
burkear@nih.gov?subject=Web Inquiry on [TAB-5074] Selective Expansion of Engineered TCR-T Cells for Use in Adoptive Cell Immunotherapy&body=Please send me information about technology [TAB-5074] Selective Expansion of Engineered TCR-T Cells for Use in Adoptive Cell Immunotherapy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts[].value
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
burkear@nih.gov?subject=Web Inquiry on [TAB-5074] Selective Expansion of Engineered TCR-T Cells for Use in Adoptive Cell Immunotherapy&body=Please send me information about technology [TAB-5074] Selective Expansion of Engineered TCR-T Cells for Use in Adoptive Cell Immunotherapy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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Status: Abandoned

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Filed on 2018-09-24
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National Stage 201880076862.9
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China
National Stage 201880076862.9
Filed on 2018-09-24
Status: Issued

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European Patent
National Stage 18786145.5
Filed on 2020-05-05
Status: Issued

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European Patent
National Stage 18786145.5
Filed on 2020-05-05
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National Stage 273698
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National Stage 10-2020-7012314
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National Stage 11202003112Q
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US Patent 12,227,554
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European patent (EP) 62020020943.0
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Filed on 2023-07-17
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Divisional (DIV) 23185846.5
Filed on 2023-07-17
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European patent (EP) 18786145.5
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European patent (EP) 18786145.5
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European patent (EP) 18786145.5
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European patent (EP) 18786145.5
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European patent (EP) 18786145.5
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Divisional (DIV) 10202302822Q
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National Stage 2018345400
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National Stage 3077595
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National Stage 201880076862.9
Filed on 2018-09-24
Status: Issued

# data[].attributes.field_patent_htmls[]
European Patent
National Stage 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
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National Stage 273698
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National Stage 2020-519092
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National Stage 10-2020-7012314
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National Stage 11202003112Q
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US Patent 12,227,554
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European patent (EP) 62020020943.0
Filed on 2020-11-26
Status: Issued

# data[].attributes.field_patent_htmls[]
European Patent
Divisional (DIV) 23185846.5
Filed on 2023-07-17
Status: Pending

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Spain
European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
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European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
France
European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
Italy
European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
Germany
European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
United Kingdom
European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
Switzerland
European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
Norway
European patent (EP) 18786145.5
Filed on 2020-05-05
Status: Issued

# data[].attributes.field_patent_htmls[]
Singapore
Divisional (DIV) 10202302822Q
Filed on 2023-10-03
Status: Pending

# data[].attributes.field_patent_htmls[]
Japan
Divisional (DIV) 2023-220106
Filed on 2023-12-26
Status: Issued

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_patent_titles[]
METHODS FOR SELECTIVELY EXPANDING CELLS EXPRESSING A TCR WITH A MURINE CONSTANT REGION

# data[].attributes.field_publications[].value
Parkhurst M, et al. Adoptive transfer of personalized neoantigen-reactive TCR-transduced T cells in metastatic colorectal cancer: phase 2 trial interim results. (PMID 38992)

# data[].attributes.field_publications[].processed
Parkhurst M, et al. Adoptive transfer of personalized neoantigen-reactive TCR-transduced T cells in metastatic colorectal cancer: phase 2 trial interim results. (PMID 38992)

# data[].attributes.field_publications[].value
Kim SP, et al. Adoptive cellular therapy with autologous tumor-infiltrating lymphocytes and T-cell receptor-engineered T cells targeting common p53 neoantigens in human solid tumors. (PMID 35749374)

# data[].attributes.field_publications[].processed
Kim SP, et al. Adoptive cellular therapy with autologous tumor-infiltrating lymphocytes and T-cell receptor-engineered T cells targeting common p53 neoantigens in human solid tumors. (PMID 35749374)

# data[].attributes.field_publications[].value
Lowery FL, et al. Molecular signatures of antitumor neoantigen-reactive T cells from metastatic human cancers. (PMID 35113651)

# data[].attributes.field_publications[].processed
Lowery FL, et al. Molecular signatures of antitumor neoantigen-reactive T cells from metastatic human cancers. (PMID 35113651)

# data[].attributes.field_technology_names[]
Sorting And/or Selective Expansion Of T Lymphocytes For Use In Adoptive Cell Immunotherapy.

# data[].attributes.title
Chimeric VLP vaccines to Prevent HTLV-1 Infection

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for Chimeric VLP Vaccines to Prevent HTLV-1 Infection.

Description of Technology:

There is currently no approved vaccine to prevent human T-cell leukemia virus type I (HTLV-1) infection, a highly oncogenic virus linked to serious diseases like adult T-cell leukemia/lymphoma (ATLL) and Tropical Spastic paraparesis /HTLV-1-Associated Myelopathy (HAM/TSP). Existing interventions are limited to behavioral prevention, leaving millions at risk, especially in underserved global regions. A safe and effective vaccine is urgently needed to fill this critical public health gap.

This invention is a nucleic acid-based vaccine that generates virus-like particles (VLPs) in the body using HTLV-1 Env and gag proteins to trigger a protective immune response against HTLV-1 infection. With no approved vaccines available and millions at risk—particularly in underserved regions—this first-of-its-kind solution addresses a critical public health need. It offers broad protection across HTLV-1 subtypes and is currently being tested in non-human primates, with strong potential for future clinical development and commercial interest.

Potential Commercial Applications:

HTLV-1 Infection

Adult T-cell leukemia/lymphoma (ATLL)

Tropical Spastic paraparesis /HTLV-1-Associated Myelopathy (HAM/TSP)

Competitive Advantages:

No approved HTLV-1 vaccines

Preventative vaccine to reduce healthcare costs and economic burden of treating people developing related diseases

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for Chimeric VLP Vaccines to Prevent HTLV-1 Infection.

Description of Technology:

There is currently no approved vaccine to prevent human T-cell leukemia virus type I (HTLV-1) infection, a highly oncogenic virus linked to serious diseases like adult T-cell leukemia/lymphoma (ATLL) and Tropical Spastic paraparesis /HTLV-1-Associated Myelopathy (HAM/TSP). Existing interventions are limited to behavioral prevention, leaving millions at risk, especially in underserved global regions. A safe and effective vaccine is urgently needed to fill this critical public health gap.

This invention is a nucleic acid-based vaccine that generates virus-like particles (VLPs) in the body using HTLV-1 Env and gag proteins to trigger a protective immune response against HTLV-1 infection. With no approved vaccines available and millions at risk—particularly in underserved regions—this first-of-its-kind solution addresses a critical public health need. It offers broad protection across HTLV-1 subtypes and is currently being tested in non-human primates, with strong potential for future clinical development and commercial interest.

Potential Commercial Applications:

HTLV-1 Infection

Adult T-cell leukemia/lymphoma (ATLL)

Tropical Spastic paraparesis /HTLV-1-Associated Myelopathy (HAM/TSP)

Competitive Advantages:

No approved HTLV-1 vaccines

Preventative vaccine to reduce healthcare costs and economic burden of treating people developing related diseases

# data[].attributes.field_collaboration_description.value
The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for development of a nucleic acid-based vaccine for use as a preventative to human T-lymphotrophic virus-1 (HTLV-1) infection.

# data[].attributes.field_collaboration_description.processed
The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for development of a nucleic acid-based vaccine for use as a preventative to human T-lymphotrophic virus-1 (HTLV-1) infection.

# data[].attributes.field_licensingcontact_hrefs[]
diptadip.dattaroy@nih.gov?subject=Web Inquiry on [TAB-5069] Chimeric VLP vaccines to Prevent HTLV-1 Infection&body=Please send me information about technology [TAB-5069] Chimeric VLP vaccines to Prevent HTLV-1 Infection.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts[].value
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
diptadip.dattaroy@nih.gov?subject=Web Inquiry on [TAB-5069] Chimeric VLP vaccines to Prevent HTLV-1 Infection&body=Please send me information about technology [TAB-5069] Chimeric VLP vaccines to Prevent HTLV-1 Infection.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/340,400
Filed on 2022-05-10
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/340,400
Filed on 2022-05-10
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2023/066839
Filed on 2023-05-10
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2023/066839
Filed on 2023-05-10
Status: Expired

# data[].attributes.field_patents[].value
Australia
National Stage 2023268543
Filed on 2024-11-14
Status: Pending

# data[].attributes.field_patents[].processed
Australia
National Stage 2023268543
Filed on 2024-11-14
Status: Pending

# data[].attributes.field_patents[].value
India
National Stage 202417088469
Filed on 2024-11-15
Status: Pending

# data[].attributes.field_patents[].processed
India
National Stage 202417088469
Filed on 2024-11-15
Status: Pending

# data[].attributes.field_patents[].value
US
National Stage 18/864,213
Filed on 2024-11-08
Status: Pending

# data[].attributes.field_patents[].processed
US
National Stage 18/864,213
Filed on 2024-11-08
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/340,400
Filed on 2022-05-10
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2023/066839
Filed on 2023-05-10
Status: Expired

# data[].attributes.field_patent_htmls[]
Australia
National Stage 2023268543
Filed on 2024-11-14
Status: Pending

# data[].attributes.field_patent_htmls[]
India
National Stage 202417088469
Filed on 2024-11-15
Status: Pending

# data[].attributes.field_patent_htmls[]
US
National Stage 18/864,213
Filed on 2024-11-08
Status: Pending

# data[].attributes.field_patent_titles[]
VACCINE FOR HUMAN T-LYMPHOTROPIC VIRUS-1

# data[].attributes.field_patent_titles[]
VACCINE FOR HUMAN T-LYMPHOTROPIC VIRUS-1

# data[].attributes.field_patent_titles[]
VACCINE FOR HUMAN T-LYMPHOTROPIC VIRUS-1

# data[].attributes.field_patent_titles[]
VACCINE FOR HUMAN T-LYMPHOTROPIC VIRUS-1

# data[].attributes.field_patent_titles[]
VACCINE FOR HUMAN T-LYMPHOTROPIC VIRUS-1

# data[].attributes.field_publications[].value
Franchini G, et al. HTLV-1 and HTLV-2: Pathogenesis and role of viral proteins. Viruses. 2022;14(10):2084.

# data[].attributes.field_publications[].processed
Franchini G, et al. HTLV-1 and HTLV-2: Pathogenesis and role of viral proteins. Viruses. 2022;14(10):2084.

# data[].attributes.field_technology_names[]
Chimeric VLP Vaccines To Prevent HTLV-1 Infection

# data[].attributes.title
Method of Detecting Circulating Cell-Free HPV 6 and 11 DNA in Patients Afflicted With Diseases Caused by Chronic HPV 6 or 11 Infection and Use Thereof

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) and Frederick National Laboratory for Cancer Research (FNLCR) seek research co-development partners and/or licensees for commercial development of a novel liquid biopsy diagnostic for non-invasive detection of cell-free HPV 6 and 11 DNA for recurrent respiratory papillomatosis (RRP).

Description of Technology:

Recurrent respiratory papillomatosis (RRP), caused by chronic infection with human papillomavirus (HPV) types 6 and 11, is a rare but potentially fatal disease characterized by the growth of papillomas throughout the respiratory tract. While HPV 6/11 infections are common, affecting approximately 40% of U.S. adults, a subset of patients can develop a range of conditions from benign papillomas to dysplasia and invasive cancers. Current treatment for RRP typically involves repetitive surgical intervention or laser ablation to alleviate symptoms, which carries significant procedural risks. A recent breakthrough with a therapeutic HPV vaccine demonstrated that 51% of patients avoided surgery for at least a year, with some experiencing durable remission. However, there remains no reliable diagnostic tool to confirm viral clearance or guide systemic therapy decisions.

Researchers at the NCI and FNLCR have developed a novel hybridization-based next-generation sequencing (NGS) liquid biopsy method to detect circulating cell-free HPV 6 and 11 DNA in the plasma of patients with RRP. This innovative approach uses the established relevance of circulating viral DNA as a valuable biomarker for disease monitoring and therapeutic decision-making in other virally-associated conditions. The method is designed to target multiple regions across the entire HPV 6 and 11 genomes. It employs a pull-down DNA technology to enhance coverage – overcoming limitations of fixed-primer PCR for small cell-free DNA fragments. While low-risk HPV-associated diseases like RRP exhibit less tumor cell turnover compared to advanced cancers, the inherent high vascularity of papillomas may facilitate the release of viral DNA into peripheral blood. This method offers a non-invasive, sensitive and potentially prognostic tool to aid in (1) diagnosis, (2) monitoring progression and (3) guiding systemic therapies such as HPV vaccination or predicting severity – including pulmonary risk.

Investigators at the NCI and FNLCR continue to evaluate circulating HPV 6 and 11 DNA in patients previously treated in clinical trials to further assess its prognostic and predictive capabilities. This technology presents a compelling opportunity for commercial development and seamless integration into existing diagnostic platforms. NCI and FNLCR offer licensing and collaborative development opportunities to advance this critical diagnostic and prognostic tool for RRP.

Potential Commercial Applications:

Liquid biopsy diagnostic for RRP confirmation

Monitoring RRP disease progression

Prognostic test for RRP severity, especially pulmonary disease

Companion diagnostic to guide systemic RRP therapies

HPV 6/11 detection assay for anogenital condyloma

Competitive Advantages:

Non-invasive, sensitive and potentially prognostic and diagnostic tool

Reduces the need for, and risk from, repeat surgical procedures

Detects disease even with a Derkay score of 0 (minimal laryngeal involvement)

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) and Frederick National Laboratory for Cancer Research (FNLCR) seek research co-development partners and/or licensees for commercial development of a novel liquid biopsy diagnostic for non-invasive detection of cell-free HPV 6 and 11 DNA for recurrent respiratory papillomatosis (RRP).

Description of Technology:

Recurrent respiratory papillomatosis (RRP), caused by chronic infection with human papillomavirus (HPV) types 6 and 11, is a rare but potentially fatal disease characterized by the growth of papillomas throughout the respiratory tract. While HPV 6/11 infections are common, affecting approximately 40% of U.S. adults, a subset of patients can develop a range of conditions from benign papillomas to dysplasia and invasive cancers. Current treatment for RRP typically involves repetitive surgical intervention or laser ablation to alleviate symptoms, which carries significant procedural risks. A recent breakthrough with a therapeutic HPV vaccine demonstrated that 51% of patients avoided surgery for at least a year, with some experiencing durable remission. However, there remains no reliable diagnostic tool to confirm viral clearance or guide systemic therapy decisions.

Researchers at the NCI and FNLCR have developed a novel hybridization-based next-generation sequencing (NGS) liquid biopsy method to detect circulating cell-free HPV 6 and 11 DNA in the plasma of patients with RRP. This innovative approach uses the established relevance of circulating viral DNA as a valuable biomarker for disease monitoring and therapeutic decision-making in other virally-associated conditions. The method is designed to target multiple regions across the entire HPV 6 and 11 genomes. It employs a pull-down DNA technology to enhance coverage – overcoming limitations of fixed-primer PCR for small cell-free DNA fragments. While low-risk HPV-associated diseases like RRP exhibit less tumor cell turnover compared to advanced cancers, the inherent high vascularity of papillomas may facilitate the release of viral DNA into peripheral blood. This method offers a non-invasive, sensitive and potentially prognostic tool to aid in (1) diagnosis, (2) monitoring progression and (3) guiding systemic therapies such as HPV vaccination or predicting severity – including pulmonary risk.

Investigators at the NCI and FNLCR continue to evaluate circulating HPV 6 and 11 DNA in patients previously treated in clinical trials to further assess its prognostic and predictive capabilities. This technology presents a compelling opportunity for commercial development and seamless integration into existing diagnostic platforms. NCI and FNLCR offer licensing and collaborative development opportunities to advance this critical diagnostic and prognostic tool for RRP.

Potential Commercial Applications:

Liquid biopsy diagnostic for RRP confirmation

Monitoring RRP disease progression

Prognostic test for RRP severity, especially pulmonary disease

Companion diagnostic to guide systemic RRP therapies

HPV 6/11 detection assay for anogenital condyloma

Competitive Advantages:

Non-invasive, sensitive and potentially prognostic and diagnostic tool

Reduces the need for, and risk from, repeat surgical procedures

Detects disease even with a Derkay score of 0 (minimal laryngeal involvement)

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for commercial development of a novel liquid biopsy diagnostic for non-invasive detection of cell-free HPV 6 and 11 DNA for Recurrent Respiratory Papillomatosis (RRP).

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for commercial development of a novel liquid biopsy diagnostic for non-invasive detection of cell-free HPV 6 and 11 DNA for Recurrent Respiratory Papillomatosis (RRP).

# data[].attributes.field_licensingcontact_hrefs[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5071] Method of Detecting Circulating Cell-Free HPV 6 and 11 DNA in Patients Afflicted With Diseases Caused by Chronic HPV 6 or 11 Infection and Use Thereof&body=Please send me information about technology [TAB-5071] Method of Detecting Circulating Cell-Free HPV 6 and 11 DNA in Patients Afflicted With Diseases Caused by Chronic HPV 6 or 11 Infection and Use Thereof.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].value
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5071] Method of Detecting Circulating Cell-Free HPV 6 and 11 DNA in Patients Afflicted With Diseases Caused by Chronic HPV 6 or 11 Infection and Use Thereof&body=Please send me information about technology [TAB-5071] Method of Detecting Circulating Cell-Free HPV 6 and 11 DNA in Patients Afflicted With Diseases Caused by Chronic HPV 6 or 11 Infection and Use Thereof.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/803,323
Filed on 2025-05-09
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/803,323
Filed on 2025-05-09
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2026/027273
Filed on 2026-05-08
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2026/027273
Filed on 2026-05-08
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/803,323
Filed on 2025-05-09
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2026/027273
Filed on 2026-05-08
Status: Pending

# data[].attributes.field_patent_titles[]
METHODS OF DETECTING CIRCULATING CELL-FREE HPV 6 AND HPV 11 DNA IN LIQUID BIOPSIES

# data[].attributes.field_patent_titles[]
METHODS OF DETECTING CIRCULATING CELL-FREE HPV 6 AND HPV 11 DNA IN LIQUID BIOPSIES

# data[].attributes.field_publications[].value
Norberg SM, et al. PRGN-2012 gene therapy in adults with recurrent respiratory papillomatosis: a pivotal phase 1/2 clinical trial. (PMID 39855244)

# data[].attributes.field_publications[].processed
Norberg SM, et al. PRGN-2012 gene therapy in adults with recurrent respiratory papillomatosis: a pivotal phase 1/2 clinical trial. (PMID 39855244)

# data[].attributes.field_technology_names[]
Method of detecting circulating cell-free HPV 6 and 11 DNA in patients afflicted with disease caused by chronic HPV 6 or 11 infection and use thereof (LBR# 25-004)
(LBR Greater Rights Requested)

# data[].attributes.title
Establishment and characterization of the A 1847 human ovarian carcinoma line

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks licensees for a tumorigenic cell line, A1847, from a patient with metastatic ovarian cancer. As a BRCA1 deficient cell line, it serves as a model to researchers studying cell cycle regulation, tumor suppression and effective drugs aiding in repair of DNA damage.

Description of Technology:

Mutations, such as loss of function, in the BRCA1 gene increase the risk of developing ovarian cancer. In its early stages, ovarian cancer may not cause any definitive symptoms but can rapidly progress within a year to advanced stage. This metastatic growth can occur by shedding cancerous cells into peritoneal fluid, often associated with epithelial ovarian cancer, its most common type. While treatments exist, it is limited by the development of drug resistance that is not succumbed to damage in cell death.

The National Cancer Institute (NCI) researchers derived a metastatic ovarian carcinoma cell line, A1847, from a 50-year-old female. It was established as a continuous tumorigenic cell line and characterized by isozyme phenotype, short tandem repeat (STR) analysis and karyotypically with modal number 68 and 3 marker chromosomes. This cell line may be used to identify therapeutic targets and to screen drug candidates against ovarian cancer.

NCI is seeking parties to nonexclusively license the A1847 human ovarian carcinoma cell line.

Potential Commercial Applications:

Tool to conduct preclinical proof-of-concept studies required for commercial development of anti-cancer agents and targeted therapies in ovarian cancer

Research model to investigate epithelial ovarian cancer

Research model for mechanistic studies of ovarian cancer and BRCA1-deficient tumors

Competitive Advantages:

Well-characterized metastatic ovarian cancer cell line

Tumorigenic cell line to generate animal models of metastatic ovarian cancer for commercial and research development

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks licensees for a tumorigenic cell line, A1847, from a patient with metastatic ovarian cancer. As a BRCA1 deficient cell line, it serves as a model to researchers studying cell cycle regulation, tumor suppression and effective drugs aiding in repair of DNA damage.

Description of Technology:

Mutations, such as loss of function, in the BRCA1 gene increase the risk of developing ovarian cancer. In its early stages, ovarian cancer may not cause any definitive symptoms but can rapidly progress within a year to advanced stage. This metastatic growth can occur by shedding cancerous cells into peritoneal fluid, often associated with epithelial ovarian cancer, its most common type. While treatments exist, it is limited by the development of drug resistance that is not succumbed to damage in cell death.

The National Cancer Institute (NCI) researchers derived a metastatic ovarian carcinoma cell line, A1847, from a 50-year-old female. It was established as a continuous tumorigenic cell line and characterized by isozyme phenotype, short tandem repeat (STR) analysis and karyotypically with modal number 68 and 3 marker chromosomes. This cell line may be used to identify therapeutic targets and to screen drug candidates against ovarian cancer.

NCI is seeking parties to nonexclusively license the A1847 human ovarian carcinoma cell line.

Potential Commercial Applications:

Tool to conduct preclinical proof-of-concept studies required for commercial development of anti-cancer agents and targeted therapies in ovarian cancer

Research model to investigate epithelial ovarian cancer

Research model for mechanistic studies of ovarian cancer and BRCA1-deficient tumors

Competitive Advantages:

Well-characterized metastatic ovarian cancer cell line

Tumorigenic cell line to generate animal models of metastatic ovarian cancer for commercial and research development

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing for the A1847 ovarian cancer cell line.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing for the A1847 ovarian cancer cell line.

# data[].attributes.field_licensingcontact_hrefs[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5060] Establishment and characterization of the A 1847 human ovarian carcinoma line&body=Please send me information about technology [TAB-5060] Establishment and characterization of the A 1847 human ovarian carcinoma line.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].value
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5060] Establishment and characterization of the A 1847 human ovarian carcinoma line&body=Please send me information about technology [TAB-5060] Establishment and characterization of the A 1847 human ovarian carcinoma line.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_publications[].value
Standing, D., et al. Selective targeting of IRAK1 attenuates low molecular weight hyaluronic acid-induced stemness and non-canonical STAT3 activation in epithelial ovarian cancer. (PMID 38796478)

# data[].attributes.field_publications[].processed
Standing, D., et al. Selective targeting of IRAK1 attenuates low molecular weight hyaluronic acid-induced stemness and non-canonical STAT3 activation in epithelial ovarian cancer. (PMID 38796478)

# data[].attributes.field_publications[].value
Sethi, G., et al. An RNA interference lethality screen of the human druggable genome to identify molecular vulnerabilities in epithelial ovarian cancer. (PMID 23056589)

# data[].attributes.field_publications[].processed
Sethi, G., et al. An RNA interference lethality screen of the human druggable genome to identify molecular vulnerabilities in epithelial ovarian cancer. (PMID 23056589)

# data[].attributes.field_publications[].value
Godwin, A.K., et al. High resistance to cisplatin in human ovarian cancer cell lines is associated with marked increase of glutathione synthesis. (PMID 1348364)

# data[].attributes.field_publications[].processed
Godwin, A.K., et al. High resistance to cisplatin in human ovarian cancer cell lines is associated with marked increase of glutathione synthesis. (PMID 1348364)

# data[].attributes.field_related_inventions[].processed
E-018-2020-0

# data[].attributes.field_technology_names[]
Establishment and characterization of the A 1847 human ovarian carcinoma line

# data[].attributes.title
Compositions and Methods for Producing Dendritic Cell-based Vaccines with Enhanced Efficacy

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) is seeking research co-development partners and/or licensees for NCI’s compositions and methods to enhance the efficacy of dendritic cell (DC)-based cancer vaccines.

Description of Technology:

Current dendritic cell (DC)-based cancer vaccines are limited by impaired DC function due to cancer-driven lipid imbalances and other immunosuppressive factors reducing vaccine effectiveness. To address this issue, NCI has generated dendritic cells in the presence of omega-3 fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) and their derivatives, or specialized pro-resolving lipid mediators, to restore and enhance the dendritic cells’ antigen-presenting function and anti-tumor efficacy. This approach could significantly improve the potency of DC-based cancer vaccines, offering a promising strategy to overcome a major limitation in current cancer immunotherapies. NCI is actively continuing development of this technology and seeks licensing and/or collaboration partners to support further preclinical validation and potential clinical translation.

Potential Commercial Applications:

Cancer immunotherapy

Development of human DC vaccines

Formulations involving omega-3 fatty acids or pro-resolving lipids

Competitive Advantages:

Production of DCs with enhanced antigen-presenting function, anti-tumor efficacy and potency

Significant tumor reduction and improved survival compared in animals compared with wild-type DCs

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) is seeking research co-development partners and/or licensees for NCI’s compositions and methods to enhance the efficacy of dendritic cell (DC)-based cancer vaccines.

Description of Technology:

Current dendritic cell (DC)-based cancer vaccines are limited by impaired DC function due to cancer-driven lipid imbalances and other immunosuppressive factors reducing vaccine effectiveness. To address this issue, NCI has generated dendritic cells in the presence of omega-3 fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) and their derivatives, or specialized pro-resolving lipid mediators, to restore and enhance the dendritic cells’ antigen-presenting function and anti-tumor efficacy. This approach could significantly improve the potency of DC-based cancer vaccines, offering a promising strategy to overcome a major limitation in current cancer immunotherapies. NCI is actively continuing development of this technology and seeks licensing and/or collaboration partners to support further preclinical validation and potential clinical translation.

Potential Commercial Applications:

Cancer immunotherapy

Development of human DC vaccines

Formulations involving omega-3 fatty acids or pro-resolving lipids

Competitive Advantages:

Production of DCs with enhanced antigen-presenting function, anti-tumor efficacy and potency

Significant tumor reduction and improved survival compared in animals compared with wild-type DCs

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for the development of NCI’s compositions and methods to enhance the efficacy of dendritic cell (DC)-based cancer vaccines by using omega-3 fatty acids or pro-resolving lipid mediators.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for the development of NCI’s compositions and methods to enhance the efficacy of dendritic cell (DC)-based cancer vaccines by using omega-3 fatty acids or pro-resolving lipid mediators.

# data[].attributes.field_licensingcontact_hrefs[]
diptadip.dattaroy@nih.gov?subject=Web Inquiry on [TAB-5066] Compositions and Methods for Producing Dendritic Cell-based Vaccines with Enhanced Efficacy&body=Please send me information about technology [TAB-5066] Compositions and Methods for Producing Dendritic Cell-based Vaccines with Enhanced Efficacy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts[].value
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Dattaroy, Diptadip
diptadip.dattaroy@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
diptadip.dattaroy@nih.gov?subject=Web Inquiry on [TAB-5066] Compositions and Methods for Producing Dendritic Cell-based Vaccines with Enhanced Efficacy&body=Please send me information about technology [TAB-5066] Compositions and Methods for Producing Dendritic Cell-based Vaccines with Enhanced Efficacy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/586,629
Filed on 2023-09-29
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/586,629
Filed on 2023-09-29
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2024/049057
Filed on 2024-09-27
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2024/049057
Filed on 2024-09-27
Status: Expired

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/586,629
Filed on 2023-09-29
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2024/049057
Filed on 2024-09-27
Status: Expired

# data[].attributes.field_patent_titles[]
COMPOSITIONS AND METHODS FOR PRODUCING DENDRITIC CELL-BASED VACCINES WITH ENHANCED EFFICACY

# data[].attributes.field_patent_titles[]
COMPOSITIONS AND METHODS FOR PRODUCING DENDRITIC CELL-BASED VACCINES WITH ENHANCED EFFICACY

# data[].attributes.field_publications[].value
Tiwary, S., "Endogenously high Omega-3 levels lead to a less suppressive tumor microenvironment."

# data[].attributes.field_publications[].processed
Tiwary, S., "Endogenously high Omega-3 levels lead to a less suppressive tumor microenvironment."

# data[].attributes.field_publications[].value
Tiwary, S., K. Hsu, K. C. Goldfarbmuren, Z. Xia, and J. A. Berzofsky.  High levels of endogenous omega-3 fatty acids prolong the lifespan, promote antigen presentation, and improve DC-based cancer vaccine efficacy in mice. 2025.  Cancer Immunology Research, in press.

# data[].attributes.field_publications[].processed
Tiwary, S., K. Hsu, K. C. Goldfarbmuren, Z. Xia, and J. A. Berzofsky.  High levels of endogenous omega-3 fatty acids prolong the lifespan, promote antigen presentation, and improve DC-based cancer vaccine efficacy in mice. 2025.  Cancer Immunology Research, in press.

# data[].attributes.field_technology_names[]
Improving the efficacy of dendric cell-based cancer vaccines by DHA treatment

# data[].attributes.title
A conserved viral peptide for use in cancer immunotherapy

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for viral peptide (CE1)-based therapeutics for HCC prevention and treatment.

Description of Technology:

Hepatocellular carcinoma (HCC) is a common and aggressive primary liver cancer. It develops mainly from at-risk individuals with underlying chronic liver diseases, such as hepatitis and cirrhosis. HCC is a leading cause of cancer-related death worldwide and its global incidence and mortality rate continues to rise. The current methods for early detection, surveillance and treatment are suboptimal due to complex etiologies and intricate tumor biology.

Through serological profiling across three independent cohorts, researchers at the National Cancer Institute (NCI) have identified a common epitope (CE1) shared among protective viral antigens enriched in healthy individuals compared to HCC patients. A synthetic CE1 peptide was demonstrated to have utility in eliciting a T cell response to HCC cells and can be developed as an immunotherapy for HCC, such as a CE1-based HCC vaccine. Currently, as there are limited therapeutic options for HCC patients, novel treatments would offer tremendous commercial and public health benefits.

Potential Commercial Applications:

HCC prevention and treatment

Predictive biomarker for HCC risk

Serological response test

Patient stratification for CE1-based therapy

Monitoring the efficacy of the CE1-based vaccine

Competitive Advantages:

VirScan data support that this peptide correlates with better outcomes in HCC and breast cancer

CE1 peptide shows an immunomodulatory effect; immunomodulators are a promising approach to cancer treatment

CE1 peptide is biologically active in inducing T cell cytolytic activity

HCC cell killing in an HLA-specific manner

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for viral peptide (CE1)-based therapeutics for HCC prevention and treatment.

Description of Technology:

Hepatocellular carcinoma (HCC) is a common and aggressive primary liver cancer. It develops mainly from at-risk individuals with underlying chronic liver diseases, such as hepatitis and cirrhosis. HCC is a leading cause of cancer-related death worldwide and its global incidence and mortality rate continues to rise. The current methods for early detection, surveillance and treatment are suboptimal due to complex etiologies and intricate tumor biology.

Through serological profiling across three independent cohorts, researchers at the National Cancer Institute (NCI) have identified a common epitope (CE1) shared among protective viral antigens enriched in healthy individuals compared to HCC patients. A synthetic CE1 peptide was demonstrated to have utility in eliciting a T cell response to HCC cells and can be developed as an immunotherapy for HCC, such as a CE1-based HCC vaccine. Currently, as there are limited therapeutic options for HCC patients, novel treatments would offer tremendous commercial and public health benefits.

Potential Commercial Applications:

HCC prevention and treatment

Predictive biomarker for HCC risk

Serological response test

Patient stratification for CE1-based therapy

Monitoring the efficacy of the CE1-based vaccine

Competitive Advantages:

VirScan data support that this peptide correlates with better outcomes in HCC and breast cancer

CE1 peptide shows an immunomodulatory effect; immunomodulators are a promising approach to cancer treatment

CE1 peptide is biologically active in inducing T cell cytolytic activity

HCC cell killing in an HLA-specific manner

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations  for viral peptide (CE1)-based therapeutics for HCC prevention and treatment

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations  for viral peptide (CE1)-based therapeutics for HCC prevention and treatment

# data[].attributes.field_licensingcontact_hrefs[]
changke@mail.nih.gov?subject=Web Inquiry on [TAB-5067] A conserved viral peptide for use in cancer immunotherapy&body=Please send me information about technology [TAB-5067] A conserved viral peptide for use in cancer immunotherapy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Chang, Kevin
changke@mail.nih.gov

# data[].attributes.field_licensing_contacts[].value
Chang, Kevin
changke@mail.nih.gov

# data[].attributes.field_licensing_contacts[].processed
Chang, Kevin
changke@mail.nih.gov

# data[].attributes.field_licensing_contacts_uris[]
changke@mail.nih.gov?subject=Web Inquiry on [TAB-5067] A conserved viral peptide for use in cancer immunotherapy&body=Please send me information about technology [TAB-5067] A conserved viral peptide for use in cancer immunotherapy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/735,040
Filed on 2024-12-17
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/735,040
Filed on 2024-12-17
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/059785
Filed on 2025-12-16
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/059785
Filed on 2025-12-16
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/735,040
Filed on 2024-12-17
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/059785
Filed on 2025-12-16
Status: Pending

# data[].attributes.field_patent_titles[]
VIRUS ANTIGEN-DERIVED IMMUNOGENIC PEPTIDES AND THEIR USE FOR THE PREVENTION AND TREATMENT OF HEPATOCELLULAR CARCINOMA

# data[].attributes.field_patent_titles[]
VIRUS ANTIGEN-DERIVED IMMUNOGENIC PEPTIDES AND THEIR USE FOR THE EARLY INTERVENTION AND TREATMENT OF LIVER CANCER

# data[].attributes.field_publications[].value
Ma L, et al. Beneficial infections of the enterovirus genus in patients with liver cancer. (PMID: 40345802)

# data[].attributes.field_publications[].processed
Ma L, et al. Beneficial infections of the enterovirus genus in patients with liver cancer. (PMID: 40345802)

# data[].attributes.field_related_inventions[].processed
E-171-2022

# data[].attributes.field_related_inventions[].processed
E-174-2019

# data[].attributes.field_technology_names[]
A conserved viral peptide for use in cancer immunotherapy

# data[].attributes.title
T Cell Receptor Targeting HPV6 E2 and a Panel of Cos7 Cells Expressing Different HLA Class I Proteins for Use in Validation and Potency Studies

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks licensees for this invention comprising (1) a novel T cell receptor (TCR) specific to the E2 protein of Human papillomavirus (HPV) type 6  in the context of the human leukocyte antigen, HLA-B55, and (2) a panel of Cos7 cells expressing different HLA proteins for validation of T cell responses in immunotherapies for low-risk HPV-related diseases such as recurrent respiratory papillomatosis and anogenital condyloma.

Description of Technology:

Chronic infections with low-risk HPV types 6 and 11 can lead to such diseases as recurrent respiratory papillomatosis and anogenital condyloma. Such diseases can lower quality of life considerably, expose patients to repeated invasive procedures (such as surgery) and are often recurrent and unresponsive to standard treatments. There are few targeted treatments in development against these diseases. Therefore, there may be a need for reliable research tools to test the potency of targeted treatments, particularly immunotherapies, prior to the product’s release for patient use.

The researchers at the National Cancer Institute (NCI) identified a novel T cell receptor (TCR) specific for an antigen derived from HPV6 E2, restricted to HLA-B55. This TCR was reconstructed with a mouse constant region for tracking in donor T cells and may be used in potency testing and release assays of vaccines and other immunotherapies that target HPV6.

The NCI seeks licensees for the research-use TCR and the panel of Cos7 cells. This invention offers a unique opportunity for developing new TCR-based therapies and validation tools for HPV-related diseases.

Potential Commercial Applications:

Research materials to support therapeutic or diagnostic development against HPV-related diseases

Potency testing and other release assays of HPV 6-containing immunotherapy products

Competitive Advantages:

Unique TCR and cell line panel to validate T cell responses in immunotherapies for low-risk HPV-related diseases such as recurrent respiratory papillomatosis and anogenital condyloma

Superior tools – together or separately – in release assays for HPV 6-targeting immunotherapy products

Unique tools for lot release assays for low- or high-risk HPV-targeting immunotherapy products

Unique tools for lot release, stability and comparability studies

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks licensees for this invention comprising (1) a novel T cell receptor (TCR) specific to the E2 protein of Human papillomavirus (HPV) type 6  in the context of the human leukocyte antigen, HLA-B55, and (2) a panel of Cos7 cells expressing different HLA proteins for validation of T cell responses in immunotherapies for low-risk HPV-related diseases such as recurrent respiratory papillomatosis and anogenital condyloma.

Description of Technology:

Chronic infections with low-risk HPV types 6 and 11 can lead to such diseases as recurrent respiratory papillomatosis and anogenital condyloma. Such diseases can lower quality of life considerably, expose patients to repeated invasive procedures (such as surgery) and are often recurrent and unresponsive to standard treatments. There are few targeted treatments in development against these diseases. Therefore, there may be a need for reliable research tools to test the potency of targeted treatments, particularly immunotherapies, prior to the product’s release for patient use.

The researchers at the National Cancer Institute (NCI) identified a novel T cell receptor (TCR) specific for an antigen derived from HPV6 E2, restricted to HLA-B55. This TCR was reconstructed with a mouse constant region for tracking in donor T cells and may be used in potency testing and release assays of vaccines and other immunotherapies that target HPV6.

The NCI seeks licensees for the research-use TCR and the panel of Cos7 cells. This invention offers a unique opportunity for developing new TCR-based therapies and validation tools for HPV-related diseases.

Potential Commercial Applications:

Research materials to support therapeutic or diagnostic development against HPV-related diseases

Potency testing and other release assays of HPV 6-containing immunotherapy products

Competitive Advantages:

Unique TCR and cell line panel to validate T cell responses in immunotherapies for low-risk HPV-related diseases such as recurrent respiratory papillomatosis and anogenital condyloma

Superior tools – together or separately – in release assays for HPV 6-targeting immunotherapy products

Unique tools for lot release assays for low- or high-risk HPV-targeting immunotherapy products

Unique tools for lot release, stability and comparability studies

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing for this invention that comprises a novel T cell receptor (TCR) targeting HPV6 E2 in the context of HLA-B55 and a panel of Cos7 cells expressing different Class I human leukocyte antigen (HLA) proteins, that may be used in development of validation and potency assays for vaccines and other therapies designed to induce HPV6-specific T cell responses.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing for this invention that comprises a novel T cell receptor (TCR) targeting HPV6 E2 in the context of HLA-B55 and a panel of Cos7 cells expressing different Class I human leukocyte antigen (HLA) proteins, that may be used in development of validation and potency assays for vaccines and other therapies designed to induce HPV6-specific T cell responses.

# data[].attributes.field_licensingcontact_hrefs[]
zehra.sherwani@nih.gov?subject=Web Inquiry on [TAB-5068] T Cell Receptor Targeting HPV6 E2 and a Panel of Cos7 Cells Expressing Different HLA Class I Proteins for Use in Validation and Potency Studies&body=Please send me information about technology [TAB-5068] T Cell Receptor Targeting HPV6 E2 and a Panel of Cos7 Cells Expressing Different HLA Class I Proteins for Use in Validation and Potency Studies.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Sherwani, Zehra
zehra.sherwani@nih.gov

# data[].attributes.field_licensing_contacts[].value
Sherwani, Zehra
zehra.sherwani@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Sherwani, Zehra
zehra.sherwani@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
zehra.sherwani@nih.gov?subject=Web Inquiry on [TAB-5068] T Cell Receptor Targeting HPV6 E2 and a Panel of Cos7 Cells Expressing Different HLA Class I Proteins for Use in Validation and Potency Studies&body=Please send me information about technology [TAB-5068] T Cell Receptor Targeting HPV6 E2 and a Panel of Cos7 Cells Expressing Different HLA Class I Proteins for Use in Validation and Potency Studies.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_publications[].value
Bai K, Norberg SM, Sievers C, Meyer T, et al. Durable response in a patient with recurrent respiratory papillomatosis treated with immune checkpoint blockade. Case Reports Head Neck. 2022 Oct;44(10):E31-E37. doi: 10.1002/hed.27144.

# data[].attributes.field_publications[].processed
Bai K, Norberg SM, Sievers C, Meyer T, et al. Durable response in a patient with recurrent respiratory papillomatosis treated with immune checkpoint blockade. Case Reports Head Neck. 2022 Oct;44(10):E31-E37. doi: 10.1002/hed.27144.

# data[].attributes.field_technology_names[]
Discovery of a T cell receptor targeting an antigen derived from HPV6 E2 and a panel of Cos7 cells expressing different HLA class I
proteins

# data[].attributes.title
Method of Manufacturing Papilloma Infiltrating Lymphocyte (PIL) Cell Therapy Products as a Treatment for Patients with Chronic Viral Infection(s)

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for development of papilloma-infiltrating lymphocytes (PIL) as treatment for patients with chronic human papillomavirus (HPV) 6 or 11 infections.

Description of Technology:

Recurrent Respiratory Papillomatosis (RRP) and anogenital condyloma are caused by chronic infection with human papillomavirus (HPV) types 6 or 11. These conditions lead to the development of papillomatous growths in different regions of the body – RRP affects the upper aerodigestive tract, while condylomas involve the anogenital area. In RRP, growths in the aerodigestive tract can cause dysphonia, dyspnea, and, in severe cases, airway obstruction, which may lead to recurrent pneumonia or respiratory failure.

Current treatment for RRP primarily involves repeated surgical debulking or laser ablation to manage symptoms. However, the virus often persists in a latent state, resulting in continual papilloma regrowth. The need for frequent procedures exposes patients to cumulative anesthetic and surgical risks, emotional distress, and significantly diminished quality of life. Despite progress in localized treatments such as surgery and laser ablation, there are no approved systemic therapies for chronic HPV 6 or 11-related conditions. This highlights a clear unmet need for effective, curative therapy options.

Researchers at the National Cancer Institute (NCI) have developed a novel adoptive cell therapy approach to target conditions driven by HPV types 6 or 11. They have successfully identified and preferentially expanded HPV 6 and/or 11-specific T cells from papilloma tissue obtained from patients with RRP. These papilloma-infiltrating lymphocytes (PILs) have demonstrated the ability to eliminate papillomatous tissue. This T cell manufacturing method holds promise for developing cell-based therapies for chronic HPV 6/11-related conditions, including RRP and potentially anogenital condyloma. Notably, the ability to isolate and expand antigen-specific lymphocytes from non-cancerous growths represents an exciting advancement in the field of adoptive cell therapy – potentially paving the way for treating a broader range of non-malignant diseases.

This technology is available for licensing and offers a compelling opportunity for companies developing next-generation immunotherapies. The Center for Immuno-Oncology and the Surgical Oncology Program of the NCI, Center for Cancer Research are actively seeking industry partners to support the clinical development and commercialization of this approach. It is particularly well-suited for biotech firms focused on T cell therapies or addressing HPV-related diseases. Strategic collaboration could accelerate market entry and unlock significant value in an area with high unmet medical need.

Potential Commercial Applications:

Immunotherapy for chronic HPV-related conditions such as recurrent respiratory papillomatosis (RRP) and anogenital condyloma.

Development of personalized T cell therapies targeting HPV 6 or HPV 11 infections.

Generation of T cell receptor (TCR) libraries for research and therapeutic purposes.

Competitive Advantages:

Selective expansion of T cells with high specificity for HPV 6 or HPV 11 antigens.

Potential to treat both non-cancerous and cancerous HPV-related conditions.

Ability to produce oligoclonal T cell populations, increasing the efficacy of the therapy.

Methodology applicable to both therapeutic and preventative treatments for chronic HPV infections.

Drug development for RRP may qualify for regulatory incentives due to the rarity of the disease.

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for development of papilloma-infiltrating lymphocytes (PIL) as treatment for patients with chronic human papillomavirus (HPV) 6 or 11 infections.

Description of Technology:

Recurrent Respiratory Papillomatosis (RRP) and anogenital condyloma are caused by chronic infection with human papillomavirus (HPV) types 6 or 11. These conditions lead to the development of papillomatous growths in different regions of the body – RRP affects the upper aerodigestive tract, while condylomas involve the anogenital area. In RRP, growths in the aerodigestive tract can cause dysphonia, dyspnea, and, in severe cases, airway obstruction, which may lead to recurrent pneumonia or respiratory failure.

Current treatment for RRP primarily involves repeated surgical debulking or laser ablation to manage symptoms. However, the virus often persists in a latent state, resulting in continual papilloma regrowth. The need for frequent procedures exposes patients to cumulative anesthetic and surgical risks, emotional distress, and significantly diminished quality of life. Despite progress in localized treatments such as surgery and laser ablation, there are no approved systemic therapies for chronic HPV 6 or 11-related conditions. This highlights a clear unmet need for effective, curative therapy options.

Researchers at the National Cancer Institute (NCI) have developed a novel adoptive cell therapy approach to target conditions driven by HPV types 6 or 11. They have successfully identified and preferentially expanded HPV 6 and/or 11-specific T cells from papilloma tissue obtained from patients with RRP. These papilloma-infiltrating lymphocytes (PILs) have demonstrated the ability to eliminate papillomatous tissue. This T cell manufacturing method holds promise for developing cell-based therapies for chronic HPV 6/11-related conditions, including RRP and potentially anogenital condyloma. Notably, the ability to isolate and expand antigen-specific lymphocytes from non-cancerous growths represents an exciting advancement in the field of adoptive cell therapy – potentially paving the way for treating a broader range of non-malignant diseases.

This technology is available for licensing and offers a compelling opportunity for companies developing next-generation immunotherapies. The Center for Immuno-Oncology and the Surgical Oncology Program of the NCI, Center for Cancer Research are actively seeking industry partners to support the clinical development and commercialization of this approach. It is particularly well-suited for biotech firms focused on T cell therapies or addressing HPV-related diseases. Strategic collaboration could accelerate market entry and unlock significant value in an area with high unmet medical need.

Potential Commercial Applications:

Immunotherapy for chronic HPV-related conditions such as recurrent respiratory papillomatosis (RRP) and anogenital condyloma.

Development of personalized T cell therapies targeting HPV 6 or HPV 11 infections.

Generation of T cell receptor (TCR) libraries for research and therapeutic purposes.

Competitive Advantages:

Selective expansion of T cells with high specificity for HPV 6 or HPV 11 antigens.

Potential to treat both non-cancerous and cancerous HPV-related conditions.

Ability to produce oligoclonal T cell populations, increasing the efficacy of the therapy.

Methodology applicable to both therapeutic and preventative treatments for chronic HPV infections.

Drug development for RRP may qualify for regulatory incentives due to the rarity of the disease.

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations  for papilloma-infiltrating lymphocytes (PIL) in treatment for chronic HPV6/11-associated diseases

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations  for papilloma-infiltrating lymphocytes (PIL) in treatment for chronic HPV6/11-associated diseases

# data[].attributes.field_licensingcontact_hrefs[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5072] Method of Manufacturing Papilloma Infiltrating Lymphocyte (PIL) Cell Therapy Products as a Treatment for Patients with Chronic Viral Infection(s)&body=Please send me information about technology [TAB-5072] Method of Manufacturing Papilloma Infiltrating Lymphocyte (PIL) Cell Therapy Products as a Treatment for Patients with Chronic Viral Infection(s).&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].value
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Gulay French, Suna
suna.gulay@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
suna.gulay@nih.gov?subject=Web Inquiry on [TAB-5072] Method of Manufacturing Papilloma Infiltrating Lymphocyte (PIL) Cell Therapy Products as a Treatment for Patients with Chronic Viral Infection(s)&body=Please send me information about technology [TAB-5072] Method of Manufacturing Papilloma Infiltrating Lymphocyte (PIL) Cell Therapy Products as a Treatment for Patients with Chronic Viral Infection(s).&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/709,683
Filed on 2024-10-21
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/709,683
Filed on 2024-10-21
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/051640
Filed on 2025-10-20
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/051640
Filed on 2025-10-20
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/709,683
Filed on 2024-10-21
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/051640
Filed on 2025-10-20
Status: Pending

# data[].attributes.field_patent_titles[]
METHODS OF PREPARING CELL THERAPY PRODUCTS FOR THE TREATMENT OF CONDITIONS CAUSED BY HUMAN PAPILLOMAVIRUS 6 OR 11 INFECTION

# data[].attributes.field_patent_titles[]
METHODS OF PREPARING CELL THERAPY PRODUCTS FOR THE TREATMENT OF CONDITIONS CAUSED BY HUMAN PAPILLOMAVIRUS 6 OR 11 INFECTION

# data[].attributes.field_publications[].value
Bai K, Norberg SM, Sievers C, Meyer T, et al. Durable response in a patient with recurrent respiratory papillomatosis treated with immune checkpoint blockade. Case Reports Head Neck. 2022 Oct;44(10):E31-E37. doi: 10.1002/hed.27144.

# data[].attributes.field_publications[].processed
Bai K, Norberg SM, Sievers C, Meyer T, et al. Durable response in a patient with recurrent respiratory papillomatosis treated with immune checkpoint blockade. Case Reports Head Neck. 2022 Oct;44(10):E31-E37. doi: 10.1002/hed.27144.

# data[].attributes.field_technology_names[]
Method of Manufacturing Papilloma Infiltrating Lymphocyte Cell Therapy Products as a Treatment for Patients with Chronic Viral Infection(s)

# data[].attributes.title
Enhanced Tumor Reactivity of T Cells Lacking SIT1, LAX1 or TRAT1

# data[].attributes.body.value
Summary:

The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) is actively seeking potential licensees interested in further developing these inhibitory transmembrane adapter proteins as targets for T-cell immunotherapy for the treatment of cancer, infectious diseases, and autoimmune diseases.

Description of Technology:

Cellular immunotherapy holds much promise for the treatment of cancer. However, certain cellular therapies have limited success because of immunosuppression in the tumor microenvironment. Thus, there is an unmet need for improved methods of cellular immunotherapy.

T cells constitutively express inhibitory molecules that limit the activation response to antigens by the T cell antigen receptor (TCR). Among these are the transmembrane adapter proteins SIT1, LAX 1 and TRA T1. These appear to tonically associate with the TCR and inhibit signal transduction. Researchers at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) have identified SIT1, LAX 1 and TRA T1 as potential targets for T-cell immunotherapy. Mouse models have demonstrated that deletion of SIT1, LAX1 and TRA T1 – or expression of nonfunctional mutant versions of these proteins in mouse T cells – enhances TCR signaling and significantly increases T cell cytotoxicity against tumor cells. Experiments confirming these results in human T cells are currently underway. This discovery provides a new therapeutic approach to greatly improve clinical outcomes of T-cell immunotherapy in treating cancers. It also holds potential to treat infectious diseases or autoimmune diseases

Potential Commercial Applications:

Treatment for cancer

Treatment for infectious diseases

Treatment for autoimmune diseases

Competitive Advantages:

Potentially superior therapeutic benefit in cancer by:

Enhancing tumoricidal activity of T-cell immunotherapy

Overcoming immunosuppression in the tumor microenvironment

Potentially superior therapeutic benefit in infectious diseases by enhancing immune responses to pathogens

Potentially superior therapeutic benefit in autoimmune disease by enhancing the generation or function of antigen-specific regulator T cells (Tregs)

# data[].attributes.body.processed
Summary:

The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) is actively seeking potential licensees interested in further developing these inhibitory transmembrane adapter proteins as targets for T-cell immunotherapy for the treatment of cancer, infectious diseases, and autoimmune diseases.

Description of Technology:

Cellular immunotherapy holds much promise for the treatment of cancer. However, certain cellular therapies have limited success because of immunosuppression in the tumor microenvironment. Thus, there is an unmet need for improved methods of cellular immunotherapy.

T cells constitutively express inhibitory molecules that limit the activation response to antigens by the T cell antigen receptor (TCR). Among these are the transmembrane adapter proteins SIT1, LAX 1 and TRA T1. These appear to tonically associate with the TCR and inhibit signal transduction. Researchers at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) have identified SIT1, LAX 1 and TRA T1 as potential targets for T-cell immunotherapy. Mouse models have demonstrated that deletion of SIT1, LAX1 and TRA T1 – or expression of nonfunctional mutant versions of these proteins in mouse T cells – enhances TCR signaling and significantly increases T cell cytotoxicity against tumor cells. Experiments confirming these results in human T cells are currently underway. This discovery provides a new therapeutic approach to greatly improve clinical outcomes of T-cell immunotherapy in treating cancers. It also holds potential to treat infectious diseases or autoimmune diseases

Potential Commercial Applications:

Treatment for cancer

Treatment for infectious diseases

Treatment for autoimmune diseases

Competitive Advantages:

Potentially superior therapeutic benefit in cancer by:

Enhancing tumoricidal activity of T-cell immunotherapy

Overcoming immunosuppression in the tumor microenvironment

Potentially superior therapeutic benefit in infectious diseases by enhancing immune responses to pathogens

Potentially superior therapeutic benefit in autoimmune disease by enhancing the generation or function of antigen-specific regulator T cells (Tregs)

# data[].attributes.field_collaboration_description.value
Researchers at the NICHD seek licensing for further developing these inhibitory transmembrane adapter proteins as targets for T-cell immunotherapy for the treatment of cancer, infectious diseases, and autoimmune diseases.

# data[].attributes.field_collaboration_description.processed
Researchers at the NICHD seek licensing for further developing these inhibitory transmembrane adapter proteins as targets for T-cell immunotherapy for the treatment of cancer, infectious diseases, and autoimmune diseases.

# data[].attributes.field_licensingcontact_hrefs[]
darackn@mail.nih.gov?subject=Web Inquiry on [TAB-5065] Enhanced Tumor Reactivity of T Cells Lacking SIT1, LAX1 or TRAT1&body=Please send me information about technology [TAB-5065] Enhanced Tumor Reactivity of T Cells Lacking SIT1, LAX1 or TRAT1.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Guyton, Nicole
darackn@mail.nih.gov

# data[].attributes.field_licensing_contacts[].value
Guyton, Nicole
darackn@mail.nih.gov

# data[].attributes.field_licensing_contacts[].processed
Guyton, Nicole
darackn@mail.nih.gov

# data[].attributes.field_licensing_contacts_uris[]
darackn@mail.nih.gov?subject=Web Inquiry on [TAB-5065] Enhanced Tumor Reactivity of T Cells Lacking SIT1, LAX1 or TRAT1&body=Please send me information about technology [TAB-5065] Enhanced Tumor Reactivity of T Cells Lacking SIT1, LAX1 or TRAT1.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/625,354
Filed on 2024-01-26
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/625,354
Filed on 2024-01-26
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/013054
Filed on 2025-01-24
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/013054
Filed on 2025-01-24
Status: Expired

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/625,354
Filed on 2024-01-26
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/013054
Filed on 2025-01-24
Status: Expired

# data[].attributes.field_patent_titles[]
Enhanced Tumor Reactivity of T cells lacking SIT1, LAX1 or TRAT1

# data[].attributes.field_patent_titles[]
Enhanced Tumor Reactivity of T cells lacking SIT1, LAX1 or TRAT1

# data[].attributes.field_technology_names[]
Enhanced tumor of T cells lacking SIT1, LAX1 or TRAT1

# data[].attributes.title
Chimeric Antigen Receptors Targeting the Gamma Delta (γδ) T-Cell Receptor

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a set of Chimeric Antigen Receptors (CARs) that target the γδ T-Cell Receptor.

Description of Technology:

T cells express two main types of receptors based on the proteins that make up the T-cell receptor (TCR) heterodimers: ab (alpha beta) and gd (gamma delta). T cells expressing the gd TCR are detected at lower frequencies compared with T cells expressing the ab TCR. gd T cells make up 0.3-10% of peripheral blood T cells. The gd TCR is expressed on the cell surface of several aggressive cancers, including – but not limited to – hepatosplenic T-cell lymphoma, primary cutaneous gd T-cell lymphoma and T-cell acute lymphoblastic leukemia (T-ALL). These cancers carry poor prognosis as they are often resistant to chemotherapy. In addition, to their roles in cancer development, gd T cells may also play role in autoimmune diseases, including psoriasis, rheumatoid arthritis, multiple sclerosis and myositis. There is evidence that gd T cells are involved in initiation or persistence of these autoimmune diseases. To this end, new treatment options are needed for gd T-cell malignancies and autoimmune diseases.

Researchers at the National Cancer Institute (NCI) have developed several CARs targeting the gd TCR. These CARs can specifically bind to and immunologically recognize human gd TCR. Binding of the CAR to the gd TCR elicits an immune response that allows for killing of cells expressing this TCR.

Potential Commercial Applications:

Treatment of γδ T cell cancers

hepatosplenic T-cell lymphoma

primary cutaneous gd T-cell lymphoma

T-ALL

Treatment of γδ T cell autoimmune diseases

psoriasis

rheumatoid arthritis

multiple sclerosis

myositis

Competitive Advantages:

Promising new treatment option for several major market opportunities, including gd T cell malignancies and autoimmune diseases

Promising new treatment option for patients resistant to chemotherapy

In vivo proof-of-concept studies completed

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a set of Chimeric Antigen Receptors (CARs) that target the γδ T-Cell Receptor.

Description of Technology:

T cells express two main types of receptors based on the proteins that make up the T-cell receptor (TCR) heterodimers: ab (alpha beta) and gd (gamma delta). T cells expressing the gd TCR are detected at lower frequencies compared with T cells expressing the ab TCR. gd T cells make up 0.3-10% of peripheral blood T cells. The gd TCR is expressed on the cell surface of several aggressive cancers, including – but not limited to – hepatosplenic T-cell lymphoma, primary cutaneous gd T-cell lymphoma and T-cell acute lymphoblastic leukemia (T-ALL). These cancers carry poor prognosis as they are often resistant to chemotherapy. In addition, to their roles in cancer development, gd T cells may also play role in autoimmune diseases, including psoriasis, rheumatoid arthritis, multiple sclerosis and myositis. There is evidence that gd T cells are involved in initiation or persistence of these autoimmune diseases. To this end, new treatment options are needed for gd T-cell malignancies and autoimmune diseases.

Researchers at the National Cancer Institute (NCI) have developed several CARs targeting the gd TCR. These CARs can specifically bind to and immunologically recognize human gd TCR. Binding of the CAR to the gd TCR elicits an immune response that allows for killing of cells expressing this TCR.

Potential Commercial Applications:

Treatment of γδ T cell cancers

hepatosplenic T-cell lymphoma

primary cutaneous gd T-cell lymphoma

T-ALL

Treatment of γδ T cell autoimmune diseases

psoriasis

rheumatoid arthritis

multiple sclerosis

myositis

Competitive Advantages:

Promising new treatment option for several major market opportunities, including gd T cell malignancies and autoimmune diseases

Promising new treatment option for patients resistant to chemotherapy

In vivo proof-of-concept studies completed

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations  for a set of Chimeric Antigen Receptors (CARs) that target the γδ T-Cell Receptor, and if applicable, CARs that target the αβ T-Cell Receptor, too.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations  for a set of Chimeric Antigen Receptors (CARs) that target the γδ T-Cell Receptor, and if applicable, CARs that target the αβ T-Cell Receptor, too.

# data[].attributes.field_licensingcontact_hrefs[]
burkear@nih.gov?subject=Web Inquiry on [TAB-5073] Chimeric Antigen Receptors Targeting the Gamma Delta (γδ) T-Cell Receptor&body=Please send me information about technology [TAB-5073] Chimeric Antigen Receptors Targeting the Gamma Delta (γδ) T-Cell Receptor.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts[].value
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
burkear@nih.gov?subject=Web Inquiry on [TAB-5073] Chimeric Antigen Receptors Targeting the Gamma Delta (γδ) T-Cell Receptor&body=Please send me information about technology [TAB-5073] Chimeric Antigen Receptors Targeting the Gamma Delta (γδ) T-Cell Receptor.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/678,625
Filed on 2024-08-02
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/678,625
Filed on 2024-08-02
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/040252
Filed on 2025-08-01
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/040252
Filed on 2025-08-01
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/678,625
Filed on 2024-08-02
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/040252
Filed on 2025-08-01
Status: Pending

# data[].attributes.field_patent_titles[]
CHIMERIC ANTIGEN RECEPTORS TARGETING THE GAMMA DELTA T CELL RECEPTOR

# data[].attributes.field_patent_titles[]
CHIMERIC ANTIGEN RECEPTORS TARGETING THE GAMMA DELTA T CELL RECEPTOR

# data[].attributes.field_publications[].value
Kochenderfer JN, et al. Development of Novel Chimeric Antigen Receptors Targeting the Gamma-Delta (γδ) T-Cell Receptor.

# data[].attributes.field_publications[].processed
Kochenderfer JN, et al. Development of Novel Chimeric Antigen Receptors Targeting the Gamma-Delta (γδ) T-Cell Receptor.

# data[].attributes.field_technology_names[]
Development of chimeric antigen receptors targeting the gamma-delta T-cell receptor

# data[].attributes.title
Generating Conditional and Reverse Conditional Loss-of-Function Alleles in Mouse Casq2

# data[].attributes.body.value
Summary:

The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) is seeking potential licensees interested in further developing or utilizing these Casq2 mouse strains. As a research tool, patent protection is not being pursued for this technology. More information to access these strains can be found here: https://www.jax.org/strain/036291 and https://www.jax.org/strain/036290.

Description of Technology:

Cardiac calsequestrin (Casq2) plays an essential role in maintaining cardiac Ca2+ homeostasis. Human CASQ2 mutations are associated with catecholaminergic polymorphic ventricular tachycardia (CPVT), a rare familial arrhythmogenic disorder within a group of diseases characterized as Sudden Arrhythmic Death.

The inventors have generated Casq2Flox and Casq2RevFlox mouse strains that model CPVT. The two novel strains successfully phenocopy aspects of CPVT, including stress-induced arrhythmias and reduced basal heart rates. The strains allow investigators to determine the importance of Casq2 gene function in specific tissues and at specific developmental time points. They also allow investigators to determine the efficacy of gene therapy and to address key mechanism questions. The materials are validated and fully functional.

Potential Commercial Applications:

Study of Casq2 function

Study of calcium storage in cardiac muscle and CPVT

Determining the efficacy of gene therapy for CPVT

Competitive Advantages:

Only available conditional and reverse conditional loss-of-function alleles in mouse Casq2

Allows the study of Casq2 gene function in specific tissues and at specific developmental points

# data[].attributes.body.processed
Summary:

The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) is seeking potential licensees interested in further developing or utilizing these Casq2 mouse strains. As a research tool, patent protection is not being pursued for this technology. More information to access these strains can be found here: https://www.jax.org/strain/036291 and https://www.jax.org/strain/036290.

Description of Technology:

Cardiac calsequestrin (Casq2) plays an essential role in maintaining cardiac Ca2+ homeostasis. Human CASQ2 mutations are associated with catecholaminergic polymorphic ventricular tachycardia (CPVT), a rare familial arrhythmogenic disorder within a group of diseases characterized as Sudden Arrhythmic Death.

The inventors have generated Casq2Flox and Casq2RevFlox mouse strains that model CPVT. The two novel strains successfully phenocopy aspects of CPVT, including stress-induced arrhythmias and reduced basal heart rates. The strains allow investigators to determine the importance of Casq2 gene function in specific tissues and at specific developmental time points. They also allow investigators to determine the efficacy of gene therapy and to address key mechanism questions. The materials are validated and fully functional.

Potential Commercial Applications:

Study of Casq2 function

Study of calcium storage in cardiac muscle and CPVT

Determining the efficacy of gene therapy for CPVT

Competitive Advantages:

Only available conditional and reverse conditional loss-of-function alleles in mouse Casq2

Allows the study of Casq2 gene function in specific tissues and at specific developmental points

# data[].attributes.field_collaboration_description.value
NICHD seeks licensing for further developing or utilizing these Casq2 mouse strains.

# data[].attributes.field_collaboration_description.processed
NICHD seeks licensing for further developing or utilizing these Casq2 mouse strains.

# data[].attributes.field_licensingcontact_hrefs[]
nathan.whitman@nih.gov?subject=Web Inquiry on [TAB-5081] Generating Conditional and Reverse Conditional Loss-of-Function Alleles in Mouse Casq2&body=Please send me information about technology [TAB-5081] Generating Conditional and Reverse Conditional Loss-of-Function Alleles in Mouse Casq2.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Whitman, Nathan
nathan.whitman@nih.gov

# data[].attributes.field_licensing_contacts[].value
Whitman, Nathan
nathan.whitman@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Whitman, Nathan
nathan.whitman@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
nathan.whitman@nih.gov?subject=Web Inquiry on [TAB-5081] Generating Conditional and Reverse Conditional Loss-of-Function Alleles in Mouse Casq2&body=Please send me information about technology [TAB-5081] Generating Conditional and Reverse Conditional Loss-of-Function Alleles in Mouse Casq2.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_publications[].value
Knollmann BC, et al. Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia. (PMID 16932808)

# data[].attributes.field_publications[].processed
Knollmann BC, et al. Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia. (PMID 16932808)

# data[].attributes.field_publications[].value
Flores DJ, et al. Conditional ablation and conditional rescue models for Casq2 elucidate the role of development and of cell-type specific expression of Casq2 in the CPVT2 phenotype. (PMID 29452352)

# data[].attributes.field_publications[].processed
Flores DJ, et al. Conditional ablation and conditional rescue models for Casq2 elucidate the role of development and of cell-type specific expression of Casq2 in the CPVT2 phenotype. (PMID 29452352)

# data[].attributes.field_publications[].value
Blackwell DJ, et al. The Purkinje–myocardial junction is the anatomic origin of ventricular arrhythmia in CPVT. (PMID 34990403)

# data[].attributes.field_publications[].processed
Blackwell DJ, et al. The Purkinje–myocardial junction is the anatomic origin of ventricular arrhythmia in CPVT. (PMID 34990403)

# data[].attributes.field_technology_names[]
Generating conditional and reverse conditional loss-of-function alleles in mouse Casq2

# data[].attributes.title
Identification and Characterization of HLA-A24 Agonist Epitopes of MUC1 Oncoprotein

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks co-development partners and licensees for a human cytotoxic T lymphocyte agonist epitope from the C-terminal subunit of mucin 1 (MUC1-C), which can be used as a peptide, polypeptide (protein), in a cancer vaccine or T-cell targeted therapy to target many tumor types.

Description of Technology:

Many human carcinomas and hematologic malignancies overexpress mucin 1 (MUC1), a transmembrane glycoprotein composed of heterodimers formed by a large, N-terminal subunit (MUC1-N) and a smaller, C-terminal subunit (MUC1-C). In tumors, the MUC-1 heterodimer becomes abnormally hypoglycosylated – leading to the exposure of antigenic epitopes to the immune system. Aberrant MUC1 expression, and in particular its MUC1-C subunit, has been associated with poor prognosis and correlates with cancer metastasis – further establishing MUC1 as a target for cancer therapy.

Inventors at the National Cancer Institute have identified epitopes of MUC1-C and enhancer agonist peptides that can activate cytotoxic T lymphocytes. These epitopes and enhancers may be suitable to develop into immunotherapies, such as cancer vaccines against various malignancies. In particular, the agonist peptides are expected to further enhance responses in patients when used in vaccines or T-cell therapy. The epitopes span the human leukocyte antigen HLA-A24 allele and facilitate recognition of MUC1-C in the context of HLA-A24.

This technology is available for collaboration and licensing opportunities.

Potential Commercial Applications:

Treatment of MUC1-expressing cancers

Cancer vaccine compositions

MUC1-targeting epitopes and agonists

Activation of cytotoxic T cell response as an enhanced cancer treatment

Competitive Advantages:

Agonist epitopes can be incorporated into various vaccine platforms

Agonist epitopes can be used for the ex vivo generation of human T cells

Epitopes span the HLA-A24 allele and facilitate recognition and killing of human tumor cells in an MHC-restricted manner

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks co-development partners and licensees for a human cytotoxic T lymphocyte agonist epitope from the C-terminal subunit of mucin 1 (MUC1-C), which can be used as a peptide, polypeptide (protein), in a cancer vaccine or T-cell targeted therapy to target many tumor types.

Description of Technology:

Many human carcinomas and hematologic malignancies overexpress mucin 1 (MUC1), a transmembrane glycoprotein composed of heterodimers formed by a large, N-terminal subunit (MUC1-N) and a smaller, C-terminal subunit (MUC1-C). In tumors, the MUC-1 heterodimer becomes abnormally hypoglycosylated – leading to the exposure of antigenic epitopes to the immune system. Aberrant MUC1 expression, and in particular its MUC1-C subunit, has been associated with poor prognosis and correlates with cancer metastasis – further establishing MUC1 as a target for cancer therapy.

Inventors at the National Cancer Institute have identified epitopes of MUC1-C and enhancer agonist peptides that can activate cytotoxic T lymphocytes. These epitopes and enhancers may be suitable to develop into immunotherapies, such as cancer vaccines against various malignancies. In particular, the agonist peptides are expected to further enhance responses in patients when used in vaccines or T-cell therapy. The epitopes span the human leukocyte antigen HLA-A24 allele and facilitate recognition of MUC1-C in the context of HLA-A24.

This technology is available for collaboration and licensing opportunities.

Potential Commercial Applications:

Treatment of MUC1-expressing cancers

Cancer vaccine compositions

MUC1-targeting epitopes and agonists

Activation of cytotoxic T cell response as an enhanced cancer treatment

Competitive Advantages:

Agonist epitopes can be incorporated into various vaccine platforms

Agonist epitopes can be used for the ex vivo generation of human T cells

Epitopes span the HLA-A24 allele and facilitate recognition and killing of human tumor cells in an MHC-restricted manner

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for agonist epitopes of the MUC1-C oncoprotein.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for agonist epitopes of the MUC1-C oncoprotein.

# data[].attributes.field_licensingcontact_hrefs[]
michael.pollack@nih.gov?subject=Web Inquiry on [TAB-5083] Identification and Characterization of HLA-A24 Agonist Epitopes of MUC1 Oncoprotein&body=Please send me information about technology [TAB-5083] Identification and Characterization of HLA-A24 Agonist Epitopes of MUC1 Oncoprotein.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Pollack, Michael
michael.pollack@nih.gov

# data[].attributes.field_licensing_contacts[].value
Pollack, Michael
michael.pollack@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Pollack, Michael
michael.pollack@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
michael.pollack@nih.gov?subject=Web Inquiry on [TAB-5083] Identification and Characterization of HLA-A24 Agonist Epitopes of MUC1 Oncoprotein&body=Please send me information about technology [TAB-5083] Identification and Characterization of HLA-A24 Agonist Epitopes of MUC1 Oncoprotein.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 61/894,482
Filed on 2013-10-23
Status: Abandoned

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 61/894,482
Filed on 2013-10-23
Status: Abandoned

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2014/061723
Filed on 2014-10-22
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2014/061723
Filed on 2014-10-22
Status: Expired

# data[].attributes.field_patents[].value
US Patent 11,732,017
Filed on 2021-04-26
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 11,732,017
Filed on 2021-04-26
Status: Issued

# data[].attributes.field_patents[].value
US Patent 12,325,731
Filed on 2023-06-29
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 12,325,731
Filed on 2023-06-29
Status: Issued

# data[].attributes.field_patents[].value
US Patent 10,035,832
Filed on 2016-04-22
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 10,035,832
Filed on 2016-04-22
Status: Issued

# data[].attributes.field_patents[].value
US Patent 10,508,141
Filed on 2018-07-13
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 10,508,141
Filed on 2018-07-13
Status: Issued

# data[].attributes.field_patents[].value
US Patent 11,155,588
Filed on 2019-12-16
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 11,155,588
Filed on 2019-12-16
Status: Issued

# data[].attributes.field_patents[].value
Canada
Divisional (DIV) 3205348
Filed on 2023-06-30
Status: Pending

# data[].attributes.field_patents[].processed
Canada
Divisional (DIV) 3205348
Filed on 2023-06-30
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 61/894,482
Filed on 2013-10-23
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2014/061723
Filed on 2014-10-22
Status: Expired

# data[].attributes.field_patent_htmls[]
US Patent 11,732,017
Filed on 2021-04-26
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 12,325,731
Filed on 2023-06-29
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 10,035,832
Filed on 2016-04-22
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 10,508,141
Filed on 2018-07-13
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 11,155,588
Filed on 2019-12-16
Status: Issued

# data[].attributes.field_patent_htmls[]
Canada
Divisional (DIV) 3205348
Filed on 2023-06-30
Status: Pending

# data[].attributes.field_patent_titles[]
Identification And Characterization Of HLA-A24 Agonist Epitopes Of MUC1-Oncoprotein

# data[].attributes.field_patent_titles[]
HLA-A24 Agonist Epitopes Of MUC1-C Oncoprotein and Compositions and Methods of Use

# data[].attributes.field_patent_titles[]
Identification And Characterization Of HLA-A24 Agonist Epitopes Of MUC1-Oncoprotein

# data[].attributes.field_patent_titles[]
HLA-A24 AGONIST EPITOPES OF MUC1-C ONCOPROTEIN AND COMPOSITIONS AND METHODS OF USE

# data[].attributes.field_patent_titles[]
HLA-A24 Agonist Epitopes Of MUC1-Oncoprotein and Compositions and Methods of Use

# data[].attributes.field_patent_titles[]
Identification And Characterization Of HLA-A24 Agonist Epitopes Of MUC1-Oncoprotein

# data[].attributes.field_patent_titles[]
Identification And Characterization Of HLA-A24 Agonist Epitopes Of MUC1-Oncoprotein

# data[].attributes.field_patent_titles[]
HLA-A24 Agonist Epitopes Of MUC1-C Oncoprotein and Compositions and Methods of Use

# data[].attributes.field_publications[].value
Jochems C, et al. Identification and characterization of agonist epitopes of the MUC1-C oncoprotein. (PMID 24233342)

# data[].attributes.field_publications[].processed
Jochems C, et al. Identification and characterization of agonist epitopes of the MUC1-C oncoprotein. (PMID 24233342)

# data[].attributes.field_technology_names[]
Identification And Characterization Of HLA-A24 Agonist Epitopes Of MUC1-Oncoprotein

# data[].attributes.title
Photoactivatable Dye Compounds For Conjugate Formation And Methods of Making And Using the Same

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a new series of photo-absorbing silicon-phthalocyanine derivatives (IR702HKT) for use in near-infrared photoimmunotherapy (NIR-PIT) in the treatment of cancer.

Description of Technology:

Near-infrared photoimmunotherapy (NIR-PIT) is a method of treating cancers that utilizes an antibody-photoabsorber conjugate (APC), which is activated by near-infrared light to kill cells. The antibody binds to the appropriate cell surface antigen and a photo-activatable compound induces lethal damage to the cell membrane after NIR-light exposure. NIR-light exposure induces highly selective, necrotic cancer cell death within minutes without damage to adjoining cells.

Researchers at the National Cancer Institute (NCI) and Kansai Medical University (KMU) have developed the current invention which is a new series of photo-absorbing silicon-phthalocyanine derivatives (IR702HKT) as alternatives to the current IRDye700DX. This series of IR702HKTs have modified linkers that improve the efficacy of cellular cytotoxicity of IR702HKT bound to target cancer cells. Additionally, appropriate modifications improved in vivo stability of these new APCs and required less energetic therapeutic light exposure, which should improve clinical therapeutic efficacy and safety of NIR-PIT.

The inventors are open to co-development partners and/or licensing opportunities.

Potential Commercial Applications:

Cancer treatment

Cancer diagnosis

Cancer imaging

Treatment against viral, fungus, parasite, or bacterial infection

Age-related macular degeneration and lymphangioma, via depletion of abnormal vessels

Improved metabolic and physical function, via targeting of senile senescent cells

Competitive Advantages:

Improved in vivo stability

Improved cytotoxicity against APC-bound target cells by the same light exposure

Reduced therapeutic light exposure clinical therapeutic efficacy and safety, compared to current photo-absorbing silicon-phthalocyanine derivatives

Improved synthesis yields

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a new series of photo-absorbing silicon-phthalocyanine derivatives (IR702HKT) for use in near-infrared photoimmunotherapy (NIR-PIT) in the treatment of cancer.

Description of Technology:

Near-infrared photoimmunotherapy (NIR-PIT) is a method of treating cancers that utilizes an antibody-photoabsorber conjugate (APC), which is activated by near-infrared light to kill cells. The antibody binds to the appropriate cell surface antigen and a photo-activatable compound induces lethal damage to the cell membrane after NIR-light exposure. NIR-light exposure induces highly selective, necrotic cancer cell death within minutes without damage to adjoining cells.

Researchers at the National Cancer Institute (NCI) and Kansai Medical University (KMU) have developed the current invention which is a new series of photo-absorbing silicon-phthalocyanine derivatives (IR702HKT) as alternatives to the current IRDye700DX. This series of IR702HKTs have modified linkers that improve the efficacy of cellular cytotoxicity of IR702HKT bound to target cancer cells. Additionally, appropriate modifications improved in vivo stability of these new APCs and required less energetic therapeutic light exposure, which should improve clinical therapeutic efficacy and safety of NIR-PIT.

The inventors are open to co-development partners and/or licensing opportunities.

Potential Commercial Applications:

Cancer treatment

Cancer diagnosis

Cancer imaging

Treatment against viral, fungus, parasite, or bacterial infection

Age-related macular degeneration and lymphangioma, via depletion of abnormal vessels

Improved metabolic and physical function, via targeting of senile senescent cells

Competitive Advantages:

Improved in vivo stability

Improved cytotoxicity against APC-bound target cells by the same light exposure

Reduced therapeutic light exposure clinical therapeutic efficacy and safety, compared to current photo-absorbing silicon-phthalocyanine derivatives

Improved synthesis yields

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing for a new series of photo-absorbing silicon-phthalocyanine derivatives (IR702HKT) as alternatives to the current IRDye700DX.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing for a new series of photo-absorbing silicon-phthalocyanine derivatives (IR702HKT) as alternatives to the current IRDye700DX.

# data[].attributes.field_licensingcontact_hrefs[]
eric.cheng2@nih.gov?subject=Web Inquiry on [TAB-5086] Photoactivatable Dye Compounds For Conjugate Formation And Methods of Making And Using the Same&body=Please send me information about technology [TAB-5086] Photoactivatable Dye Compounds For Conjugate Formation And Methods of Making And Using the Same.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_licensing_contacts[].value
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
eric.cheng2@nih.gov?subject=Web Inquiry on [TAB-5086] Photoactivatable Dye Compounds For Conjugate Formation And Methods of Making And Using the Same&body=Please send me information about technology [TAB-5086] Photoactivatable Dye Compounds For Conjugate Formation And Methods of Making And Using the Same.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/690,585
Filed on 2024-09-04
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/690,585
Filed on 2024-09-04
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/044361
Filed on 2025-09-03
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/044361
Filed on 2025-09-03
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/690,585
Filed on 2024-09-04
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/044361
Filed on 2025-09-03
Status: Pending

# data[].attributes.field_patent_titles[]
PHOTOACTIVATABLE DYE COMPOUNDS FOR CONJUGATE FORMATION AND METHODS OF MAKING AND USING THE SAME

# data[].attributes.field_patent_titles[]
PHOTOACTIVATABLE DYE COMPOUNDS FOR CONJUGATE FORMATION AND METHODS OF MAKING AND USING THE SAME

# data[].attributes.field_related_inventions[].processed
E-137-2024-1

# data[].attributes.field_technology_names[]
Photoabsorbing Dyes (IR702HKTs) for Near Infrared PhotoImmuno Therapy (NIR-PIT)

# data[].attributes.field_technology_owners[]
Kansai Medical University, Molecular Imaging Branch

# data[].attributes.title
Acyloxyacyl Hydrolase (AOAH) and Methods of Use

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for the development of AOAH as a cancer immunotherapy.

Description of Technology:

Immune CheckPoint Inhibitors (ICIs) and T-cell based therapies are part of the emerging immunology-based therapies being used to treat cancers.  However, the efficacy of ICI therapies can be limited and a substantial portion of patients develop resistance or tolerance to treatment.  T-cell based cancer immunotherapies have only been approved for hematological cancers. They are suboptimal in solid tumor cancers due to physical barriers and the immuno-suppressive tumor microenvironment.  Thus, additional therapies and strategies are needed to improve efficacy and expand the types of cancer amendable to treatment.

Scientists at the National Cancer Institute have identified a secreted lipase, Acyloxyacyl Hydrolase (AOAH), produced by cells such as macrophages and dendritic cells that can potentiate immunotherapies in murine tumor models.  The protein sensitizes T cell receptors to weak antigens and protects dendritic cells through depleting immunosuppressive arachidonyl phoshatidylcholines and oxidized derivatives.  Thus, the protein can potentially enhance the efficacy and types of cancers treated by ICI based and T-cell based immunotherapies.

The National Cancer Institute is seeking collaborators and/or licensees to develop this technology as a cancer immunotherapy.

Potential Commercial Applications:

Cancer immunotherapy

Combination therapy with ICIs or T-cell based therapies

Competitive Advantages:

Novel therapeutic entity

Potentially improved efficacy

Increased types of addressable cancers

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for the development of AOAH as a cancer immunotherapy.

Description of Technology:

Immune CheckPoint Inhibitors (ICIs) and T-cell based therapies are part of the emerging immunology-based therapies being used to treat cancers.  However, the efficacy of ICI therapies can be limited and a substantial portion of patients develop resistance or tolerance to treatment.  T-cell based cancer immunotherapies have only been approved for hematological cancers. They are suboptimal in solid tumor cancers due to physical barriers and the immuno-suppressive tumor microenvironment.  Thus, additional therapies and strategies are needed to improve efficacy and expand the types of cancer amendable to treatment.

Scientists at the National Cancer Institute have identified a secreted lipase, Acyloxyacyl Hydrolase (AOAH), produced by cells such as macrophages and dendritic cells that can potentiate immunotherapies in murine tumor models.  The protein sensitizes T cell receptors to weak antigens and protects dendritic cells through depleting immunosuppressive arachidonyl phoshatidylcholines and oxidized derivatives.  Thus, the protein can potentially enhance the efficacy and types of cancers treated by ICI based and T-cell based immunotherapies.

The National Cancer Institute is seeking collaborators and/or licensees to develop this technology as a cancer immunotherapy.

Potential Commercial Applications:

Cancer immunotherapy

Combination therapy with ICIs or T-cell based therapies

Competitive Advantages:

Novel therapeutic entity

Potentially improved efficacy

Increased types of addressable cancers

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations  for the development of AOAH as an immunotherapy for cancer treatment.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations  for the development of AOAH as an immunotherapy for cancer treatment.

# data[].attributes.field_licensingcontact_hrefs[]
changke@mail.nih.gov?subject=Web Inquiry on [TAB-5087] Acyloxyacyl Hydrolase (AOAH) and Methods of Use&body=Please send me information about technology [TAB-5087] Acyloxyacyl Hydrolase (AOAH) and Methods of Use.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Chang, Kevin
changke@mail.nih.gov

# data[].attributes.field_licensing_contacts[].value
Chang, Kevin
changke@mail.nih.gov

# data[].attributes.field_licensing_contacts[].processed
Chang, Kevin
changke@mail.nih.gov

# data[].attributes.field_licensing_contacts_uris[]
changke@mail.nih.gov?subject=Web Inquiry on [TAB-5087] Acyloxyacyl Hydrolase (AOAH) and Methods of Use&body=Please send me information about technology [TAB-5087] Acyloxyacyl Hydrolase (AOAH) and Methods of Use.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/717,036
Filed on 2024-11-06
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/717,036
Filed on 2024-11-06
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/053940
Filed on 2025-11-04
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/053940
Filed on 2025-11-04
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/717,036
Filed on 2024-11-06
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/053940
Filed on 2025-11-04
Status: Pending

# data[].attributes.field_patent_titles[]
ACYLOXYACYL HYDROLASE AND METHODS OF USE

# data[].attributes.field_patent_titles[]
ACYLOXYACYL HYDROLASE AND METHODS OF USE

# data[].attributes.field_publications[].value
Gong L et al. Cancer Immunology Data Engine Reveals Secreted AOAH as a Potential Immunotherapy. (PMID 40730154)

# data[].attributes.field_publications[].processed
Gong L et al. Cancer Immunology Data Engine Reveals Secreted AOAH as a Potential Immunotherapy. (PMID 40730154)

# data[].attributes.field_technology_names[]
Big data-driven discovery and development of AOAH as new immunotherapy

# data[].attributes.title
Automated Cell Radiolabeling Device Using Acoustophoresis Micro-Fluidic Technology

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) sees research co-development partners and/or licensees for an automated acoustophoresis device to radio-label and isolate cells.

Description of Technology:

This technology includes an automated cell radiolabeling device that utilizes acoustophoresis microfluidic technology. The device streamlines the radiolabeling process by integrating cell washing and concentrating steps, which enhances reproducibility and standardization. This innovation simplifies the GMP (Good Manufacturing Practice) compliance for radiolabeling cells intended for human use. It also addresses the limitations of current manual methods that rely on centrifugation. The result is a benchtop system designed for clinical radio-pharmacies, ensuring efficient and reliable cell preparation for diagnostic and therapeutic applications.

Automated Acoustophoresis Device to Radio-Label & Isolate Cells for Immunotherapy and Isolated Cells for Immunotherapy Treatment

Potential Commercial Applications:

Clinical radio-pharmacies for radiolabeled cell diagnostics

Research institutions focused on cellular therapies and diagnostics

Pharmaceutical companies developing radiolabeled therapeutics

Competitive Advantages:

Fully automated process reduces manual intervention, increasing efficiency and consistency

Micron-scale acoustophoresis technology enhances reproducibility and standardization of cell radiolabeling

Streamlined GMP compliance simplifies regulatory processes for clinical applications

Benchtop system

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) sees research co-development partners and/or licensees for an automated acoustophoresis device to radio-label and isolate cells.

Description of Technology:

This technology includes an automated cell radiolabeling device that utilizes acoustophoresis microfluidic technology. The device streamlines the radiolabeling process by integrating cell washing and concentrating steps, which enhances reproducibility and standardization. This innovation simplifies the GMP (Good Manufacturing Practice) compliance for radiolabeling cells intended for human use. It also addresses the limitations of current manual methods that rely on centrifugation. The result is a benchtop system designed for clinical radio-pharmacies, ensuring efficient and reliable cell preparation for diagnostic and therapeutic applications.

Automated Acoustophoresis Device to Radio-Label & Isolate Cells for Immunotherapy and Isolated Cells for Immunotherapy Treatment

Potential Commercial Applications:

Clinical radio-pharmacies for radiolabeled cell diagnostics

Research institutions focused on cellular therapies and diagnostics

Pharmaceutical companies developing radiolabeled therapeutics

Competitive Advantages:

Fully automated process reduces manual intervention, increasing efficiency and consistency

Micron-scale acoustophoresis technology enhances reproducibility and standardization of cell radiolabeling

Streamlined GMP compliance simplifies regulatory processes for clinical applications

Benchtop system

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations  for an automated acoustophoresis device to radio-label and isolate cells.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations  for an automated acoustophoresis device to radio-label and isolate cells.

# data[].attributes.field_licensingcontact_htmls[]
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_licensing_contacts[].value
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/191,103
Filed on 2021-05-20
Status: Abandoned

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/191,103
Filed on 2021-05-20
Status: Abandoned

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2022/028819
Filed on 2022-05-11
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2022/028819
Filed on 2022-05-11
Status: Expired

# data[].attributes.field_patents[].value
US
National Stage 18/290,442
Filed on 2023-11-13
Status: Pending

# data[].attributes.field_patents[].processed
US
National Stage 18/290,442
Filed on 2023-11-13
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/191,103
Filed on 2021-05-20
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2022/028819
Filed on 2022-05-11
Status: Expired

# data[].attributes.field_patent_htmls[]
US
National Stage 18/290,442
Filed on 2023-11-13
Status: Pending

# data[].attributes.field_publications[].value
Adler, S, et al. Using Acoustophoresis Cell Washing In The Immune Cell Radiolabeling Procedure.

# data[].attributes.field_publications[].processed
Adler, S, et al. Using Acoustophoresis Cell Washing In The Immune Cell Radiolabeling Procedure.

# data[].attributes.field_technology_names[]
Novel Device For Cell Radiolabeling Using Acoustophoresis Micro-fluidic Technology

# data[].attributes.body.value
Summary:

The NCI seeks research co-development partners or licensees for monoclonal antibodies that specifically target cancer-expressed EGFR.

Description of Technology:

Epidermal growth factor receptor (EGFR) is a well-known oncogenic driver in lung cancer, head and neck cancer, glioblastoma multiforme (GBM) and other cancers. NCI inventors have previously isolated a mouse monoclonal antibody that binds to the human EGFRvIII – but not wildtype EGFR known as the 40H3 antibody (NCI Ref: E-103-2019). To improve the 40H3 antibody’s suitability for the clinic, the inventors humanized the antibody through the generation of multiple variants with distinct sequences. The inventors produced about 14 humanized candidates of the 40H3 antibody. Significantly, CAR Ts using one of the antibodies (A10) showed potent killing of cancer cells in various pre-clinical models overexpressing EGFR. The pre-clinical results obtained to date suggest that the A10 antibody is a promising candidate for development as various therapeutics for the treatment of EGFRvIII-expressing cancers.

Potential Commercial Applications:

Cancer therapeutic against numerous EGFRvIII-expressing tumor types – including, but not limited to, lung cancer, head and neck cancer and GBM.

Therapeutic applications of the unconjugated antibodies

Use of the unconjugated antibodies as a targeting moiety in antibody-drug conjugates (ADCs), radio-immunotherapies (RITs) and chimeric antigen receptors (CARs)

Diagnostic agent for detection and monitoring levels of EGFRvIII-expressing cancers

Competitive Advantages:

Less non-specific cell killing using humanized EGFRvIII antibodies with high EGFRvIII binding specificity will result in fewer and lower grade potential side effects

Therapeutic development against various common and rare cancers represent many paths to market and out-licensing opportunities

CAR Ts using the A10 antibody are available for immediate testing

A10 binding EGFR when over-expressed from amplified EGFR is specific to various cancers

# data[].attributes.body.processed
Summary:

The NCI seeks research co-development partners or licensees for monoclonal antibodies that specifically target cancer-expressed EGFR.

Description of Technology:

Epidermal growth factor receptor (EGFR) is a well-known oncogenic driver in lung cancer, head and neck cancer, glioblastoma multiforme (GBM) and other cancers. NCI inventors have previously isolated a mouse monoclonal antibody that binds to the human EGFRvIII – but not wildtype EGFR known as the 40H3 antibody (NCI Ref: E-103-2019). To improve the 40H3 antibody’s suitability for the clinic, the inventors humanized the antibody through the generation of multiple variants with distinct sequences. The inventors produced about 14 humanized candidates of the 40H3 antibody. Significantly, CAR Ts using one of the antibodies (A10) showed potent killing of cancer cells in various pre-clinical models overexpressing EGFR. The pre-clinical results obtained to date suggest that the A10 antibody is a promising candidate for development as various therapeutics for the treatment of EGFRvIII-expressing cancers.

Potential Commercial Applications:

Cancer therapeutic against numerous EGFRvIII-expressing tumor types – including, but not limited to, lung cancer, head and neck cancer and GBM.

Therapeutic applications of the unconjugated antibodies

Use of the unconjugated antibodies as a targeting moiety in antibody-drug conjugates (ADCs), radio-immunotherapies (RITs) and chimeric antigen receptors (CARs)

Diagnostic agent for detection and monitoring levels of EGFRvIII-expressing cancers

Competitive Advantages:

Less non-specific cell killing using humanized EGFRvIII antibodies with high EGFRvIII binding specificity will result in fewer and lower grade potential side effects

Therapeutic development against various common and rare cancers represent many paths to market and out-licensing opportunities

CAR Ts using the A10 antibody are available for immediate testing

A10 binding EGFR when over-expressed from amplified EGFR is specific to various cancers

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for monoclonal antibodies that specifically target cancer-expressed EGFR.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for monoclonal antibodies that specifically target cancer-expressed EGFR.

# data[].attributes.field_licensingcontact_htmls[]
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts[].value
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/525,493
Filed on 2023-07-07
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/525,493
Filed on 2023-07-07
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2024/037091
Filed on 2024-07-08
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2024/037091
Filed on 2024-07-08
Status: Expired

# data[].attributes.field_patents[].value
Japan
National Stage 2026-500043
Filed on 2026-01-05
Status: Pending

# data[].attributes.field_patents[].processed
Japan
National Stage 2026-500043
Filed on 2026-01-05
Status: Pending

# data[].attributes.field_patents[].value
Canada
National Stage 3297257
Filed on 2025-12-30
Status: Pending

# data[].attributes.field_patents[].processed
Canada
National Stage 3297257
Filed on 2025-12-30
Status: Pending

# data[].attributes.field_patents[].value
Australia
National Stage 2024296940
Filed on 2026-01-13
Status: Pending

# data[].attributes.field_patents[].processed
Australia
National Stage 2024296940
Filed on 2026-01-13
Status: Pending

# data[].attributes.field_patents[].value
China
National Stage 202480057586.7
Filed on 2026-04-01
Status: Pending

# data[].attributes.field_patents[].processed
China
National Stage 202480057586.7
Filed on 2026-04-01
Status: Pending

# data[].attributes.field_patents[].value
US
National Stage 19/497,173
Filed on 2025-12-24
Status: Pending

# data[].attributes.field_patents[].processed
US
National Stage 19/497,173
Filed on 2025-12-24
Status: Pending

# data[].attributes.field_patents[].value
European Patent
National Stage 24748511.3
Filed on 2026-01-27
Status: Pending

# data[].attributes.field_patents[].processed
European Patent
National Stage 24748511.3
Filed on 2026-01-27
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/525,493
Filed on 2023-07-07
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2024/037091
Filed on 2024-07-08
Status: Expired

# data[].attributes.field_patent_htmls[]
Japan
National Stage 2026-500043
Filed on 2026-01-05
Status: Pending

# data[].attributes.field_patent_htmls[]
Canada
National Stage 3297257
Filed on 2025-12-30
Status: Pending

# data[].attributes.field_patent_htmls[]
Australia
National Stage 2024296940
Filed on 2026-01-13
Status: Pending

# data[].attributes.field_patent_htmls[]
China
National Stage 202480057586.7
Filed on 2026-04-01
Status: Pending

# data[].attributes.field_patent_htmls[]
US
National Stage 19/497,173
Filed on 2025-12-24
Status: Pending

# data[].attributes.field_patent_htmls[]
European Patent
National Stage 24748511.3
Filed on 2026-01-27
Status: Pending

# data[].attributes.field_related_inventions[].processed
E-103-2019

# data[].attributes.field_technology_names[]
Humanization of the monoclonal antibody, 40H3:  generation of improved variants

# data[].attributes.field_technology_owners[]
Laboratory of Molecular Biology, National Cancer Institute (NCI), NIH - NCI

# data[].attributes.title
Novel Human Immunogenic Epitopes of the Human Endogenous Retrovirus ERVMER34-1

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for the clinical translation of novel peptide-based therapeutic cancer vaccines derived from ERVMER34-1, a human endogenous retrovirus (HERV) antigen, offering a unique opportunity to address a significant unmet need in the treatment of various carcinomas.

Description of Technology:

Human Endogenous Retroviruses (HERVs), remnants of ancient retroviral germline infections that comprise ~8% of the human genome, represent a promising yet underexplored frontier in targeted cancer therapy. Although typically epigenetically silenced in normal adult tissues, select HERV components, including RNAs and envelope proteins, are frequently overexpressed in various carcinomas due to epigenetic dysregulation – a hallmark of cancer. The challenge lies in identifying specific, highly immunogenic HERV targets that elicit potent anti-tumor immune responses without triggering autoimmunity. Addressing this need is critical to advancing broadly applicable cancer immunotherapies.

Inventors at the NCI have developed and characterized a novel cancer immunotherapy platform targeting ERVMER34-1, a specific HERV envelope protein that is highly expressed across multiple human carcinomas while exhibiting minimal expression in normal tissues. Using transcriptomic and proteomic datasets, the team confirmed the tumor-selective expression profile of ERVMER34-1. To improve safety and specificity, they engineered an artificial antigen-presenting cell line to express the full-length ERVMER34-1 protein, HLA-A2 and CD80 to facilitate efficient priming and expansion of ERVMER34-1-reactive CD8+ T cells. To therapeutically target ERVMER34-1, they modified the ERVMER34-1 protein by removing the signal peptide, cleavage site, predicted immunosuppressive domain, transmembrane domain and a 170-amino acid region homologous to human proteins. These modifications prevent surface trafficking, antigen shedding, immune dampening, and off-target reactivity. This modified sequence was incorporated into a recombinant adenoviral vector as a therapeutic cancer vaccine. In preclinical murine models (e.g., MC38 colon cancer, EMT6 breast cancer), vaccination with this construct alone or in combination with immune checkpoint blockade or an IL-15 superagonist elicited robust, multifunctional CD4⁺ and CD8⁺ T cell responses. Those enhanced T cell responses induced tumor clearance, increased intratumoral lymphocyte infiltration, broadened neoantigen spreading and prolonged tumor control. ERVMER34-1-reactive T cells could be expanded from both healthy donor and cancer patient Peripheral Blood Mononuclear Cells (PBMCs) and demonstrated specific cytolytic activity against ERVMER34-1⁺ human carcinoma cell lines in vitro. To support peptide-based approaches, researchers developed an overlapping 15-mer peptide library spanning the modified ERVMER34-1 protein sequence. These peptides elicited strong, polyfunctional T cell responses in vitro – including both CD4⁺ and HLA-A2-restricted CD8⁺ T cell activation, enabling precise epitope mapping and facilitating future peptide vaccine design and adoptive T cell receptor (TCR)-based therapies.

The NCI invites industry partners and translational researchers to collaborate on or license this pioneering HERV ERVMER34-1 protein targeted vaccine technology. With promising preclinical data, this technology addresses a critical gap in the cancer vaccine landscape. It offers a unique opportunity to advance a novel therapeutic targeting widespread carcinomas, opening a substantial market for cancer treatment.

Potential Commercial Applications:

Peptide-based therapeutic cancer vaccines

Adenoviral vector-based therapeutic cancer vaccines

Liposome- or nanoparticle-formulated therapeutic cancer vaccines

Artificial Antigen-Presenting Cell platforms expressing ERVMER34-1 with HLA-A2 and CD80 to expand antigen-specific T cells for adoptive cell therapies

Adoptive T cell therapies using ERVMER34-1-specific TCRs isolated from PBMCs or engineered T cells redirected against shared HERV antigens

Combination immunotherapies pairing the ERVMER34-1 vaccine with checkpoint inhibitors and/or epigenetic modifiers to boost response breadth and tumor infiltration

Cytokine or immuno-cytokine-enhanced combination regimens incorporating immune-oncology agents to amplify tumor-specific T cell activation

Companion diagnostic tools to identify ERVMER34-1-expressing tumors for patient selection and treatment stratification

Competitive Advantages:

Broad tumor coverage across ~62% of carcinomas

Minimal expression in normal tissues reduces toxicity risk and expands market potential

Engineered antigen design in vaccine eliminates immunosuppressive and off-target domains, improving safety and therapeutic precision

Elicits potent, multifunctional T cell responses with cytokine production and broad epitope recognition, enhancing anti-tumor efficacy

Selectively clears tumor cells based on ERVMER34-1 expression, enabling precise targeting across variable antigen levels

Demonstrates remarkable synergistic efficacy with immune checkpoint inhibitors, achieving ~89% tumor clearance in established large tumors in mouse models

Exhibits synergistic interaction with cytokine agonists such as N-803 (Anktiva), significantly enhancing neoepitope-reactive T cell responses and improving tumor control in combination therapies

Potential for use in combination with epigenetic modulators to enhance expression of targeted antigen in human carcinomas

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for the clinical translation of novel peptide-based therapeutic cancer vaccines derived from ERVMER34-1, a human endogenous retrovirus (HERV) antigen, offering a unique opportunity to address a significant unmet need in the treatment of various carcinomas.

Description of Technology:

Human Endogenous Retroviruses (HERVs), remnants of ancient retroviral germline infections that comprise ~8% of the human genome, represent a promising yet underexplored frontier in targeted cancer therapy. Although typically epigenetically silenced in normal adult tissues, select HERV components, including RNAs and envelope proteins, are frequently overexpressed in various carcinomas due to epigenetic dysregulation – a hallmark of cancer. The challenge lies in identifying specific, highly immunogenic HERV targets that elicit potent anti-tumor immune responses without triggering autoimmunity. Addressing this need is critical to advancing broadly applicable cancer immunotherapies.

Inventors at the NCI have developed and characterized a novel cancer immunotherapy platform targeting ERVMER34-1, a specific HERV envelope protein that is highly expressed across multiple human carcinomas while exhibiting minimal expression in normal tissues. Using transcriptomic and proteomic datasets, the team confirmed the tumor-selective expression profile of ERVMER34-1. To improve safety and specificity, they engineered an artificial antigen-presenting cell line to express the full-length ERVMER34-1 protein, HLA-A2 and CD80 to facilitate efficient priming and expansion of ERVMER34-1-reactive CD8+ T cells. To therapeutically target ERVMER34-1, they modified the ERVMER34-1 protein by removing the signal peptide, cleavage site, predicted immunosuppressive domain, transmembrane domain and a 170-amino acid region homologous to human proteins. These modifications prevent surface trafficking, antigen shedding, immune dampening, and off-target reactivity. This modified sequence was incorporated into a recombinant adenoviral vector as a therapeutic cancer vaccine. In preclinical murine models (e.g., MC38 colon cancer, EMT6 breast cancer), vaccination with this construct alone or in combination with immune checkpoint blockade or an IL-15 superagonist elicited robust, multifunctional CD4⁺ and CD8⁺ T cell responses. Those enhanced T cell responses induced tumor clearance, increased intratumoral lymphocyte infiltration, broadened neoantigen spreading and prolonged tumor control. ERVMER34-1-reactive T cells could be expanded from both healthy donor and cancer patient Peripheral Blood Mononuclear Cells (PBMCs) and demonstrated specific cytolytic activity against ERVMER34-1⁺ human carcinoma cell lines in vitro. To support peptide-based approaches, researchers developed an overlapping 15-mer peptide library spanning the modified ERVMER34-1 protein sequence. These peptides elicited strong, polyfunctional T cell responses in vitro – including both CD4⁺ and HLA-A2-restricted CD8⁺ T cell activation, enabling precise epitope mapping and facilitating future peptide vaccine design and adoptive T cell receptor (TCR)-based therapies.

The NCI invites industry partners and translational researchers to collaborate on or license this pioneering HERV ERVMER34-1 protein targeted vaccine technology. With promising preclinical data, this technology addresses a critical gap in the cancer vaccine landscape. It offers a unique opportunity to advance a novel therapeutic targeting widespread carcinomas, opening a substantial market for cancer treatment.

Potential Commercial Applications:

Peptide-based therapeutic cancer vaccines

Adenoviral vector-based therapeutic cancer vaccines

Liposome- or nanoparticle-formulated therapeutic cancer vaccines

Artificial Antigen-Presenting Cell platforms expressing ERVMER34-1 with HLA-A2 and CD80 to expand antigen-specific T cells for adoptive cell therapies

Adoptive T cell therapies using ERVMER34-1-specific TCRs isolated from PBMCs or engineered T cells redirected against shared HERV antigens

Combination immunotherapies pairing the ERVMER34-1 vaccine with checkpoint inhibitors and/or epigenetic modifiers to boost response breadth and tumor infiltration

Cytokine or immuno-cytokine-enhanced combination regimens incorporating immune-oncology agents to amplify tumor-specific T cell activation

Companion diagnostic tools to identify ERVMER34-1-expressing tumors for patient selection and treatment stratification

Competitive Advantages:

Broad tumor coverage across ~62% of carcinomas

Minimal expression in normal tissues reduces toxicity risk and expands market potential

Engineered antigen design in vaccine eliminates immunosuppressive and off-target domains, improving safety and therapeutic precision

Elicits potent, multifunctional T cell responses with cytokine production and broad epitope recognition, enhancing anti-tumor efficacy

Selectively clears tumor cells based on ERVMER34-1 expression, enabling precise targeting across variable antigen levels

Demonstrates remarkable synergistic efficacy with immune checkpoint inhibitors, achieving ~89% tumor clearance in established large tumors in mouse models

Exhibits synergistic interaction with cytokine agonists such as N-803 (Anktiva), significantly enhancing neoepitope-reactive T cell responses and improving tumor control in combination therapies

Potential for use in combination with epigenetic modulators to enhance expression of targeted antigen in human carcinomas

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for the clinical translation of novel peptide-based therapeutic cancer vaccines derived from ERVMER34-1, a human endogenous retrovirus (HERV) antigen, offering a unique opportunity to address a significant unmet need in the treatment of various carcinomas.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for the clinical translation of novel peptide-based therapeutic cancer vaccines derived from ERVMER34-1, a human endogenous retrovirus (HERV) antigen, offering a unique opportunity to address a significant unmet need in the treatment of various carcinomas.

# data[].attributes.field_licensingcontact_hrefs[]
michael.pollack@nih.gov?subject=Web Inquiry on [TAB-5082] Novel Human Immunogenic Epitopes of the Human Endogenous Retrovirus ERVMER34-1&body=Please send me information about technology [TAB-5082] Novel Human Immunogenic Epitopes of the Human Endogenous Retrovirus ERVMER34-1.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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Pollack, Michael
michael.pollack@nih.gov

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Pollack, Michael
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michael.pollack@nih.gov?subject=Web Inquiry on [TAB-5082] Novel Human Immunogenic Epitopes of the Human Endogenous Retrovirus ERVMER34-1&body=Please send me information about technology [TAB-5082] Novel Human Immunogenic Epitopes of the Human Endogenous Retrovirus ERVMER34-1.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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# data[].attributes.field_patent_titles[]
HUMAN IMMUNOGENIC EPITOPES OF HEMO AND HHLA2 HUMAN ENDOGENOUS RETROVIRUSES (HERVs)

# data[].attributes.field_patent_titles[]
HUMAN IMMUNOGENIC EPITOPES OF HEMO and HHLA2 HUMAN ENDOGENOUS RETROVIRUSES (HERVS)

# data[].attributes.field_patent_titles[]
HUMAN IMMUNOGENIC EPITOPES OF HEMO and HHLA2 HUMAN ENDOGENOUS RETROVIRUSES (HERVS)

# data[].attributes.field_patent_titles[]
HUMAN IMMUNOGENIC EPITOPES OF HEMO and HHLA2 HUMAN ENDOGENOUS RETROVIRUSES (HERVS)

# data[].attributes.field_patent_titles[]
HUMAN IMMUNOGENIC EPITOPES OF HEMO and HHLA2 HUMAN ENDOGENOUS RETROVIRUSES (HERVS)

# data[].attributes.field_patent_titles[]
HUMAN IMMUNOGENIC EPITOPES OF HEMO AND HHLA2 HUMAN ENDOGENOUS RETROVIRUSES (HERVS)

# data[].attributes.field_patent_titles[]
HUMAN IMMUNOGENIC EPITOPES OF HEMO and HHLA2 HUMAN ENDOGENOUS RETROVIRUSES (HERVS)

# data[].attributes.field_publications[].value
Maldonado MDM, et al. Combination of a therapeutic cancer vaccine targeting the endogenous retroviral envelope protein ERVMER34-1 with immune-oncology agents facilitates expansion of neoepitope-specific T cells and promotes tumor control (PMID: 40360436)

# data[].attributes.field_publications[].processed
Maldonado MDM, et al. Combination of a therapeutic cancer vaccine targeting the endogenous retroviral envelope protein ERVMER34-1 with immune-oncology agents facilitates expansion of neoepitope-specific T cells and promotes tumor control (PMID: 40360436)

# data[].attributes.field_publications[].value
Gracia-Hernandez M, et al. Combination Therapy Approaches to Enhance the Efficacy of ERV-Targeting Vaccines in Cancer (PMID: 40387511)

# data[].attributes.field_publications[].processed
Gracia-Hernandez M, et al. Combination Therapy Approaches to Enhance the Efficacy of ERV-Targeting Vaccines in Cancer (PMID: 40387511)

# data[].attributes.field_related_inventions[].processed
E-056-2023

# data[].attributes.field_technology_names[]
Identification Of Novel Human Immunogenic Epitopes Of HEMO And HHLA2 Human Endogenous Retroviruses (HERVs)

# data[].attributes.field_technology_owners[]
Chan Soon-Shiong Institute of Molecular Medicine at Windber, MDR Global Systems, LLC, NCI, NIH - NCI, Uniformed Services University of the Health Sciences

# data[].attributes.title
Real-time AI System for Echocardiography Analysis and Quantification

# data[].attributes.body.value
Summary:

We are seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate or commercialize this technology.

Description of Technology:

Scientists have developed an artificial intelligence (AI) system to automatically extract predictive biomarkers from echocardiography. This AI system takes an echocardiography study as input and produces predictive biomarkers as output in real-time. It performs several automated image analysis tasks including echocardiography quality (quality for the acquired echo clips) assessment, echocardiography view retrieval (e.g., 2D four chamber or parasternal long axis view, Doppler), echocardiography cardiac region segmentation (e.g. inferior vena cava) and cardiac biomarker quantification (e.g. right atrial pressure). This system is:

1. efficient (in terms of time and space)

2. robust (can handle missing data)

3. interpretable (can provide human-understandable insights)

Such features allow its use in embedded devices for real-world clinical practice and point of care testing. This technology can be used to assist the diagnosis of a wide range of common cardiac diseases as well as to evaluate cardiac function in minority populations such as sickle cell disease patients.

Potential Commercial Applications:

Cardiologists in clinical practice, to:

streamline cross-functional workflows

obtain temporal biomarkers of a full study in a single run

Cardiology researchers, to:

Enable systematic comparison across millions of echocardiograms

rapidly analyze cardiac data across hospitals and research centers

perform analysis and quantification for pattern detection, verification, and informed hypothesis testing

Perform diagnosis and assessment of wide range of cardiac diseases including coronary artery disease, heart failure, and cardiopulmonary complications in sickle cell disease patients

Once converted into a software application, can be installed in bedside and handheld ultrasound devices to extract imaging biomarkers

Can combine the extracted imaging biomarkers with non-imaging biomarkers (e.g., lab tests, age)

Applicable to other clinical fields; e.g., endocrinology

Competitive Advantages:

Real-time medical imaging

No comparable system in the market that performs a series of medical image tasks in real-time to extract predictive imaging biomarkers from different echo types and views including Doppler, M-model, and B-mode (A2C, A4C, PLAX, IVC, etc.)

Enhance efficiency and save time – hours to minutes or seconds

Enable deeper analysis of a patient’s condition

Enables the streamlining of tedious clinical tasks (e.g., image analysis tasks and visual biomarkers observation), potentially saving hours of physicians’ time

Reduced costs to payers and patients resulting from decreased physician time

Reproducible and precise image analysis anywhere

Enables unprecedented portability and standardized access to care — including visual analytics, predictive biomarker calculation, diagnosis, assessment, and prognosis

# data[].attributes.body.processed
Summary:

We are seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate or commercialize this technology.

Description of Technology:

Scientists have developed an artificial intelligence (AI) system to automatically extract predictive biomarkers from echocardiography. This AI system takes an echocardiography study as input and produces predictive biomarkers as output in real-time. It performs several automated image analysis tasks including echocardiography quality (quality for the acquired echo clips) assessment, echocardiography view retrieval (e.g., 2D four chamber or parasternal long axis view, Doppler), echocardiography cardiac region segmentation (e.g. inferior vena cava) and cardiac biomarker quantification (e.g. right atrial pressure). This system is:

1. efficient (in terms of time and space)

2. robust (can handle missing data)

3. interpretable (can provide human-understandable insights)

Such features allow its use in embedded devices for real-world clinical practice and point of care testing. This technology can be used to assist the diagnosis of a wide range of common cardiac diseases as well as to evaluate cardiac function in minority populations such as sickle cell disease patients.

Potential Commercial Applications:

Cardiologists in clinical practice, to:

streamline cross-functional workflows

obtain temporal biomarkers of a full study in a single run

Cardiology researchers, to:

Enable systematic comparison across millions of echocardiograms

rapidly analyze cardiac data across hospitals and research centers

perform analysis and quantification for pattern detection, verification, and informed hypothesis testing

Perform diagnosis and assessment of wide range of cardiac diseases including coronary artery disease, heart failure, and cardiopulmonary complications in sickle cell disease patients

Once converted into a software application, can be installed in bedside and handheld ultrasound devices to extract imaging biomarkers

Can combine the extracted imaging biomarkers with non-imaging biomarkers (e.g., lab tests, age)

Applicable to other clinical fields; e.g., endocrinology

Competitive Advantages:

Real-time medical imaging

No comparable system in the market that performs a series of medical image tasks in real-time to extract predictive imaging biomarkers from different echo types and views including Doppler, M-model, and B-mode (A2C, A4C, PLAX, IVC, etc.)

Enhance efficiency and save time – hours to minutes or seconds

Enable deeper analysis of a patient’s condition

Enables the streamlining of tedious clinical tasks (e.g., image analysis tasks and visual biomarkers observation), potentially saving hours of physicians’ time

Reduced costs to payers and patients resulting from decreased physician time

Reproducible and precise image analysis anywhere

Enables unprecedented portability and standardized access to care — including visual analytics, predictive biomarker calculation, diagnosis, assessment, and prognosis

# data[].attributes.field_collaboration_description.value
Researchers at the NLM are seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate or commercialize this technology.

# data[].attributes.field_collaboration_description.processed
Researchers at the NLM are seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate or commercialize this technology.

# data[].attributes.field_licensingcontact_hrefs[]
ricquita.pollard@nih.gov?subject=Web Inquiry on [TAB-5089] Real-time AI System for Echocardiography Analysis and Quantification&body=Please send me information about technology [TAB-5089] Real-time AI System for Echocardiography Analysis and Quantification.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Pollard, Ricquita
ricquita.pollard@nih.gov

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Pollard, Ricquita
ricquita.pollard@nih.gov

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Pollard, Ricquita
ricquita.pollard@nih.gov

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ricquita.pollard@nih.gov?subject=Web Inquiry on [TAB-5089] Real-time AI System for Echocardiography Analysis and Quantification&body=Please send me information about technology [TAB-5089] Real-time AI System for Echocardiography Analysis and Quantification.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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# data[].attributes.field_patent_titles[]
ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

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ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

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ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A
LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

# data[].attributes.field_patent_titles[]
ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

# data[].attributes.field_patent_titles[]
ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

# data[].attributes.field_patent_titles[]
ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

# data[].attributes.field_patent_titles[]
ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

# data[].attributes.field_patent_titles[]
ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

# data[].attributes.field_patent_titles[]
ECHOCARDIOGRAPHIC ESTIMATION OF RIGHT ATRIAL PRESSURE USING A LIGHTWEIGHT AND OPEN-WORLD ARTIFICIAL INTELLIGENCE SYSTEM

# data[].attributes.field_publications[].value
Zamzmia G, et al. Evaluation of An Artificial Intelligence-Based System for Echocardiographic Estimation of Right Atrial Pressure, International Journal of Cardiovascular Imaging, DOI: 10.1007/s10554-023-02941-8, September 2023.

# data[].attributes.field_publications[].processed
Zamzmia G, et al. Evaluation of An Artificial Intelligence-Based System for Echocardiographic Estimation of Right Atrial Pressure, International Journal of Cardiovascular Imaging, DOI: 10.1007/s10554-023-02941-8, September 2023.

# data[].attributes.field_publications[].value
Zamzmi G, et al. Real-time echocardiography image analysis and quantification of cardiac indices. Medical image analysis, 80, 102438. (2022). https://doi.org/10.1016/j.media.2022.102438

# data[].attributes.field_publications[].processed
Zamzmi G, et al. Real-time echocardiography image analysis and quantification of cardiac indices. Medical image analysis, 80, 102438. (2022). https://doi.org/10.1016/j.media.2022.102438

# data[].attributes.field_publications[].value
Zamzmi G, et al. Open-world active learning for echocardiography view classification. Medical Imaging 2022: Computer-Aided Diagnosis. Vol. 12033. SPIE, 2022. DOI: https://doi.org/10.1117/12.2612578

# data[].attributes.field_publications[].processed
Zamzmi G, et al. Open-world active learning for echocardiography view classification. Medical Imaging 2022: Computer-Aided Diagnosis. Vol. 12033. SPIE, 2022. DOI: https://doi.org/10.1117/12.2612578

# data[].attributes.field_publications[].value
Zamzmi G, et al. Fully automated spectral envelope and peak velocity detection from Doppler echocardiography images. Medical Imaging 2020: Computer-Aided Diagnosis. Vol. 11314G. SPIE, 2020. DOI: https://doi.org/10.1117/12.2551183

# data[].attributes.field_publications[].processed
Zamzmi G, et al. Fully automated spectral envelope and peak velocity detection from Doppler echocardiography images. Medical Imaging 2020: Computer-Aided Diagnosis. Vol. 11314G. SPIE, 2020. DOI: https://doi.org/10.1117/12.2551183

# data[].attributes.field_publications[].value
Zamzmi G, Hsu LY, Li W, Sachdev V, Antani S. Echo doppler flow classification and goodness assessment with convolutional neural networks. 2019 18th IEEE International Conference On Machine Learning And Applications (ICMLA), 2019. DOI: https://doi.org/10.1109/ICMLA.2019.00283

# data[].attributes.field_publications[].processed
Zamzmi G, Hsu LY, Li W, Sachdev V, Antani S. Echo doppler flow classification and goodness assessment with convolutional neural networks. 2019 18th IEEE International Conference On Machine Learning And Applications (ICMLA), 2019. DOI: https://doi.org/10.1109/ICMLA.2019.00283

# data[].attributes.field_technology_names[]
Real-time AI System For Echocardiography Analysis And Quantification

# data[].attributes.field_technology_names[]
Real-time AI System For Echocardiography Analysis And Quantification

# data[].attributes.field_technology_names[]
Real-time AI System For Echocardiography Analysis And Quantification

# data[].attributes.field_technology_owners[]
Clinical Center (CC), National Heart, Lung, and Blood Institute (NHLBI), NLM

# data[].attributes.field_technology_owners[]
Clinical Center (CC), National Heart, Lung, and Blood Institute (NHLBI), NIH - NLM, NLM

# data[].attributes.title
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.body.value
Summary:

The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of an eyedrop formulation to deliver a series of peptides as a gene-agnostic approach to treating inherited retinal diseases.

Description of Technology:

Retinitis pigmentosa (RP) is one of the most common inherited retinal diseases (IRDs) that is estimated to affect 1 in 4,000 people in the United States and worldwide. Over 100,000 people in the US, and 1.5 million people worldwide suffer from RP. RP leads to progressive photoreceptor cell degeneration and ultimately vision loss, with more than 90 genes implicated in molecular pathways towards photoreceptor cell death. Due to this high heterogeneity, therapeutic approaches targeting specific genes generally benefit few patients, while for most forms of RP few or no medical options are available.

Peptide drug development has made great progress recently thanks to new production, modification, and analytical technologies. Solutions of chemically synthesized bioactive peptides have unique advantages over mixed formulations. They are free of inactive ingredients that cause secondary effects. Structural biology and recombinant biologics aid in peptide design to modify amino acids, enhancing target affinity, specificity, and regulating bioactivity, as well as improving the solubility and stability of peptide drugs. Peptides can diffuse better than biologics (proteins, antibodies) with better penetrability. Compared with biologics, therapeutic peptides have demonstrably less immunogenicity and lower production costs.

This technology optimizes synthetic peptides that are soluble, stable, and protect the retina. A series of peptides derived from the neurotrophic region of PEDF 17-mer (human sequence 98-114 amino acids, N- and C-terminus uncapped) is designed and synthesized. They have a series of truncations from the amino and carboxy ends, and internal region, as well as isosteric amino acid replacements, and amino terminal additions such as capping (X) and amidation (Y) to prevent exopeptidases from degrading the peptide. The peptides are optimized to protect photoreceptors and other retinal cells against death and degeneration. They optimized for solubility, stability, efficacy, in protecting the retina at the structural, morphological and functional level. The peptides can be tested in vitro, ex vivo, in cells and in vivo using models of retinal degeneration. The peptides can be used as eyedrops in vivo.

Potential Commercial Applications:

Potential simple and effective treatment for inherited eye diseases contributing to Retinitis Pigmentosa (RP) and macular degenerations, such as AMD and geographic atrophy

Prevent disease progression by protecting degenerating photoreceptors

Competitive Advantages:

Chemically synthesized bioactive peptide solutions are free of inactive ingredients that cause secondary effects as compared to mixed formulations

Enhanced target affinity, specificity, bioactivity, as well as in improved solubility, and stability

Peptides can diffuse better than biologics (proteins, antibodies) with better penetrability

Compared to biologics, therapeutic peptides have demonstrably less immunogenicity and lower production costs

Eye drop formulation is accessible to more patients and provides an easy administration route

PEDF formulation mimics the natural protective process lost in patients with inherited eye diseases, contributing to RP

# data[].attributes.body.processed
Summary:

The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of an eyedrop formulation to deliver a series of peptides as a gene-agnostic approach to treating inherited retinal diseases.

Description of Technology:

Retinitis pigmentosa (RP) is one of the most common inherited retinal diseases (IRDs) that is estimated to affect 1 in 4,000 people in the United States and worldwide. Over 100,000 people in the US, and 1.5 million people worldwide suffer from RP. RP leads to progressive photoreceptor cell degeneration and ultimately vision loss, with more than 90 genes implicated in molecular pathways towards photoreceptor cell death. Due to this high heterogeneity, therapeutic approaches targeting specific genes generally benefit few patients, while for most forms of RP few or no medical options are available.

Peptide drug development has made great progress recently thanks to new production, modification, and analytical technologies. Solutions of chemically synthesized bioactive peptides have unique advantages over mixed formulations. They are free of inactive ingredients that cause secondary effects. Structural biology and recombinant biologics aid in peptide design to modify amino acids, enhancing target affinity, specificity, and regulating bioactivity, as well as improving the solubility and stability of peptide drugs. Peptides can diffuse better than biologics (proteins, antibodies) with better penetrability. Compared with biologics, therapeutic peptides have demonstrably less immunogenicity and lower production costs.

This technology optimizes synthetic peptides that are soluble, stable, and protect the retina. A series of peptides derived from the neurotrophic region of PEDF 17-mer (human sequence 98-114 amino acids, N- and C-terminus uncapped) is designed and synthesized. They have a series of truncations from the amino and carboxy ends, and internal region, as well as isosteric amino acid replacements, and amino terminal additions such as capping (X) and amidation (Y) to prevent exopeptidases from degrading the peptide. The peptides are optimized to protect photoreceptors and other retinal cells against death and degeneration. They optimized for solubility, stability, efficacy, in protecting the retina at the structural, morphological and functional level. The peptides can be tested in vitro, ex vivo, in cells and in vivo using models of retinal degeneration. The peptides can be used as eyedrops in vivo.

Potential Commercial Applications:

Potential simple and effective treatment for inherited eye diseases contributing to Retinitis Pigmentosa (RP) and macular degenerations, such as AMD and geographic atrophy

Prevent disease progression by protecting degenerating photoreceptors

Competitive Advantages:

Chemically synthesized bioactive peptide solutions are free of inactive ingredients that cause secondary effects as compared to mixed formulations

Enhanced target affinity, specificity, bioactivity, as well as in improved solubility, and stability

Peptides can diffuse better than biologics (proteins, antibodies) with better penetrability

Compared to biologics, therapeutic peptides have demonstrably less immunogenicity and lower production costs

Eye drop formulation is accessible to more patients and provides an easy administration route

PEDF formulation mimics the natural protective process lost in patients with inherited eye diseases, contributing to RP

# data[].attributes.field_collaboration_description.value
The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of an eyedrop formulation to deliver a series of peptides as a gene-agnostic approach to treating inherited retinal diseases.

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The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of an eyedrop formulation to deliver a series of peptides as a gene-agnostic approach to treating inherited retinal diseases.

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National Heart, Lung, and Blood Institute (NHLBI)

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National Heart, Lung, and Blood Institute (NHLBI)

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National Heart, Lung, and Blood Institute (NHLBI)

# data[].attributes.field_inventor_companies[]
National Heart, Lung, and Blood Institute (NHLBI)

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ricquita.pollard@nih.gov?subject=Web Inquiry on [TAB-5092] MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE&body=Please send me information about technology [TAB-5092] MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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Pollard, Ricquita
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# data[].attributes.field_patent_titles[]
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.field_patent_titles[]
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.field_patent_titles[]
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.field_patent_titles[]
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.field_patent_titles[]
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.field_patent_titles[]
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.field_patent_titles[]
MODIFIED PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND METHODS OF USE

# data[].attributes.field_publications[].value
Bernardo-Colon A, et al. H105A peptide eye drops promote photoreceptor survival in murine and human models of retinal degeneration. (PMID: 40118996)

# data[].attributes.field_publications[].processed
Bernardo-Colon A, et al. H105A peptide eye drops promote photoreceptor survival in murine and human models of retinal degeneration. (PMID: 40118996)

# data[].attributes.field_publications[].value
Valiente-Soriano FJ, et al. Pigment Epithelium-Derived Factor (PEDF) Fragments Prevent Mouse Cone Photoreceptor Cell Loss Induced by Focal Phototoxicity In Vivo. (PMID: 33008127)

# data[].attributes.field_publications[].processed
Valiente-Soriano FJ, et al. Pigment Epithelium-Derived Factor (PEDF) Fragments Prevent Mouse Cone Photoreceptor Cell Loss Induced by Focal Phototoxicity In Vivo. (PMID: 33008127)

# data[].attributes.field_publications[].value
Hernández-Pinto A, et al. PEDF peptides promote photoreceptor survival in rd10 retina models. (PMID: 30980815)

# data[].attributes.field_publications[].processed
Hernández-Pinto A, et al. PEDF peptides promote photoreceptor survival in rd10 retina models. (PMID: 30980815)

# data[].attributes.field_publications[].value
Kenealey J, et al. Small Retinoprotective Peptides Reveal a Receptor-binding Region on Pigment Epithelium-derived Factor. (PMID: 26304116)

# data[].attributes.field_publications[].processed
Kenealey J, et al. Small Retinoprotective Peptides Reveal a Receptor-binding Region on Pigment Epithelium-derived Factor. (PMID: 26304116)

# data[].attributes.field_related_inventions[].processed
E-028-2023

# data[].attributes.field_technology_names[]
Photoreceptor-protective Peptides based on truncated PEDF

# data[].attributes.field_technology_owners[]
National Eye Institute (NEI), National Heart, Lung, and Blood Institute (NHLBI), National Heart, Lung, and Blood Institute (NHLBI)

# data[].attributes.title
Pigment Epithelium-Derived Factor Peptides and Their Use for Treating Retinal Degeneration

# data[].attributes.body.value
Summary:

The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of an AAV2-based delivery system or an eyedrop formulation to deliver a Pigment Epithelium-Derived Factor (PEDF) peptide as a gene-agnostic approach to treating inherited retinal diseases.

Description of Technology:

Retinitis pigmentosa (RP) is one of the most common inherited retinal diseases (IRDs) – estimated to affect 1 in 4,000 people worldwide. Over 100,000 people in the US and 1.5 million people worldwide suffer from RP. This disease leads to progressive photoreceptor cell degeneration and, ultimately, vision loss. More than 90 genes are implicated in molecular pathways towards photoreceptor cell death. Due to this high heterogeneity, therapeutic approaches targeting specific genes generally benefit few patients. For most forms of RP, few or no medical options are available. Thus, there remains a need to identify new and more effective treatments for RP and other inherited retinal degenerations. Mutation-independent strategies to protect photoreceptors against continued damage and degradation are appealing approaches.

To delay photoreceptor degeneration, we propose using neurotrophic molecules as a mutation-independent approach using pigment epithelium-derived factor (PEDF). PEDF is a multifunctional member of the serine proteinase inhibitor (serpin) family with neurotrophic and antiangiogenic properties in the retina. Researchers at the NEI developed a peptide of 17 amino acid residues (17-mer) from the receptor-binding domain of PEDF. It contains amino acid substitution at position 105 from a histidine to an alanine (PEDF 17-mer[H105A]). H105A exhibits a highly potent protective effect on photoreceptors using in vivo mouse models of RP.

The technology encompasses two delivery approaches for this proprietary peptide: (1) an eyedrop formulation and/or (2) an Adeno-Associated Vector 2 (AAV2). A sustained delivery system delivers the 17-mer [H105A] to treat or prevent photoreceptor degradation and vision loss in patients with IRDs (e.g., retinitis pigmentosa, Leber congenital amaurosis, cone-rod dystrophy, Stargardt-like macular degeneration or maculopathy) or age-related macular degenerations (AMD). The technology is available for licensing and co-development.

Potential Commercial Applications:

Minimally invasive therapy to prevent photoreceptor degeneration in retinal disorders (IRDs and AMD)

Retinitis Pigmentosa (RP), macular degeneration, and other related diseases

AAV2 vectors for delivery of genes to retinal cells both preventative and therapeutic

Prevent disease progression to late-stage RP

Competitive Advantages:

Favorable safety profile

Large addressable market given applications to IRDs and AMD (USD 13.7 billion in 2023 and an estimated compound annual growth rate (CAGR) of 9.6% from 2024 to 2032

Partially established regulatory path, as their AAV2 vector is identical to Luxturna, an FDA-approved therapy for retinal dystrophy

Superior diffusion and penetrability than biologics

Demonstrably less immunogenicity and lower production costs than biologics

Eye drop formulation has larger addressable market

Eye drop formulation provides easy administration route

Broad-spectrum therapeutic approach:

PEDF mimics the natural protective process lost in patients with inherited eye diseases

Protective effects on photoreceptors are independent of the gene mutations causing degeneration

Chemically synthesized bioactive peptide solutions are free of inactive ingredients, causing fewer secondary effects than mixed formulations

# data[].attributes.body.processed
Summary:

The National Eye Institute (NEI) seeks research co-development partners and/or licensees for the development of an AAV2-based delivery system or an eyedrop formulation to deliver a Pigment Epithelium-Derived Factor (PEDF) peptide as a gene-agnostic approach to treating inherited retinal diseases.

Description of Technology:

Retinitis pigmentosa (RP) is one of the most common inherited retinal diseases (IRDs) – estimated to affect 1 in 4,000 people worldwide. Over 100,000 people in the US and 1.5 million people worldwide suffer from RP. This disease leads to progressive photoreceptor cell degeneration and, ultimately, vision loss. More than 90 genes are implicated in molecular pathways towards photoreceptor cell death. Due to this high heterogeneity, therapeutic approaches targeting specific genes generally benefit few patients. For most forms of RP, few or no medical options are available. Thus, there remains a need to identify new and more effective treatments for RP and other inherited retinal degenerations. Mutation-independent strategies to protect photoreceptors against continued damage and degradation are appealing approaches.

To delay photoreceptor degeneration, we propose using neurotrophic molecules as a mutation-independent approach using pigment epithelium-derived factor (PEDF). PEDF is a multifunctional member of the serine proteinase inhibitor (serpin) family with neurotrophic and antiangiogenic properties in the retina. Researchers at the NEI developed a peptide of 17 amino acid residues (17-mer) from the receptor-binding domain of PEDF. It contains amino acid substitution at position 105 from a histidine to an alanine (PEDF 17-mer[H105A]). H105A exhibits a highly potent protective effect on photoreceptors using in vivo mouse models of RP.

The technology encompasses two delivery approaches for this proprietary peptide: (1) an eyedrop formulation and/or (2) an Adeno-Associated Vector 2 (AAV2). A sustained delivery system delivers the 17-mer [H105A] to treat or prevent photoreceptor degradation and vision loss in patients with IRDs (e.g., retinitis pigmentosa, Leber congenital amaurosis, cone-rod dystrophy, Stargardt-like macular degeneration or maculopathy) or age-related macular degenerations (AMD). The technology is available for licensing and co-development.

Potential Commercial Applications:

Minimally invasive therapy to prevent photoreceptor degeneration in retinal disorders (IRDs and AMD)

Retinitis Pigmentosa (RP), macular degeneration, and other related diseases

AAV2 vectors for delivery of genes to retinal cells both preventative and therapeutic

Prevent disease progression to late-stage RP

Competitive Advantages:

Favorable safety profile

Large addressable market given applications to IRDs and AMD (USD 13.7 billion in 2023 and an estimated compound annual growth rate (CAGR) of 9.6% from 2024 to 2032

Partially established regulatory path, as their AAV2 vector is identical to Luxturna, an FDA-approved therapy for retinal dystrophy

Superior diffusion and penetrability than biologics

Demonstrably less immunogenicity and lower production costs than biologics

Eye drop formulation has larger addressable market

Eye drop formulation provides easy administration route

Broad-spectrum therapeutic approach:

PEDF mimics the natural protective process lost in patients with inherited eye diseases

Protective effects on photoreceptors are independent of the gene mutations causing degeneration

Chemically synthesized bioactive peptide solutions are free of inactive ingredients, causing fewer secondary effects than mixed formulations

# data[].attributes.field_collaboration_description.value
Researchers at the ​NEI​ seek ​licensing and/or co-development research collaborations ​ for the development of an AVV2-based delivery system or an eyedrop formulation to deliver a PEDF peptide as a gene-agnostic approach to treating inherited retinal diseases.

# data[].attributes.field_collaboration_description.processed
Researchers at the ​NEI​ seek ​licensing and/or co-development research collaborations ​ for the development of an AVV2-based delivery system or an eyedrop formulation to deliver a PEDF peptide as a gene-agnostic approach to treating inherited retinal diseases.

# data[].attributes.field_licensingcontact_hrefs[]
ricquita.pollard@nih.gov?subject=Web Inquiry on [TAB-5091] Pigment Epithelium-Derived Factor Peptides and Their Use for Treating Retinal Degeneration&body=Please send me information about technology [TAB-5091] Pigment Epithelium-Derived Factor Peptides and Their Use for Treating Retinal Degeneration.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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Pollard, Ricquita
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PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

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PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

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PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

# data[].attributes.field_patent_titles[]
PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

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PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

# data[].attributes.field_patent_titles[]
PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

# data[].attributes.field_patent_titles[]
PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

# data[].attributes.field_patent_titles[]
PIGMENT EPITHELIUM-DERIVED FACTOR PEPTIDES AND USE FOR TREATING RETINAL
DEGENERATION

# data[].attributes.field_publications[].value
Bernardo-Colón A, et al. H105A peptide eye drops promote photoreceptor survival in murine and human models of retinal degeneration. (PMID: 40118996)

# data[].attributes.field_publications[].processed
Bernardo-Colón A, et al. H105A peptide eye drops promote photoreceptor survival in murine and human models of retinal degeneration. (PMID: 40118996)

# data[].attributes.field_publications[].value
Valiente-Soriano FJ, et al. Pigment Epithelium-Derived Factor (PEDF) Fragments Prevent Mouse Cone Photoreceptor Cell Loss Induced by Focal Phototoxicity In Vivo. (PMID: 33008127)

# data[].attributes.field_publications[].processed
Valiente-Soriano FJ, et al. Pigment Epithelium-Derived Factor (PEDF) Fragments Prevent Mouse Cone Photoreceptor Cell Loss Induced by Focal Phototoxicity In Vivo. (PMID: 33008127)

# data[].attributes.field_publications[].value
Hernández-Pinto A, et al. PEDF peptides promote photoreceptor survival in rd10 retina models. (PMID: 30980815)

# data[].attributes.field_publications[].processed
Hernández-Pinto A, et al. PEDF peptides promote photoreceptor survival in rd10 retina models. (PMID: 30980815)

# data[].attributes.field_publications[].value
Kenealey J, et al. Small Retinoprotective Peptides Reveal a Receptor-binding Region on Pigment Epithelium-derived Factor. (PMID: 26304116)

# data[].attributes.field_publications[].processed
Kenealey J, et al. Small Retinoprotective Peptides Reveal a Receptor-binding Region on Pigment Epithelium-derived Factor. (PMID: 26304116)

# data[].attributes.field_related_inventions[].processed
E-156-2023

# data[].attributes.field_technology_names[]
In Vivo Assay For Drug Discovery And Detection Of Photoreceptor Survival Factors: Discovery Of The PEDF Peptide 17-
mer[H105A]

# data[].attributes.field_technology_owners[]
National Eye Institute (NEI), University of Modena and Reggio Emilia, University of Modena and Reggio Emilia

# data[].attributes.title
Nucleophosmin 1 (NPM1) Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia

# data[].attributes.body.value
Summary:

The NCI seeks research co-development partners or licensees for Nucleophosmin 1 (NPM1) Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia.

Description of Technology:

Acute myeloid leukemia (AML) is a rare form of blood cancer affecting myeloid stem and progenitor cells, associated with a poor prognosis and a 5-year survival rate of ~33%. Current treatments, including intensive chemotherapy and stem cell transplantation, are not suitable for all patients and can cause significant toxicities, including low blood cell counts, infection and graft-versus-host disease. Therefore, there is a need for safer and more effective treatments.

This specific invention concerns the isolation of two highly specific T cell receptors (TCRs), known as TCR6 and TCR7, recognizing a neoepitope, AVEEVSLRK. The neoepitope is derived from mutant Nucleophosmin 1 (NPM1) and presented in the context of HLA-A*11:01. Pre-clinical results for these TCRs revealed robust and specific cytotoxicity against a leukemia cell line and several patient-derived AML samples expressing the NPM1 mutation and HLA-A*11:01. Furthermore, they showed no cross-reactivity to normal peripheral blood mononuclear cells, structurally similar peptides or unrelated HLA alleles. These results suggest these novel TCRs represent a potential adoptive T cell therapy for the treatment of AML.

Potential Commercial Applications:

Acute myeloid leukemia patients expressing HLA-A*11:01.

Competitive Advantages:

Highly specific targeting of mutant NPM1

Minimed off-target effects with enhanced safety profile

•Significant unmet medical need for AML patients

# data[].attributes.body.processed
Summary:

The NCI seeks research co-development partners or licensees for Nucleophosmin 1 (NPM1) Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia.

Description of Technology:

Acute myeloid leukemia (AML) is a rare form of blood cancer affecting myeloid stem and progenitor cells, associated with a poor prognosis and a 5-year survival rate of ~33%. Current treatments, including intensive chemotherapy and stem cell transplantation, are not suitable for all patients and can cause significant toxicities, including low blood cell counts, infection and graft-versus-host disease. Therefore, there is a need for safer and more effective treatments.

This specific invention concerns the isolation of two highly specific T cell receptors (TCRs), known as TCR6 and TCR7, recognizing a neoepitope, AVEEVSLRK. The neoepitope is derived from mutant Nucleophosmin 1 (NPM1) and presented in the context of HLA-A*11:01. Pre-clinical results for these TCRs revealed robust and specific cytotoxicity against a leukemia cell line and several patient-derived AML samples expressing the NPM1 mutation and HLA-A*11:01. Furthermore, they showed no cross-reactivity to normal peripheral blood mononuclear cells, structurally similar peptides or unrelated HLA alleles. These results suggest these novel TCRs represent a potential adoptive T cell therapy for the treatment of AML.

Potential Commercial Applications:

Acute myeloid leukemia patients expressing HLA-A*11:01.

Competitive Advantages:

Highly specific targeting of mutant NPM1

Minimed off-target effects with enhanced safety profile

•Significant unmet medical need for AML patients

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for NPM1 Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for NPM1 Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia.

# data[].attributes.field_licensingcontact_hrefs[]
abritee.dhal@nih.gov?subject=Web Inquiry on [TAB-5097] Nucleophosmin 1 (NPM1) Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia&body=Please send me information about technology [TAB-5097] Nucleophosmin 1 (NPM1) Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia.&bcc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts[].value
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
abritee.dhal@nih.gov?subject=Web Inquiry on [TAB-5097] Nucleophosmin 1 (NPM1) Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia&body=Please send me information about technology [TAB-5097] Nucleophosmin 1 (NPM1) Mutation-Specific T Cell Receptors for Targeted Treatment of Acute Myeloid Leukemia.&bcc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/908,266
Filed on 2025-10-30
Status: Pending

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/908,266
Filed on 2025-10-30
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/908,266
Filed on 2025-10-30
Status: Pending

# data[].attributes.field_patent_titles[]
NUCLEOPHOSMIN 1 MUTATION-SPECIFIC T CELL RECEPTORS

# data[].attributes.field_technology_names[]
NPM1 mutation-specific T cell receptors for treatment of HLA-A*11:01-positive acute myeloid leukemia

# data[].attributes.title
DNA Methylation-Based Cancer Diagnostics for Accurate Tumor Classification

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a collection of T-cell receptors (TCRs) that specifically target the mutated KRAS antigen.

This technology encompasses a DNA methylation–based diagnostic platform designed to improve the accuracy and consistency of cancer classification, with demonstrated utility for tumors of the central nervous system, kidney, and hematopoietic system. By identifying disease-specific methylation signatures, the approach reduces interobserver variability and enhances diagnostic confidence. The central nervous system (CNS) classifier is built from a curated reference set of 16,567 methylation profiles and organizes tumors into 22 families and 133 clinically relevant diagnostic classes, including 21 newly developed methylation classes not represented in other existing tools. Across multiple independent validation cohorts (n = 5,875), the classifier demonstrated robust performance, and in a clinical-impact analysis of 1,204 NIH validation cases, methylation profiling materially influenced final diagnosis in 74.4% of cases by refining, increasing precision, or reclassifying. The CNS classifier was deployed as a user-facing software tool, MethylScape Analysis, which streamlines methylation-based classification workflows for CNS tumors (https://methylscape.ccr.cancer.gov/). The development of multiple specialized classifiers supports a more granular understanding of tumor biology and  informed clinical decision-making.

Description of Technology:

Accurate CNS tumor classification can be challenging when tumors show overlapping histology, limited tissue or atypical features. A meaningful fraction of cases remains unclassified or assigned with limited confidence with current molecular tools. These diagnostic ambiguities directly affect subtype and grade assignment which, in turn, influence treatment planning, prognosis, and clinical trial eligibility. Variability across observers and institutions can lead to additional testing, delays, and inconsistent diagnoses.

The NCI/Bethesda classifier addresses this gap using DNA methylation patterns as a robust molecular fingerprint. It applies a stratified machine learning framework to extend diagnostic coverage and improve assignment confidence for CNS tumors. The classifier was developed from a rigorously curated reference set of over 16k methylation profiles, structured into 22 tumor families and 133 clinically relevant diagnostic classes and includes 21 recently developed methylation classes not represented in existing tools. The approach has been validated across multiple independent cohorts (n = 5,875) and supports deployment through MethylScape, a public web-based portal that streamlines classifier execution for broad accessibility. In an NIH validation cohort analysis of 1,204 high-confidence matches with pre-methylation diagnoses available, methylation profiling confirmed the initial diagnosis in 25.6% of cases while driving clinically meaningful diagnostic evolution in the remainder, including refined diagnosis (subtyping) in 14.6%, new diagnosis with increased precision in 54.7%, and substantial diagnostic reclassification in 5.0%—changes that are expected to affect patient management in the reclassification subset.

Renal neoplasms present a parallel diagnostic challenge due to morphologic and molecular heterogeneity, overlapping microscopic features, and interobserver variability. As a result, a subset of cases are unclassifiable even after immunohistochemical, mutation and cytogenetic workups. To address this, the Kidney Classifier component of this platform leverages genome-wide DNA methylation profiling (feasible on formalin-fixed paraffin-embedded tissue using robust array-based methods). It was developed through examination of methylation signatures from over 2,000 renal neoplasms, identifying 23 coherent methylation groups that correlate with known tumor types and reveal clinically relevant novel subtypes. A machine learning classifier trained on 1,284 samples was externally tested on 287 renal neoplasms, demonstrating >90% concordance between expected neoplasm type and high-score methylation-based classification, with discordant cases highlighting opportunities for diagnostic reclassification and improved precision in challenging renal tumor evaluations.

Licensing and collaboration opportunities include commercial development of methylation-based diagnostic tests and/or software-enabled classification solutions for clinical laboratories, reference labs, and diagnostic companies. Partners may engage in external validation (retrospective and prospective), assay standardization, integration into pathology workflows and reporting systems, and extension of classifier coverage to additional tumor types and multi-institutional datasets. Consistent with consensus recommendations for complementary classifiers, the inventors are also interested in collaborations that: (1) operationalize multi-classifier strategies (concordant/complementary prediction to increase confidence; (2) leverage discordance to trigger orthogonal follow-up) and (3) accelerate clinical translation through scalable deployment models- including CLIA laboratory workflows and regulated diagnostic pathways.

Potential Commercial Applications:

Molecular classification and diagnosis of CNS and kidney tumors, including difficult-to-classify and low-confidence cases

Diagnostic subtyping aligned to WHO-guided entities

Reference-lab and hospital-lab deployment

Clinical trial stratification and translational research cohort harmonization

Multi-classifier diagnostic decision support

Cancer treatment development

Competitive Advantages:

Developed from a rigorously curated, large reference set of methylation profiles

Clinically relevant CNS diagnostic

CNS tumor methylation classes not represented in existing tools, expanding diagnostic coverage

Clinical-impact analysis creating superior diagnostic precision

Superior classifier for kidney cancer

Superior classifiers for multiple solid, difficult-to-diagnose tumors

Integrative into clinical workflows, improving diagnostic practices and enhancing patient care

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a collection of T-cell receptors (TCRs) that specifically target the mutated KRAS antigen.

This technology encompasses a DNA methylation–based diagnostic platform designed to improve the accuracy and consistency of cancer classification, with demonstrated utility for tumors of the central nervous system, kidney, and hematopoietic system. By identifying disease-specific methylation signatures, the approach reduces interobserver variability and enhances diagnostic confidence. The central nervous system (CNS) classifier is built from a curated reference set of 16,567 methylation profiles and organizes tumors into 22 families and 133 clinically relevant diagnostic classes, including 21 newly developed methylation classes not represented in other existing tools. Across multiple independent validation cohorts (n = 5,875), the classifier demonstrated robust performance, and in a clinical-impact analysis of 1,204 NIH validation cases, methylation profiling materially influenced final diagnosis in 74.4% of cases by refining, increasing precision, or reclassifying. The CNS classifier was deployed as a user-facing software tool, MethylScape Analysis, which streamlines methylation-based classification workflows for CNS tumors (https://methylscape.ccr.cancer.gov/). The development of multiple specialized classifiers supports a more granular understanding of tumor biology and  informed clinical decision-making.

Description of Technology:

Accurate CNS tumor classification can be challenging when tumors show overlapping histology, limited tissue or atypical features. A meaningful fraction of cases remains unclassified or assigned with limited confidence with current molecular tools. These diagnostic ambiguities directly affect subtype and grade assignment which, in turn, influence treatment planning, prognosis, and clinical trial eligibility. Variability across observers and institutions can lead to additional testing, delays, and inconsistent diagnoses.

The NCI/Bethesda classifier addresses this gap using DNA methylation patterns as a robust molecular fingerprint. It applies a stratified machine learning framework to extend diagnostic coverage and improve assignment confidence for CNS tumors. The classifier was developed from a rigorously curated reference set of over 16k methylation profiles, structured into 22 tumor families and 133 clinically relevant diagnostic classes and includes 21 recently developed methylation classes not represented in existing tools. The approach has been validated across multiple independent cohorts (n = 5,875) and supports deployment through MethylScape, a public web-based portal that streamlines classifier execution for broad accessibility. In an NIH validation cohort analysis of 1,204 high-confidence matches with pre-methylation diagnoses available, methylation profiling confirmed the initial diagnosis in 25.6% of cases while driving clinically meaningful diagnostic evolution in the remainder, including refined diagnosis (subtyping) in 14.6%, new diagnosis with increased precision in 54.7%, and substantial diagnostic reclassification in 5.0%—changes that are expected to affect patient management in the reclassification subset.

Renal neoplasms present a parallel diagnostic challenge due to morphologic and molecular heterogeneity, overlapping microscopic features, and interobserver variability. As a result, a subset of cases are unclassifiable even after immunohistochemical, mutation and cytogenetic workups. To address this, the Kidney Classifier component of this platform leverages genome-wide DNA methylation profiling (feasible on formalin-fixed paraffin-embedded tissue using robust array-based methods). It was developed through examination of methylation signatures from over 2,000 renal neoplasms, identifying 23 coherent methylation groups that correlate with known tumor types and reveal clinically relevant novel subtypes. A machine learning classifier trained on 1,284 samples was externally tested on 287 renal neoplasms, demonstrating >90% concordance between expected neoplasm type and high-score methylation-based classification, with discordant cases highlighting opportunities for diagnostic reclassification and improved precision in challenging renal tumor evaluations.

Licensing and collaboration opportunities include commercial development of methylation-based diagnostic tests and/or software-enabled classification solutions for clinical laboratories, reference labs, and diagnostic companies. Partners may engage in external validation (retrospective and prospective), assay standardization, integration into pathology workflows and reporting systems, and extension of classifier coverage to additional tumor types and multi-institutional datasets. Consistent with consensus recommendations for complementary classifiers, the inventors are also interested in collaborations that: (1) operationalize multi-classifier strategies (concordant/complementary prediction to increase confidence; (2) leverage discordance to trigger orthogonal follow-up) and (3) accelerate clinical translation through scalable deployment models- including CLIA laboratory workflows and regulated diagnostic pathways.

Potential Commercial Applications:

Molecular classification and diagnosis of CNS and kidney tumors, including difficult-to-classify and low-confidence cases

Diagnostic subtyping aligned to WHO-guided entities

Reference-lab and hospital-lab deployment

Clinical trial stratification and translational research cohort harmonization

Multi-classifier diagnostic decision support

Cancer treatment development

Competitive Advantages:

Developed from a rigorously curated, large reference set of methylation profiles

Clinically relevant CNS diagnostic

CNS tumor methylation classes not represented in existing tools, expanding diagnostic coverage

Clinical-impact analysis creating superior diagnostic precision

Superior classifier for kidney cancer

Superior classifiers for multiple solid, difficult-to-diagnose tumors

Integrative into clinical workflows, improving diagnostic practices and enhancing patient care

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations to further develop and possibly expand the classification capabilities of the software.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations to further develop and possibly expand the classification capabilities of the software.

# data[].attributes.field_licensingcontact_htmls[]
Greene, Jaime
greenejaime@mail.nih.gov

# data[].attributes.field_licensing_contacts[].value
Greene, Jaime
greenejaime@mail.nih.gov

# data[].attributes.field_licensing_contacts[].processed
Greene, Jaime
greenejaime@mail.nih.gov

# data[].attributes.field_patents[].value
US
Ordinary Patent (ORD) 18/499,833
Filed on 2023-11-01
Status: Pending

# data[].attributes.field_patents[].processed
US
Ordinary Patent (ORD) 18/499,833
Filed on 2023-11-01
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Ordinary Patent (ORD) 18/499,833
Filed on 2023-11-01
Status: Pending

# data[].attributes.field_publications[].value
Singh O., et.al.  Robust DNA Methylation-Based Diagnosis and Classification for Central Nervous 1 System Tumors, submitted

# data[].attributes.field_publications[].processed
Singh O., et.al.  Robust DNA Methylation-Based Diagnosis and Classification for Central Nervous 1 System Tumors, submitted

# data[].attributes.field_publications[].value
Aldape K., et.al. cIMPACT-NOW update 9: Recommendations on utilization of genome-wide DNA methylation profiling for central nervous system tumor diagnostics. Neurooncol Adv. 2025 Jan 3;7(1):vdae228. PMID: 39902391

# data[].attributes.field_publications[].processed
Aldape K., et.al. cIMPACT-NOW update 9: Recommendations on utilization of genome-wide DNA methylation profiling for central nervous system tumor diagnostics. Neurooncol Adv. 2025 Jan 3;7(1):vdae228. PMID: 39902391

# data[].attributes.field_publications[].value
Papanicolau-Sengos A., et.al., Mod Pathol. 2025 Nov;38(11):100884, PMID: 40939817

# data[].attributes.field_publications[].processed
Papanicolau-Sengos A., et.al., Mod Pathol. 2025 Nov;38(11):100884, PMID: 40939817

# data[].attributes.field_technology_names[]
DNA methylation-based cancer diagnostics for tumors of the central nervous system, kidney and hematopoietic system

# data[].attributes.field_technology_owners[]
Laboratory of Pathology, National Cancer Institute (NCI), NCI - CCR

# data[].attributes.title
Combined RNA and DNA Vaccination Strategy for Improving the Vaccine Immune Response

# data[].attributes.body.value
Description of Technology:

The development of an effective HIV vaccine has been ongoing. HIV sequence diversity and immunodominance are major obstacles in the design of an effective vaccine. Researchers at the National Cancer Institute (NCI) developed a novel vaccine strategy combining both DNA and mRNA vaccination to induce an effective immune response. This combination strategy could also be used to develop vaccines against cancer or other infectious diseases (ex. SARS-CoV-2).
Previous studies by NCI determined that regions of the polypeptides Gag and Env are both essential to the core structure and envelope of the HIV-1 virus. Co-administration of DNA expressing Gag and Env elicits a protective immune response and reduces infection burden.  This current technology relates to earlier technology from the same inventors describing the identification of the conserved elements (CE) within HIV-1 p24Gag. Specifically, the inventors demonstrated that priming with p24gag CE followed by vaccination with either a full-length p55gag DNA plasmid or p24gag CE DNA together with full-length p55gag DNA increased the CE responses compared to vaccination with p24CE DNA alone.

The current invention expands upon the earlier technology, combining DNA and RNA vaccination strategies to induce an effective HIV immune response.  The inventors demonstrated that administration of gag mRNA/LNP efficiently boosted both humoral and cellular responses in rhesus macaques previously immunized by a Gag DNA-based vaccine. Furthermore, the mRNA/LNP as booster vaccination induced more potent cytotoxic T cell responses than using mRNA as prime. Overall, this invention describes a heterologous prime/boost regimen including a DNA prime followed by mRNA boost vaccination with the same or similar immunogens – resulting in optimal levels of humoral and cellular immune response. The use of a mRNA booster to stimulate DNA primed immunity may be broadly applicable as a vaccination strategy for other infectious diseases and cancer.

Potential Commercial Applications:

Prophylactic and therapeutic vaccines for HIV

Prophylactic and therapeutic vaccines for infectious diseases

Prophylactic and therapeutic vaccines for cancer

Competitive Advantages:

Addresses key hurdle faced by current HIV vaccines: sequence diversity of HIV and immunodominance of specific epitopes

Induces optimal cellular and humoral responses

Reduces infectious burden

Potential vaccine strategy applicable to other non-HIV diseases, such as cancer

In vivo validation of vaccine strategy in non-human primates (rhesus macaques)

# data[].attributes.body.processed
Description of Technology:

The development of an effective HIV vaccine has been ongoing. HIV sequence diversity and immunodominance are major obstacles in the design of an effective vaccine. Researchers at the National Cancer Institute (NCI) developed a novel vaccine strategy combining both DNA and mRNA vaccination to induce an effective immune response. This combination strategy could also be used to develop vaccines against cancer or other infectious diseases (ex. SARS-CoV-2).
Previous studies by NCI determined that regions of the polypeptides Gag and Env are both essential to the core structure and envelope of the HIV-1 virus. Co-administration of DNA expressing Gag and Env elicits a protective immune response and reduces infection burden.  This current technology relates to earlier technology from the same inventors describing the identification of the conserved elements (CE) within HIV-1 p24Gag. Specifically, the inventors demonstrated that priming with p24gag CE followed by vaccination with either a full-length p55gag DNA plasmid or p24gag CE DNA together with full-length p55gag DNA increased the CE responses compared to vaccination with p24CE DNA alone.

The current invention expands upon the earlier technology, combining DNA and RNA vaccination strategies to induce an effective HIV immune response.  The inventors demonstrated that administration of gag mRNA/LNP efficiently boosted both humoral and cellular responses in rhesus macaques previously immunized by a Gag DNA-based vaccine. Furthermore, the mRNA/LNP as booster vaccination induced more potent cytotoxic T cell responses than using mRNA as prime. Overall, this invention describes a heterologous prime/boost regimen including a DNA prime followed by mRNA boost vaccination with the same or similar immunogens – resulting in optimal levels of humoral and cellular immune response. The use of a mRNA booster to stimulate DNA primed immunity may be broadly applicable as a vaccination strategy for other infectious diseases and cancer.

Potential Commercial Applications:

Prophylactic and therapeutic vaccines for HIV

Prophylactic and therapeutic vaccines for infectious diseases

Prophylactic and therapeutic vaccines for cancer

Competitive Advantages:

Addresses key hurdle faced by current HIV vaccines: sequence diversity of HIV and immunodominance of specific epitopes

Induces optimal cellular and humoral responses

Reduces infectious burden

Potential vaccine strategy applicable to other non-HIV diseases, such as cancer

In vivo validation of vaccine strategy in non-human primates (rhesus macaques)

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for development of a RNA/DNA combination vaccine against infectious diseases (ex: HIV, SARS-CoV-2) or cancer

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for development of a RNA/DNA combination vaccine against infectious diseases (ex: HIV, SARS-CoV-2) or cancer

# data[].attributes.field_licensingcontact_hrefs[]
rose.freel@nih.gov?subject=Web Inquiry on [TAB-4123] Combined RNA and DNA Vaccination Strategy for Improving the Vaccine Immune Response&body=Please send me information about technology [TAB-4123] Combined RNA and DNA Vaccination Strategy for Improving the Vaccine Immune Response.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Freel, Rose
rose.freel@nih.gov

# data[].attributes.field_licensing_contacts[].value
Freel, Rose
rose.freel@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Freel, Rose
rose.freel@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
rose.freel@nih.gov?subject=Web Inquiry on [TAB-4123] Combined RNA and DNA Vaccination Strategy for Improving the Vaccine Immune Response&body=Please send me information about technology [TAB-4123] Combined RNA and DNA Vaccination Strategy for Improving the Vaccine Immune Response.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/358,919
Filed on 2022-07-07
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/358,919
Filed on 2022-07-07
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2023/069057
Filed on 2023-06-26
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2023/069057
Filed on 2023-06-26
Status: Expired

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/358,919
Filed on 2022-07-07
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2023/069057
Filed on 2023-06-26
Status: Expired

# data[].attributes.field_patent_titles[]
IMMUNOGENS AND METHODS FOR INDUCING AN IMMUNE RESPONSE

# data[].attributes.field_patent_titles[]
IMMUNOGENS AND METHODS FOR INDUCING AN IMMUNE RESPONSE

# data[].attributes.field_publications[].value
Valentin A, et al. 2022. Comparative immunogenicity of an mRNA/LNP and a DNA vaccine targeting HIV gag conserved elements in macaques. (PMID: 35935984)

# data[].attributes.field_publications[].processed
Valentin A, et al. 2022. Comparative immunogenicity of an mRNA/LNP and a DNA vaccine targeting HIV gag conserved elements in macaques. (PMID: 35935984)

# data[].attributes.field_related_inventions[].processed
E-087-2015

# data[].attributes.field_related_inventions[].processed
E-132-2012

# data[].attributes.field_technology_names[]
Immunogens And Methods To Improve Vaccine Immune Response

# data[].attributes.title
Drug-Regulatable, Inducible Expression of Membrane-Bound Interleukin 12 (DRIM-IL-12) for Use in Adoptive Cell Therapy

# data[].attributes.body.value
Summary:

Scientists at the National Cancer Institute (NCI) have developed a novel tightly regulated drug-responsive, membrane-bound IL-12 cytokine platform, that enhances anti-tumor efficacy in adoptive cell therapy (ACT) with engineered T-cells (CAR, TCR, TILs) while improving safety. The NCI seeks research co-development partners and/or licensees to advance this technology toward clinical translation.

Description of Technology:

ACT offers hope for patients with refractory or metastatic cancers, but effectiveness is frequently undermined by the immunosuppressive tumor microenvironment and T-cell dysfunction. Interleukin-12 (IL-12), a powerful cytokine with strong anti-tumor properties, has long been recognized for its potential to invigorate T-cell responses within tumors. However, systemic administration of IL-12 results in severe toxicity. Further, prior gene therapy strategies failed to provide sufficient control over IL-12 expression. These two factors compromise safety and therapeutic performance.

This invention introduces a Nuclear Factor of Activated T cells (NFAT)-inducible, drug-regulatable, membrane-bound IL-12 (DRIM-IL-12) system that delivers spatiotemporally controlled cytokine expression within the engineered T cell therapy product. This platform ensures IL-12 is expressed only upon T-cell activation. Concurrently, the degron (D) sequence confers lenalidomide-dependent proteasome-mediated degradation–serving as a drug-controlled safety switch to limit systemic toxicity. A transmembrane (TM) domain anchors IL-12 in the plasma membrane, preventing unintended secretion and promoting localized immune modulation. When paired with tumor-specific TCRs or CARs (e.g., anti-mutant p53 or KRAS TCRs, or CD19 CAR), this platform enhances tumor cell killing and long-term survival in preclinical models. In a mouse model, DRIM-IL-12 demonstrated substantially improved safety compared to the previous generation of NFAT-inducible IL-12. The inventors also demonstrate that DRIM-IL-12 expression can be dialed down or fine-tuned to prevent T-cell exhaustion or differentiation, which can occur with uncontrolled IL-12 expression.

The NCI invites industry partners and translational researchers to collaborate or license this technology for the next generation of safer, more effective ACT-based immunotherapies.

Potential Commercial Applications:

Solid tumors expressing p53 or KRAS mutations

Hematologic malignancies

Melanoma

Competitive Advantages:

Versatile platform for inducible cytokine regulation

Superior survival in mouse models compared with TCR-only T-cells

Enhanced tumor cell killing and long-term survival in murine models

Decreased IL-12–associated toxicity

Maintenance of higher IL-12 expression

Improved sensitivity to lenalidomide-mediated degradation

# data[].attributes.body.processed
Summary:

Scientists at the National Cancer Institute (NCI) have developed a novel tightly regulated drug-responsive, membrane-bound IL-12 cytokine platform, that enhances anti-tumor efficacy in adoptive cell therapy (ACT) with engineered T-cells (CAR, TCR, TILs) while improving safety. The NCI seeks research co-development partners and/or licensees to advance this technology toward clinical translation.

Description of Technology:

ACT offers hope for patients with refractory or metastatic cancers, but effectiveness is frequently undermined by the immunosuppressive tumor microenvironment and T-cell dysfunction. Interleukin-12 (IL-12), a powerful cytokine with strong anti-tumor properties, has long been recognized for its potential to invigorate T-cell responses within tumors. However, systemic administration of IL-12 results in severe toxicity. Further, prior gene therapy strategies failed to provide sufficient control over IL-12 expression. These two factors compromise safety and therapeutic performance.

This invention introduces a Nuclear Factor of Activated T cells (NFAT)-inducible, drug-regulatable, membrane-bound IL-12 (DRIM-IL-12) system that delivers spatiotemporally controlled cytokine expression within the engineered T cell therapy product. This platform ensures IL-12 is expressed only upon T-cell activation. Concurrently, the degron (D) sequence confers lenalidomide-dependent proteasome-mediated degradation–serving as a drug-controlled safety switch to limit systemic toxicity. A transmembrane (TM) domain anchors IL-12 in the plasma membrane, preventing unintended secretion and promoting localized immune modulation. When paired with tumor-specific TCRs or CARs (e.g., anti-mutant p53 or KRAS TCRs, or CD19 CAR), this platform enhances tumor cell killing and long-term survival in preclinical models. In a mouse model, DRIM-IL-12 demonstrated substantially improved safety compared to the previous generation of NFAT-inducible IL-12. The inventors also demonstrate that DRIM-IL-12 expression can be dialed down or fine-tuned to prevent T-cell exhaustion or differentiation, which can occur with uncontrolled IL-12 expression.

The NCI invites industry partners and translational researchers to collaborate or license this technology for the next generation of safer, more effective ACT-based immunotherapies.

Potential Commercial Applications:

Solid tumors expressing p53 or KRAS mutations

Hematologic malignancies

Melanoma

Competitive Advantages:

Versatile platform for inducible cytokine regulation

Superior survival in mouse models compared with TCR-only T-cells

Enhanced tumor cell killing and long-term survival in murine models

Decreased IL-12–associated toxicity

Maintenance of higher IL-12 expression

Improved sensitivity to lenalidomide-mediated degradation

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for developing a novel tightly regulated drug-responsive, membrane-bound IL-12 cytokine platform, that enhances anti-tumor efficacy in adoptive cell therapy (ACT) with engineered T-cells (CAR, TCR, TILs).

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for developing a novel tightly regulated drug-responsive, membrane-bound IL-12 cytokine platform, that enhances anti-tumor efficacy in adoptive cell therapy (ACT) with engineered T-cells (CAR, TCR, TILs).

# data[].attributes.field_licensingcontact_hrefs[]
burkear@nih.gov?subject=Web Inquiry on [TAB-5099] Drug-Regulatable, Inducible Expression of Membrane-Bound Interleukin 12 (DRIM-IL-12) for Use in Adoptive Cell Therapy&body=Please send me information about technology [TAB-5099] Drug-Regulatable, Inducible Expression of Membrane-Bound Interleukin 12 (DRIM-IL-12) for Use in Adoptive Cell Therapy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts[].value
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Burke, Andrew
burkear@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
burkear@nih.gov?subject=Web Inquiry on [TAB-5099] Drug-Regulatable, Inducible Expression of Membrane-Bound Interleukin 12 (DRIM-IL-12) for Use in Adoptive Cell Therapy&body=Please send me information about technology [TAB-5099] Drug-Regulatable, Inducible Expression of Membrane-Bound Interleukin 12 (DRIM-IL-12) for Use in Adoptive Cell Therapy.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/652,871
Filed on 2024-05-29
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/652,871
Filed on 2024-05-29
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/031121
Filed on 2025-05-28
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/031121
Filed on 2025-05-28
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/652,871
Filed on 2024-05-29
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/031121
Filed on 2025-05-28
Status: Pending

# data[].attributes.field_publications[].value
Kim SP, et al. Drug-regulatable, inducible, and membrane-bound interleukin 12 (IL-12TM-D) for use in adoptive cell therapies against advanced cancers. https://doi.org/10.1136/jitc-2024-SITC2024.0344

# data[].attributes.field_publications[].processed
Kim SP, et al. Drug-regulatable, inducible, and membrane-bound interleukin 12 (IL-12TM-D) for use in adoptive cell therapies against advanced cancers. https://doi.org/10.1136/jitc-2024-SITC2024.0344

# data[].attributes.field_technology_names[]
Drug-regulatable, inducible expression of membrane-bound interleukin 12 for use in adoptive cell therapy.

# data[].attributes.field_technology_owners[]
National Cancer Institute (NCI), Surgery Branch

# data[].attributes.title
Soluble Tissue Factor, a Novel Target, and Antibodies, for Diagnosis, Prevention and Treatment of Thrombosis and Related Conditions

# data[].attributes.body.value
Summary:

Scientists at the National Cancer Institute (NCI) have discovered a novel therapeutic, diagnostic and prognostic target for thrombosis: Soluble Tissue Factor (sTF). NCI has generated first-in-class antibodies and platform selectively neutralizing pathological coagulation while preserving normal hemostasis. This platform technology can be used to prevent, diagnose and treat pathological thrombosis caused by a variety of clinical conditions-including cancer, sepsis, infectious diseases (e.g., COVID), autoimmune disorders, trauma, heart conditions and inflammatory conditions. It offers a much more sensitive and specific test of thrombosis than the current D-dimer test. It may be applicable to any clinical condition which induces necroptosis, pyroptosis and NETosis, such as cancer, neurodegenerative disease, ischemia-reperfusion and acute injuries, traumatic injuries, bacterial and viral infections, cardiovascular conditions, and atherosclerosis, inflammatory, autoimmune conditions, and others.

Description of Technology:

Investigators at the National Cancer Institute (NCI) have identified and therapeutically validated a distinctive, disease-restricted driver of thrombosis: soluble tissue factor (sTF). sTF is generated through proteolytic cleavage during inflammatory cell death.

Mechanistically, the researchers demonstrated that sTF generation is not limited to necroptosis but represents a conserved outcome of multiple inflammatory cell death pathways, including pyroptosis and NETtosis.

Pathological thrombosis remains a leading cause of morbidity and mortality in sepsis, cancer, autoimmune diseases, viral infections, and inflammatory disorders. Current anticoagulant and thrombosis treatments options such as Heparins and Warfarin are effective at reducing clot formation, but act indiscriminately on the coagulation cascade, disrupt normal hemostasis, and are associated with significant bleeding risk. Current thrombosis diagnostics, D-dimer, a fibrin degradation byproduct, is a late stage marker that lacks sensitivity. This invention provides an alternative for early detection based on sTF that is more sensitive and specific.

To selectively target this mechanism, the team developed novel humanized monoclonal antibodies (e.g., 58B3 and 56E5) that specifically recognize human soluble tissue factor (hsTF), but not full-length membrane-bound tissue factor (flTF). This selectivity preserves physiological hemostasis while inhibiting pathological coagulation.

In vivo validation using human samples of various clinical diseases demonstrated that administration of sTF-specific antibodies prevents fibrinogen depletion and reduces thrombin–antithrombin (TAT) complex elevation, effectively normalizing coagulation parameters. These results establish proof of concept that selective sTF neutralization can block pathological thrombosis without systemic anticoagulation.

By establishing sTF as a unifying mechanistic link between inflammatory cell death and thrombosis across sepsis, cancer, infection, autoimmune disease, cardiovascular disorders, and metabolic inflammation, this antibody platform represents a first-in-class strategy to selectively inhibit pathological coagulation while preserving normal hemostasis. The approach offers a safer, more precise therapeutic and diagnostic alternative to conventional anticoagulants.

The humanized monoclonal antibodies, as well as methods of using sTF as a target for diagnosis, treatment and prevention of thrombosis and associated diseases are available for licensing or collaborative development to advance clinical translation. Partnership opportunities include preclinical optimization, clinical development, and diagnostic assay co-development.

Potential Commercial Applications:

Diagnostic tool for early detection and monitoring of sTF in plasma. Diagnostic tool for early detection and monitoring of thrombosis, much more sensitive and specific test than the currently used D-dimer test.

Basis for diagnostic kits such as ELISA and point-of-care assays.

Diagnostic tool for early detection of DVT and PE with radiolabeled anti-sTF antibody in combination with ultrasound /CT scan

Therapeutic use for sepsis-associated thrombosis.

Therapeutic use for cancer-associated thrombosis.

Therapeutic use viral infection–associated thrombosis.

Therapeutic use autoimmune disorders.

Therapeutic use cardiovascular inflammatory diseases.

Therapeutic use for acute lung injury including Acute Respiratory Distress Syndrome ARD.

Therapeutic use for metabolic and vascular inflammatory diseases

Therapeutic use for high efficient inhibition of thrombosis with anti-sTF-based bispecific antibodies.

Competitive Advantages:

Selective targeting of pathological soluble tissue factor (sTF).

Preservation of normal hemostasis.

Potential for long-acting biologic prevention.

Specific mechanism-based intervention tied to inflammatory cell death.

# data[].attributes.body.processed
Summary:

Scientists at the National Cancer Institute (NCI) have discovered a novel therapeutic, diagnostic and prognostic target for thrombosis: Soluble Tissue Factor (sTF). NCI has generated first-in-class antibodies and platform selectively neutralizing pathological coagulation while preserving normal hemostasis. This platform technology can be used to prevent, diagnose and treat pathological thrombosis caused by a variety of clinical conditions-including cancer, sepsis, infectious diseases (e.g., COVID), autoimmune disorders, trauma, heart conditions and inflammatory conditions. It offers a much more sensitive and specific test of thrombosis than the current D-dimer test. It may be applicable to any clinical condition which induces necroptosis, pyroptosis and NETosis, such as cancer, neurodegenerative disease, ischemia-reperfusion and acute injuries, traumatic injuries, bacterial and viral infections, cardiovascular conditions, and atherosclerosis, inflammatory, autoimmune conditions, and others.

Description of Technology:

Investigators at the National Cancer Institute (NCI) have identified and therapeutically validated a distinctive, disease-restricted driver of thrombosis: soluble tissue factor (sTF). sTF is generated through proteolytic cleavage during inflammatory cell death.

Mechanistically, the researchers demonstrated that sTF generation is not limited to necroptosis but represents a conserved outcome of multiple inflammatory cell death pathways, including pyroptosis and NETtosis.

Pathological thrombosis remains a leading cause of morbidity and mortality in sepsis, cancer, autoimmune diseases, viral infections, and inflammatory disorders. Current anticoagulant and thrombosis treatments options such as Heparins and Warfarin are effective at reducing clot formation, but act indiscriminately on the coagulation cascade, disrupt normal hemostasis, and are associated with significant bleeding risk. Current thrombosis diagnostics, D-dimer, a fibrin degradation byproduct, is a late stage marker that lacks sensitivity. This invention provides an alternative for early detection based on sTF that is more sensitive and specific.

To selectively target this mechanism, the team developed novel humanized monoclonal antibodies (e.g., 58B3 and 56E5) that specifically recognize human soluble tissue factor (hsTF), but not full-length membrane-bound tissue factor (flTF). This selectivity preserves physiological hemostasis while inhibiting pathological coagulation.

In vivo validation using human samples of various clinical diseases demonstrated that administration of sTF-specific antibodies prevents fibrinogen depletion and reduces thrombin–antithrombin (TAT) complex elevation, effectively normalizing coagulation parameters. These results establish proof of concept that selective sTF neutralization can block pathological thrombosis without systemic anticoagulation.

By establishing sTF as a unifying mechanistic link between inflammatory cell death and thrombosis across sepsis, cancer, infection, autoimmune disease, cardiovascular disorders, and metabolic inflammation, this antibody platform represents a first-in-class strategy to selectively inhibit pathological coagulation while preserving normal hemostasis. The approach offers a safer, more precise therapeutic and diagnostic alternative to conventional anticoagulants.

The humanized monoclonal antibodies, as well as methods of using sTF as a target for diagnosis, treatment and prevention of thrombosis and associated diseases are available for licensing or collaborative development to advance clinical translation. Partnership opportunities include preclinical optimization, clinical development, and diagnostic assay co-development.

Potential Commercial Applications:

Diagnostic tool for early detection and monitoring of sTF in plasma. Diagnostic tool for early detection and monitoring of thrombosis, much more sensitive and specific test than the currently used D-dimer test.

Basis for diagnostic kits such as ELISA and point-of-care assays.

Diagnostic tool for early detection of DVT and PE with radiolabeled anti-sTF antibody in combination with ultrasound /CT scan

Therapeutic use for sepsis-associated thrombosis.

Therapeutic use for cancer-associated thrombosis.

Therapeutic use viral infection–associated thrombosis.

Therapeutic use autoimmune disorders.

Therapeutic use cardiovascular inflammatory diseases.

Therapeutic use for acute lung injury including Acute Respiratory Distress Syndrome ARD.

Therapeutic use for metabolic and vascular inflammatory diseases

Therapeutic use for high efficient inhibition of thrombosis with anti-sTF-based bispecific antibodies.

Competitive Advantages:

Selective targeting of pathological soluble tissue factor (sTF).

Preservation of normal hemostasis.

Potential for long-acting biologic prevention.

Specific mechanism-based intervention tied to inflammatory cell death.

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations  for developing diagnostic, prognostic, preventative and therapeutic development of sTF. NCI is seeking collaborators with Access to clinical samples of thrombosis, and with experience of in vivo detection of thrombosis (e.g. DVT) in patients with current tools. Also seeking collaborators with experience in developing bi-specific antibodies.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations  for developing diagnostic, prognostic, preventative and therapeutic development of sTF. NCI is seeking collaborators with Access to clinical samples of thrombosis, and with experience of in vivo detection of thrombosis (e.g. DVT) in patients with current tools. Also seeking collaborators with experience in developing bi-specific antibodies.

# data[].attributes.field_licensingcontact_hrefs[]
aida.cremesti@nih.gov?subject=Web Inquiry on [TAB-5085] Soluble Tissue Factor, a Novel Target, and Antibodies, for Diagnosis, Prevention and Treatment of Thrombosis and Related Conditions&body=Please send me information about technology [TAB-5085] Soluble Tissue Factor, a Novel Target, and Antibodies, for Diagnosis, Prevention and Treatment of Thrombosis and Related Conditions.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Cremesti, Aida
aida.cremesti@nih.gov

# data[].attributes.field_licensing_contacts[].value
Cremesti, Aida
aida.cremesti@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Cremesti, Aida
aida.cremesti@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
aida.cremesti@nih.gov?subject=Web Inquiry on [TAB-5085] Soluble Tissue Factor, a Novel Target, and Antibodies, for Diagnosis, Prevention and Treatment of Thrombosis and Related Conditions&body=Please send me information about technology [TAB-5085] Soluble Tissue Factor, a Novel Target, and Antibodies, for Diagnosis, Prevention and Treatment of Thrombosis and Related Conditions.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/783,685
Filed on 2025-04-04
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/783,685
Filed on 2025-04-04
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2026/022285
Filed on 2026-04-03
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2026/022285
Filed on 2026-04-03
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/783,685
Filed on 2025-04-04
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2026/022285
Filed on 2026-04-03
Status: Pending

# data[].attributes.field_patent_titles[]
HUMANIZED ANTIBODIES SPECIFIC AGAINST SOLUBLE TISSUE FACTOR

# data[].attributes.field_patent_titles[]
SOLUBLE TISSUE FACTOR, A NOVEL TARGET, AND ANTIBODIES, FOR DIAGNOSIS, PREVENTION AND TREATMENT OF THROMBOSIS AND RELATED CONDTIONS

# data[].attributes.field_publications[].value
Wan, P., Choksi, S., Park, YJ. et al. Soluble tissue factor generated by necroptosis-triggered shedding is responsible for thrombosis. Cell Res 35, 840–858 (2025). https://doi.org/10.1038/s41422-025-01167-8

# data[].attributes.field_publications[].processed
Wan, P., Choksi, S., Park, YJ. et al. Soluble tissue factor generated by necroptosis-triggered shedding is responsible for thrombosis. Cell Res 35, 840–858 (2025). https://doi.org/10.1038/s41422-025-01167-8

# data[].attributes.field_publications[].value
Yan J, Wan P, Choksi S, Liu ZG. Necroptosis and tumor progression. Trends Cancer. 2022 Jan;8(1):21-27. doi: 10.1016/j.trecan.2021.09.003.

# data[].attributes.field_publications[].processed
Yan J, Wan P, Choksi S, Liu ZG. Necroptosis and tumor progression. Trends Cancer. 2022 Jan;8(1):21-27. doi: 10.1016/j.trecan.2021.09.003.

# data[].attributes.field_technology_names[]
The soluble Tissue Factor generated by necroptosis-triggered shedding of the cell surface TF is responsible for septic shock and viral infection-induced thrombosis

# data[].attributes.field_technology_owners[]
National Institute on Alcohol Abuse and Alcoholism (NIAAA), NCI - CCR, NIH - NCI

# data[].attributes.title
Monoclonal Antibody (RO4) that Reacts with the Juxta-membrane Region of Mesothelin

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a novel monoclonal antibody (mAb), RO4, that can be used to treat mesothelin (MSLN) expressing cancers.

Description of Technology:

Mesothelin (MSLN) is a surface antigen highly expressed in many solid tumors, such as mesothelioma, ovarian, and pancreatic cancers. MSLN is present at relatively low levels in mesothelial cells of healthy individuals, making it an ideal candidate for targeted therapeutics. However, the efficacy of MSLN-targeted agents is often reduced as a portion of the protein is shed from the cell surface and binds to available anti-MSLN antibodies. This reduces therapeutic engagement at the cell surface as shed MSLN acts as a decoy within tumor microenvironments, limiting antibodies from reaching and destroying tumor cells.

Researchers at National Cancer Institute (NCI) developed a novel mAb, RO4, which specifically binds to the juxta-membrane region of MSLN to block shedding. RO4 binds to the same region of MSLN as a previously developed mAb, 15B6 (NCI Ref. #E-106-2017), but in a different conformation. This allows for increased binding affinity and specificity. CAR-T cells made with humanized RO4 demonstrated higher cytotoxicity both in vitro and in vivo compared to h15B6 CAR-Ts. Additionally, hRO4 exhibited broader binding across MSLN-positive cell types compared to h15B6, suggesting wider utility in patient populations.

Researchers at the NCI seek licensing and/or co-development research collaborations for further development of RO4 that can be used to treat MSLN-positive cancers.

Potential Commercial Applications:

Treatment of various MSLN-positive cancers – including mesothelioma, ovarian and pancreatic cancer

Development of CAR T cells and bispecific antibodies to target MSLN and CD3

Development of Antibody-Drug Conjugates (ADCs) and Antibody-nanoparticle conjugates to deliver cytotoxic payloads to MSLN-positive tumors

Competitive Advantages:

Increased therapeutic effectiveness via avoiding shed decoy interference

Enhanced binding affinity and selectivity compared to earlier antibodies

Improved cytotoxicity across various MSLN-positive tumors

Versatility in use of CAR T cells and bispecific antibodies targeting MSLN and CD3

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a novel monoclonal antibody (mAb), RO4, that can be used to treat mesothelin (MSLN) expressing cancers.

Description of Technology:

Mesothelin (MSLN) is a surface antigen highly expressed in many solid tumors, such as mesothelioma, ovarian, and pancreatic cancers. MSLN is present at relatively low levels in mesothelial cells of healthy individuals, making it an ideal candidate for targeted therapeutics. However, the efficacy of MSLN-targeted agents is often reduced as a portion of the protein is shed from the cell surface and binds to available anti-MSLN antibodies. This reduces therapeutic engagement at the cell surface as shed MSLN acts as a decoy within tumor microenvironments, limiting antibodies from reaching and destroying tumor cells.

Researchers at National Cancer Institute (NCI) developed a novel mAb, RO4, which specifically binds to the juxta-membrane region of MSLN to block shedding. RO4 binds to the same region of MSLN as a previously developed mAb, 15B6 (NCI Ref. #E-106-2017), but in a different conformation. This allows for increased binding affinity and specificity. CAR-T cells made with humanized RO4 demonstrated higher cytotoxicity both in vitro and in vivo compared to h15B6 CAR-Ts. Additionally, hRO4 exhibited broader binding across MSLN-positive cell types compared to h15B6, suggesting wider utility in patient populations.

Researchers at the NCI seek licensing and/or co-development research collaborations for further development of RO4 that can be used to treat MSLN-positive cancers.

Potential Commercial Applications:

Treatment of various MSLN-positive cancers – including mesothelioma, ovarian and pancreatic cancer

Development of CAR T cells and bispecific antibodies to target MSLN and CD3

Development of Antibody-Drug Conjugates (ADCs) and Antibody-nanoparticle conjugates to deliver cytotoxic payloads to MSLN-positive tumors

Competitive Advantages:

Increased therapeutic effectiveness via avoiding shed decoy interference

Enhanced binding affinity and selectivity compared to earlier antibodies

Improved cytotoxicity across various MSLN-positive tumors

Versatility in use of CAR T cells and bispecific antibodies targeting MSLN and CD3

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for a novel monoclonal antibody (mAb), RO4, that can be used to treat mesothelin (MSLN) expressing cancers.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for a novel monoclonal antibody (mAb), RO4, that can be used to treat mesothelin (MSLN) expressing cancers.

# data[].attributes.field_licensingcontact_hrefs[]
greenejaime@mail.nih.gov?subject=Web Inquiry on [TAB-5134] Monoclonal Antibody (RO4) that Reacts with the Juxta-membrane Region of Mesothelin&body=Please send me information about technology [TAB-5134] Monoclonal Antibody (RO4) that Reacts with the Juxta-membrane Region of Mesothelin.&bcc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Greene, Jaime
greenejaime@mail.nih.gov

# data[].attributes.field_licensing_contacts[].value
Greene, Jaime
greenejaime@mail.nih.gov

# data[].attributes.field_licensing_contacts[].processed
Greene, Jaime
greenejaime@mail.nih.gov

# data[].attributes.field_licensing_contacts_uris[]
greenejaime@mail.nih.gov?subject=Web Inquiry on [TAB-5134] Monoclonal Antibody (RO4) that Reacts with the Juxta-membrane Region of Mesothelin&body=Please send me information about technology [TAB-5134] Monoclonal Antibody (RO4) that Reacts with the Juxta-membrane Region of Mesothelin.&bcc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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US
Provisional (PRV) 63/550,703
Filed on 2024-02-07
Status: Expired

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US
Provisional (PRV) 63/550,703
Filed on 2024-02-07
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/014973
Filed on 2025-02-07
Status: Expired

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Patent Cooperation Treaty
(PCT) PCT/US2025/014973
Filed on 2025-02-07
Status: Expired

# data[].attributes.field_patents[].value
Canada
National Stage 3315513
Filed on 2026-06-17
Status: Pending

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Canada
National Stage 3315513
Filed on 2026-06-17
Status: Pending

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US
National Stage 19/613,559
Filed on 2026-08-07
Status: Pending

# data[].attributes.field_patents[].processed
US
National Stage 19/613,559
Filed on 2026-08-07
Status: Pending

# data[].attributes.field_patents[].value
European Patent
National Stage 25708322.0
Filed on 2026-06-23
Status: Pending

# data[].attributes.field_patents[].processed
European Patent
National Stage 25708322.0
Filed on 2026-06-23
Status: Pending

# data[].attributes.field_patents[].value
Australia
National Stage 2025218272
Filed on 2026-06-05
Status: Pending

# data[].attributes.field_patents[].processed
Australia
National Stage 2025218272
Filed on 2026-06-05
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/550,703
Filed on 2024-02-07
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/014973
Filed on 2025-02-07
Status: Expired

# data[].attributes.field_patent_htmls[]
Canada
National Stage 3315513
Filed on 2026-06-17
Status: Pending

# data[].attributes.field_patent_htmls[]
US
National Stage 19/613,559
Filed on 2026-08-07
Status: Pending

# data[].attributes.field_patent_htmls[]
European Patent
National Stage 25708322.0
Filed on 2026-06-23
Status: Pending

# data[].attributes.field_patent_htmls[]
Australia
National Stage 2025218272
Filed on 2026-06-05
Status: Pending

# data[].attributes.field_patent_titles[]
MONOCLONAL ANTIBODIES THAT BIND THE JUXTA-MEMBRANE REGION OF MESOTHELIN AND USES THEREOF (RO4 antibody)

# data[].attributes.field_patent_titles[]
MONOCLONAL ANTIBODIES THAT BIND THE JUXTA-MEMBRANE REGION OF MESOTHELIN AND USES THEREOF (R04 antibody)

# data[].attributes.field_patent_titles[]
MONOCLONAL ANTIBODIES THAT BIND THE JUXTAMEMBRANE REGION OF MESOTHELIN AND USES THEREOF

# data[].attributes.field_patent_titles[]
MONOCLONAL ANTIBODIES THAT BIND THE JUXTA-MEMBRANE REGION OF MESOTHELIN AND USES THEREOF

# data[].attributes.field_patent_titles[]
MONOCLONAL ANTIBODIES THAT BIND THE JUXTAMEMBRANE REGION OF MESOTHELIN AND USES THEREOF

# data[].attributes.field_patent_titles[]
MONOCLONAL ANTIBODIES THAT BIND THE JUXTA-MEMBRANE REGION OF MESOTHELIN AND USES THEREOF (R04 antibody)

# data[].attributes.field_publications[].value
Onda M, et al. RO4, a high-affinity humanized antibody against the juxtamembrane region of mesothelin for targeted cancer therapy. (PMID41550974)

# data[].attributes.field_publications[].processed
Onda M, et al. RO4, a high-affinity humanized antibody against the juxtamembrane region of mesothelin for targeted cancer therapy. (PMID41550974)

# data[].attributes.field_publications[].value
Liu X, et al. Highly active CAR T cells that bind to a juxtamembrane region of mesothelin and are not blocked by shed mesothelin. (PMID35512094)

# data[].attributes.field_publications[].processed
Liu X, et al. Highly active CAR T cells that bind to a juxtamembrane region of mesothelin and are not blocked by shed mesothelin. (PMID35512094)

# data[].attributes.field_related_inventions[].processed
E-106-2017

# data[].attributes.field_related_inventions[].processed
E-033-2022

# data[].attributes.field_technology_names[]
Monoclonal Antibody R04 that Reacts with the Juxta-membrane Region of Mesothelin

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a Quantitative Particle Identification (QPID) digital autoradiography system with particle identification capabilities.

Description of Technology:

Autoradiography is a photographic process that exposes a medium, sensitive to radiation, to a sample emitting radiation. The current state of the art involves exposing a thin slice of tissue to an ionization-sensitive film for several hours or days and then scanning the film into an autoradiography image. This image is created using the sum of the ionizations from all the decays that occurred during the time of exposure on the ionization-sensitive medium. Imaging quality of these samples can be improved by collecting information from each individual decay to enhance the autoradiographic measurement.

Researchers at National Cancer Institute (NCI) developed a Quantitative Particle Identification (QPID) digital autoradiography system to measure the energy deposition from charged particles for each individual radioactive decay. The QPID leverages the ionizing radiation detection features of the Timepix3 detector to generate autoradiograph images in units of dose per unit time and area. The high readout speed of the Timepix3 gives the detector the capability to measure separate decay ionizations. It also segregates the image into one generated only by alpha and the other only by beta particles. A gamma detector was interfaced with the Timepix3 – allowing tagging charged particle ionization events in coincidence with a gamma emission during the isotope decay. This allows for a method to distinguish between alpha and positron emitting radioisotopes when imaged concurrently in the same pathology sample. This is the most unique feature of the QPID which will aid the development of new theranostic treatments in which two similar ligands are used.

Researchers at the NCI seek licensing and/or co-development research collaborations to continue developing the QPID system for improved autoradiography imaging.

Potential Commercial Applications:

Improved radiotherapy dosing for cancer treatment

Improved radiotherapy guidance for cancer treatment

Improve accuracy of biopsy procedures through real-time tracer measurement and detection

Measuring dual radioligand pathology samples

Competitive Advantages:

QPID can measure charge particle activity for individual decays (alpha, beta, and gamma)

QPID measures absolute time of decay relative to the start of data acquisition

QPID more accurately measures radioactive dose in a tissue sample

The figure shows the unique ability of the QPID to image two radioisotopes simultaneously. A mouse was injected with a mixture of 223RaCl and Na18F, a theranostic agent pair which treats and images bone metastasis from prostate cancer. An hour after injection, a 50 micron thick spine sample was imaged on the QPID. The 223RaCl and Na18F uptake into the bone was separated into two images, one as the distribution of 223RaCl and the other as the distribution of Na18F. Because the QPID records individual decays of either radioisotope, accurate amounts of the two radioisotopes can be measured and studies of the biodistribution and micro-dosimetry are possible. The top row (panels a, b, and c) are autoradiography images generated by the QPID. The bottom row (panels d, e and f) are co-registered images of photographs of the sample overlayed  with the radioisotope distribution.

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a Quantitative Particle Identification (QPID) digital autoradiography system with particle identification capabilities.

Description of Technology:

Autoradiography is a photographic process that exposes a medium, sensitive to radiation, to a sample emitting radiation. The current state of the art involves exposing a thin slice of tissue to an ionization-sensitive film for several hours or days and then scanning the film into an autoradiography image. This image is created using the sum of the ionizations from all the decays that occurred during the time of exposure on the ionization-sensitive medium. Imaging quality of these samples can be improved by collecting information from each individual decay to enhance the autoradiographic measurement.

Researchers at National Cancer Institute (NCI) developed a Quantitative Particle Identification (QPID) digital autoradiography system to measure the energy deposition from charged particles for each individual radioactive decay. The QPID leverages the ionizing radiation detection features of the Timepix3 detector to generate autoradiograph images in units of dose per unit time and area. The high readout speed of the Timepix3 gives the detector the capability to measure separate decay ionizations. It also segregates the image into one generated only by alpha and the other only by beta particles. A gamma detector was interfaced with the Timepix3 – allowing tagging charged particle ionization events in coincidence with a gamma emission during the isotope decay. This allows for a method to distinguish between alpha and positron emitting radioisotopes when imaged concurrently in the same pathology sample. This is the most unique feature of the QPID which will aid the development of new theranostic treatments in which two similar ligands are used.

Researchers at the NCI seek licensing and/or co-development research collaborations to continue developing the QPID system for improved autoradiography imaging.

Potential Commercial Applications:

Improved radiotherapy dosing for cancer treatment

Improved radiotherapy guidance for cancer treatment

Improve accuracy of biopsy procedures through real-time tracer measurement and detection

Measuring dual radioligand pathology samples

Competitive Advantages:

QPID can measure charge particle activity for individual decays (alpha, beta, and gamma)

QPID measures absolute time of decay relative to the start of data acquisition

QPID more accurately measures radioactive dose in a tissue sample

The figure shows the unique ability of the QPID to image two radioisotopes simultaneously. A mouse was injected with a mixture of 223RaCl and Na18F, a theranostic agent pair which treats and images bone metastasis from prostate cancer. An hour after injection, a 50 micron thick spine sample was imaged on the QPID. The 223RaCl and Na18F uptake into the bone was separated into two images, one as the distribution of 223RaCl and the other as the distribution of Na18F. Because the QPID records individual decays of either radioisotope, accurate amounts of the two radioisotopes can be measured and studies of the biodistribution and micro-dosimetry are possible. The top row (panels a, b, and c) are autoradiography images generated by the QPID. The bottom row (panels d, e and f) are co-registered images of photographs of the sample overlayed  with the radioisotope distribution.

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations  for developing the QPID system for improved autoradiography imaging.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations  for developing the QPID system for improved autoradiography imaging.

# data[].attributes.field_licensingcontact_htmls[]
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_licensing_contacts[].value
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Cheng, Eric
eric.cheng2@nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/651,184
Filed on 2024-05-23
Status: Expired

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/651,184
Filed on 2024-05-23
Status: Expired

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2025/028714
Filed on 2025-05-09
Status: Pending

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2025/028714
Filed on 2025-05-09
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/651,184
Filed on 2024-05-23
Status: Expired

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2025/028714
Filed on 2025-05-09
Status: Pending

# data[].attributes.field_publications[].value
Adler SS, et al. A Quantitative Particle Identification (QPID) spectral autoradiography system. (PMID40374923)

# data[].attributes.field_publications[].processed
Adler SS, et al. A Quantitative Particle Identification (QPID) spectral autoradiography system. (PMID40374923)

# data[].attributes.field_technology_names[]
Quantitative Particle Identification (QPID) Digital Autoradiography System
Leidos EIR # 23-008

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks licensees for a CRISPR/Cas9-engineered MC38 B2m knockout murine colon cancer cell line that models tumor resistance to PD-1/PD-L1 checkpoint blockade caused by loss of MHC-I antigen presentation. This research tool provides an opportunity to study checkpoint-refractory tumors and evaluate alternative or combination immunotherapy strategies for cancers that evade conventional T-cell–mediated recognition.

Description of Technology:

Immune checkpoint blockade (ICB) is a type of cancer immunotherapy targeting proteins such as programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1), which tumors use to reduce T-cell immune activity. These therapies can be effective in some patients. However, ICB targeting PD-1/PD-L1 fails to provide clinical benefit for most cancer patients due to primary resistance. In such cases, tumors either do not respond from the outset or acquire resistance after initially responding. One important cause of resistance is defective antigen presentation, the process by which tumor cells display internal protein fragments on their surface using major histocompatibility complex class I (MHC-I) molecules for cancer-killing T cell recognition.

Researchers at the National Cancer Institute (NCI) have developed and validated an MC38 B2m knockout murine colon cancer cell line designed to reproduce a clinically relevant form of immunotherapy resistance. Using CRISPR/Cas9, NCI researchers eliminated B2m, a gene required for tumor cells to display MHC-I antigen-presenting molecules to cancer-killing T cells. The resulting MC38 B2m KO cell line produces tumors that lack this key immune-recognition signal and are resistant to anti-PD-1 and anti-PD-L1 therapy in syngeneic mouse models. This gives researchers a defined, practical preclinical model to: (1) study tumor immune escape and (2) evaluate new immunotherapy strategies in a checkpoint-resistant setting. This is a superior approach versus models only in tumors that remain responsive to checkpoint blockade. This model uses a clinically relevant checkpoint-resistance mechanism by deleting B2m, which causes loss of MHC-I antigen presentation and prevents conventional CD8+ T-cell recognition. It is based upon the MC38 colon cancer model, which has significant response to PD-1/PD-L1 immune checkpoint blockade before B2m knockout. MC38 B2m KO tumors show abrogated response to anti-PD-1 and anti-PD-L1 treatment in vivo, while wild-type MC38 tumors showed significant tumor growth reduction under the same treatment framework

The Center for Immuno-Oncology seeks licensees interested in using this cell line as a research tool for immuno-oncology studies. This model may be useful for evaluating alternative or combination immunotherapy strategies for checkpoint-refractory tumors, including cancers that evade conventional T-cell-mediated recognition due to defective antigen presentation. It facilitates mechanistic studies of tumor immune escape, CD8+ T-cell recognition, and tumor microenvironment remodeling.

Potential Commercial Applications:

Development of cancer therapeutics overcoming of PD-1/PD-L1 checkpoint blockade resistance

Development of alternative or combination immunotherapies for checkpoint-refractory tumors

Preclinical screening of alternative or combination immunotherapies for checkpoint-refractory tumors

Evaluation of cancer therapeutic strategies for cancers with defective antigen processing/presentation or loss of MHC-I expression

Companion model for comparing checkpoint-resistant MC38 B2m KO tumors against checkpoint-responsive wild-type MC38 tumors

Competitive Advantages:

Uniquely models a clinically relevant checkpoint-resistance mechanism

Uses the MC38 colon cancer model, which is well-established and regulatorily de-risked

Unique model permitting the interrogation of abrogated response to anti-PD-1 and anti-PD-L1 treatment

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks licensees for a CRISPR/Cas9-engineered MC38 B2m knockout murine colon cancer cell line that models tumor resistance to PD-1/PD-L1 checkpoint blockade caused by loss of MHC-I antigen presentation. This research tool provides an opportunity to study checkpoint-refractory tumors and evaluate alternative or combination immunotherapy strategies for cancers that evade conventional T-cell–mediated recognition.

Description of Technology:

Immune checkpoint blockade (ICB) is a type of cancer immunotherapy targeting proteins such as programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1), which tumors use to reduce T-cell immune activity. These therapies can be effective in some patients. However, ICB targeting PD-1/PD-L1 fails to provide clinical benefit for most cancer patients due to primary resistance. In such cases, tumors either do not respond from the outset or acquire resistance after initially responding. One important cause of resistance is defective antigen presentation, the process by which tumor cells display internal protein fragments on their surface using major histocompatibility complex class I (MHC-I) molecules for cancer-killing T cell recognition.

Researchers at the National Cancer Institute (NCI) have developed and validated an MC38 B2m knockout murine colon cancer cell line designed to reproduce a clinically relevant form of immunotherapy resistance. Using CRISPR/Cas9, NCI researchers eliminated B2m, a gene required for tumor cells to display MHC-I antigen-presenting molecules to cancer-killing T cells. The resulting MC38 B2m KO cell line produces tumors that lack this key immune-recognition signal and are resistant to anti-PD-1 and anti-PD-L1 therapy in syngeneic mouse models. This gives researchers a defined, practical preclinical model to: (1) study tumor immune escape and (2) evaluate new immunotherapy strategies in a checkpoint-resistant setting. This is a superior approach versus models only in tumors that remain responsive to checkpoint blockade. This model uses a clinically relevant checkpoint-resistance mechanism by deleting B2m, which causes loss of MHC-I antigen presentation and prevents conventional CD8+ T-cell recognition. It is based upon the MC38 colon cancer model, which has significant response to PD-1/PD-L1 immune checkpoint blockade before B2m knockout. MC38 B2m KO tumors show abrogated response to anti-PD-1 and anti-PD-L1 treatment in vivo, while wild-type MC38 tumors showed significant tumor growth reduction under the same treatment framework

The Center for Immuno-Oncology seeks licensees interested in using this cell line as a research tool for immuno-oncology studies. This model may be useful for evaluating alternative or combination immunotherapy strategies for checkpoint-refractory tumors, including cancers that evade conventional T-cell-mediated recognition due to defective antigen presentation. It facilitates mechanistic studies of tumor immune escape, CD8+ T-cell recognition, and tumor microenvironment remodeling.

Potential Commercial Applications:

Development of cancer therapeutics overcoming of PD-1/PD-L1 checkpoint blockade resistance

Development of alternative or combination immunotherapies for checkpoint-refractory tumors

Preclinical screening of alternative or combination immunotherapies for checkpoint-refractory tumors

Evaluation of cancer therapeutic strategies for cancers with defective antigen processing/presentation or loss of MHC-I expression

Companion model for comparing checkpoint-resistant MC38 B2m KO tumors against checkpoint-responsive wild-type MC38 tumors

Competitive Advantages:

Uniquely models a clinically relevant checkpoint-resistance mechanism

Uses the MC38 colon cancer model, which is well-established and regulatorily de-risked

Unique model permitting the interrogation of abrogated response to anti-PD-1 and anti-PD-L1 treatment

# data[].attributes.field_licensingcontact_hrefs[]
nathan.jansen@nih.gov?subject=Web Inquiry on [TAB-5137] MC38 B2m KO Cell Line&body=Please send me information about technology [TAB-5137] MC38 B2m KO Cell Line.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Jansen, Nathan
nathan.jansen@nih.gov

# data[].attributes.field_licensing_contacts[].value
Jansen, Nathan
nathan.jansen@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Jansen, Nathan
nathan.jansen@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
nathan.jansen@nih.gov?subject=Web Inquiry on [TAB-5137] MC38 B2m KO Cell Line&body=Please send me information about technology [TAB-5137] MC38 B2m KO Cell Line.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_publications[].value
Chariou, PL, et al. Generation of murine tumor models refractory to αPD-1/-L1 therapies due to defects in antigen processing/presentation or IFNγ signaling using CRISPR/Cas9 (PMID: 38427670)

# data[].attributes.field_publications[].processed
Chariou, PL, et al. Generation of murine tumor models refractory to αPD-1/-L1 therapies due to defects in antigen processing/presentation or IFNγ signaling using CRISPR/Cas9 (PMID: 38427670)

# data[].attributes.title
Human Antibodies Targeting Beneficial Viral Peptide in Liver Cancer

# data[].attributes.body.value
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees to develop a collection of anti-CE1 antibodies for liver cancer treatment.

Description of Technology:

Liver cancer is the sixth most common and the third leading cause of cancer death worldwide. The most common liver cancer in adults is hepatocellular carcinoma (HCC), an aggressive malignancy with an increasing global incidence and mortality rate. The current methods for early detection, surveillance, and treatment are suboptimal. This is due to complex etiologies, demonstrating a need for more effective treatments.

Previously, NIH investigators identified a novel viral peptide antigen known as CE1. CE1 belongs to the rhinovirus and enterovirus families (NIH Ref: E-023-2024) producing a dominant humoral response associated with reduced incidence and mortality of HCC. Through phage display from a human single-chain fragment variable (scFv) phage library, NCI inventors isolated two human antibodies (B9 and B10) against the viral peptide, CE1. Human anti-CE1 B9 and B10 antibodies were constructed. These antibodies showed specific binding to liver cancer cell lines and clinical tumor tissues. They inhibited HCC tumor growth via inducting NK cell-mediated antibody-dependent cellular cytotoxicity in vitro and in vivo. These anti-CE1 antibodies have the potential as liver cancer therapeutics, either on their own or as the targeting domain of an immunoconjugate.

Potential Commercial Applications:

Liver Cancer treatment

Recombinant immunotoxins (RITs)

Antibody drug conjugates (ADCs)

Chimeric antigen receptors (CAR)

Bispecific monoclonal antibody

Radiopharmaceuticals

Liver Cancer diagnosis

Therapeutics for tumors expressing a molecule recognized by a CE1-specific antibody, such as:

Prostate cancer

Lung cancer

Competitive Advantages:

Preferential binding to tumor cells

Potentially reduced systemic toxicity

Well-established regulatory path

Well-established antibody market

# data[].attributes.body.processed
Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees to develop a collection of anti-CE1 antibodies for liver cancer treatment.

Description of Technology:

Liver cancer is the sixth most common and the third leading cause of cancer death worldwide. The most common liver cancer in adults is hepatocellular carcinoma (HCC), an aggressive malignancy with an increasing global incidence and mortality rate. The current methods for early detection, surveillance, and treatment are suboptimal. This is due to complex etiologies, demonstrating a need for more effective treatments.

Previously, NIH investigators identified a novel viral peptide antigen known as CE1. CE1 belongs to the rhinovirus and enterovirus families (NIH Ref: E-023-2024) producing a dominant humoral response associated with reduced incidence and mortality of HCC. Through phage display from a human single-chain fragment variable (scFv) phage library, NCI inventors isolated two human antibodies (B9 and B10) against the viral peptide, CE1. Human anti-CE1 B9 and B10 antibodies were constructed. These antibodies showed specific binding to liver cancer cell lines and clinical tumor tissues. They inhibited HCC tumor growth via inducting NK cell-mediated antibody-dependent cellular cytotoxicity in vitro and in vivo. These anti-CE1 antibodies have the potential as liver cancer therapeutics, either on their own or as the targeting domain of an immunoconjugate.

Potential Commercial Applications:

Liver Cancer treatment

Recombinant immunotoxins (RITs)

Antibody drug conjugates (ADCs)

Chimeric antigen receptors (CAR)

Bispecific monoclonal antibody

Radiopharmaceuticals

Liver Cancer diagnosis

Therapeutics for tumors expressing a molecule recognized by a CE1-specific antibody, such as:

Prostate cancer

Lung cancer

Competitive Advantages:

Preferential binding to tumor cells

Potentially reduced systemic toxicity

Well-established regulatory path

Well-established antibody market

# data[].attributes.field_collaboration_description.value
Researchers at the NCI seek licensing and/or co-development research collaborations for developing a collection of anti-CE1 antibody-based therapeutics to treat liver cancer.

# data[].attributes.field_collaboration_description.processed
Researchers at the NCI seek licensing and/or co-development research collaborations for developing a collection of anti-CE1 antibody-based therapeutics to treat liver cancer.

# data[].attributes.field_licensingcontact_hrefs[]
abritee.dhal@nih.gov?subject=Web Inquiry on [TAB-5139] Human Antibodies Targeting Beneficial Viral Peptide in Liver Cancer&body=Please send me information about technology [TAB-5139] Human Antibodies Targeting Beneficial Viral Peptide in Liver Cancer.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts[].value
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Dhal, Abritee
abritee.dhal@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
abritee.dhal@nih.gov?subject=Web Inquiry on [TAB-5139] Human Antibodies Targeting Beneficial Viral Peptide in Liver Cancer&body=Please send me information about technology [TAB-5139] Human Antibodies Targeting Beneficial Viral Peptide in Liver Cancer.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
US
Provisional (PRV) 63/872,927
Filed on 2025-08-29
Status: Pending

# data[].attributes.field_patents[].processed
US
Provisional (PRV) 63/872,927
Filed on 2025-08-29
Status: Pending

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) None
Filed on None
Status: In Preparation

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) None
Filed on None
Status: In Preparation

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 63/872,927
Filed on 2025-08-29
Status: Pending

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) None
Filed on None
Status: In Preparation

# data[].attributes.field_patent_titles[]
HUMAN MONOCLONAL ANTIBODIES TARGETING A VIRAL PEPTIDE AND THEIR USE FOR
TREATING CANCER

# data[].attributes.field_patent_titles[]
HUMAN MONOCLONAL ANTIBODIES TARGETING A VIRAL PEPTIDE AND THEIR USE FOR
TREATING CANCER

# data[].attributes.field_related_inventions[].processed
E-023-2024

# data[].attributes.field_technology_names[]
Human antibodies targeting oncogenic viral peptide in liver cancer

# data[].attributes.title
D3-Selective Dopamine Agonist Platform: Eliminating D2-Mediated Side Effects in Parkinson’s and Movement Disorders

# data[].attributes.body.value
Every major dopaminergic therapy on the market today shares the same fundamental limitation: it cannot distinguish between two closely related receptor subtypes (D2 and D3). This technology changes that.

We have discovered and optimized a novel small molecule, ML417, that selectively activates the D3 dopamine receptor while leaving its close cousin, the D2 receptor, untouched. While primarily positioned for Parkinson's Disease and Restless Legs Syndrome, the D3-selective profile and strong brain penetrance demonstrated by this scaffold open high-value pipeline expansion opportunities in broader neurological and neuropsychiatric indications, including substance use disorders, schizophrenia, and cognitive decline.

# data[].attributes.body.processed
Every major dopaminergic therapy on the market today shares the same fundamental limitation: it cannot distinguish between two closely related receptor subtypes (D2 and D3). This technology changes that.

We have discovered and optimized a novel small molecule, ML417, that selectively activates the D3 dopamine receptor while leaving its close cousin, the D2 receptor, untouched. While primarily positioned for Parkinson's Disease and Restless Legs Syndrome, the D3-selective profile and strong brain penetrance demonstrated by this scaffold open high-value pipeline expansion opportunities in broader neurological and neuropsychiatric indications, including substance use disorders, schizophrenia, and cognitive decline.

# data[].attributes.field_commercial_applications.value
Current FDA-approved dopamine agonists work by activating both D2 and D3 receptors together, since the two are nearly indistinguishable at the molecular level. This lack of selectivity comes at a massive cost: patients on these medications frequently develop severe impulse control disorders (compulsive gambling, shopping, and hypersexuality)—serious, life-altering side effects tied specifically to D2 activation that limit physician dosing confidence. By contrast, D3-selective activation preserves the desired therapeutic effects (including motor symptom relief and neuroprotection) without triggering the D2-driven side effects that destroy patient quality of life.
The Market: Parkinson's Disease alone carries an estimated $14.4 billion annual economic burden in the U.S. The Opportunity: A partner collaborating on this platform has the unique strategic opportunity to replace imprecise, standard-of-care drugs (like pramipexole and ropinirole) with a safer, highly tolerated, next-generation therapeutic class.

# data[].attributes.field_commercial_applications.processed
Current FDA-approved dopamine agonists work by activating both D2 and D3 receptors together, since the two are nearly indistinguishable at the molecular level. This lack of selectivity comes at a massive cost: patients on these medications frequently develop severe impulse control disorders (compulsive gambling, shopping, and hypersexuality)—serious, life-altering side effects tied specifically to D2 activation that limit physician dosing confidence. By contrast, D3-selective activation preserves the desired therapeutic effects (including motor symptom relief and neuroprotection) without triggering the D2-driven side effects that destroy patient quality of life.
The Market: Parkinson's Disease alone carries an estimated $14.4 billion annual economic burden in the U.S. The Opportunity: A partner collaborating on this platform has the unique strategic opportunity to replace imprecise, standard-of-care drugs (like pramipexole and ropinirole) with a safer, highly tolerated, next-generation therapeutic class.

# data[].attributes.field_competitive_advantages.value
Our lead compound, ML417, represents a meaningful advance in a field where "selective" has historically only meant modest improvement. Superior Selectivity Profile: In head-to-head comparisons, ML417 outperforms the most selective D3 agonists previously reported in scientific literature, leaving the D2 receptor virtually untouched.
Demonstrated Neuroprotection: In preclinical models, our compound demonstrated stronger neuroprotective activity than pramipexole, one of the most widely prescribed D3-preferring drugs on the market today. Robust, De-Risked Foundation: The platform emerged from a systematic medicinal chemistry campaign spanning over 100 synthesized analogs. It features confirmed selectivity across multiple orthogonal assays, favorable early pharmacokinetic signals (including excellent brain penetrance), and a clean genetic toxicity profile. Secured Intellectual Property: Issued US and EP patents, offering a clean, proprietary runway for clinical development.

# data[].attributes.field_competitive_advantages.processed
Our lead compound, ML417, represents a meaningful advance in a field where "selective" has historically only meant modest improvement. Superior Selectivity Profile: In head-to-head comparisons, ML417 outperforms the most selective D3 agonists previously reported in scientific literature, leaving the D2 receptor virtually untouched.
Demonstrated Neuroprotection: In preclinical models, our compound demonstrated stronger neuroprotective activity than pramipexole, one of the most widely prescribed D3-preferring drugs on the market today. Robust, De-Risked Foundation: The platform emerged from a systematic medicinal chemistry campaign spanning over 100 synthesized analogs. It features confirmed selectivity across multiple orthogonal assays, favorable early pharmacokinetic signals (including excellent brain penetrance), and a clean genetic toxicity profile. Secured Intellectual Property: Issued US and EP patents, offering a clean, proprietary runway for clinical development.

# data[].attributes.field_inventor_companies[]
University of North Carolina, Chapel Hill

# data[].attributes.field_inventor_companies[]
University of North Carolina, Chapel Hill

# data[].attributes.field_licensingcontact_hrefs[]
susan.ano@nih.gov?subject=Web Inquiry on [TAB-5140] D3-Selective Dopamine Agonist Platform: Eliminating D2-Mediated Side Effects in Parkinson’s and Movement Disorders&body=Please send me information about technology [TAB-5140] D3-Selective Dopamine Agonist Platform: Eliminating D2-Mediated Side Effects in Parkinson’s and Movement Disorders.

# data[].attributes.field_licensingcontact_htmls[]
Ano, Susan
susan.ano@nih.gov

# data[].attributes.field_licensing_contacts[].value
Ano, Susan
susan.ano@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Ano, Susan
susan.ano@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
susan.ano@nih.gov?subject=Web Inquiry on [TAB-5140] D3-Selective Dopamine Agonist Platform: Eliminating D2-Mediated Side Effects in Parkinson’s and Movement Disorders&body=Please send me information about technology [TAB-5140] D3-Selective Dopamine Agonist Platform: Eliminating D2-Mediated Side Effects in Parkinson’s and Movement Disorders.

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2017/027618
Filed on 2017-04-14
Status: Expired

# data[].attributes.field_patents[].processed
Patent Cooperation Treaty
(PCT) PCT/US2017/027618
Filed on 2017-04-14
Status: Expired

# data[].attributes.field_patents[].value
European Patent
National Stage 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].processed
European Patent
National Stage 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].value
US Patent 11,634,404
Filed on 2018-10-12
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 11,634,404
Filed on 2018-10-12
Status: Issued

# data[].attributes.field_patents[].value
Germany
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].processed
Germany
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].value
United Kingdom
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].processed
United Kingdom
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].value
France
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].processed
France
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].value
Belgium
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].processed
Belgium
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patents[].value
Ireland
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

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European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

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European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

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European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

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US Patent 12,145,922
Filed on 2023-02-17
Status: Issued

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US Patent 12,145,922
Filed on 2023-02-17
Status: Issued

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Patent Cooperation Treaty
(PCT) PCT/US2017/027618
Filed on 2017-04-14
Status: Expired

# data[].attributes.field_patent_htmls[]
European Patent
National Stage 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 11,634,404
Filed on 2018-10-12
Status: Issued

# data[].attributes.field_patent_htmls[]
Germany
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patent_htmls[]
United Kingdom
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patent_htmls[]
France
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patent_htmls[]
Belgium
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patent_htmls[]
Ireland
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patent_htmls[]
Switzerland
European patent (EP) 17733098.2
Filed on 2018-10-23
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 12,145,922
Filed on 2023-02-17
Status: Issued

# data[].attributes.field_patent_titles[]
Selective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
Selective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
SELECTIVE D3 DOPAMINE RECEPTOR AGONISTS AND METHODS OF THEIR USE

# data[].attributes.field_patent_titles[]
Selective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
ESelective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
Selective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
Selective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
Selective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
Selective D3 Dopamine Receptor Agonists and Methods of Their Use

# data[].attributes.field_patent_titles[]
SELECTIVE D3 DOPAMINE RECEPTOR AGONISTS AND METHODS OF THEIR USE

# data[].attributes.field_publications[].value
Moritz et al., "Discovery, Optimization, and Characterization of ML417: A Novel and Highly Selective D3 Dopamine Receptor Agonist", J. Med. Chem. 2020, 63(10), 5526-5567

# data[].attributes.field_publications[].processed
Moritz et al., "Discovery, Optimization, and Characterization of ML417: A Novel and Highly Selective D3 Dopamine Receptor Agonist", J. Med. Chem. 2020, 63(10), 5526-5567

# data[].attributes.field_related_inventions[].processed
E-146-2016-0

# data[].attributes.field_related_inventions[].processed
E-146-2016-1

# data[].attributes.field_technology_names[]
Identification Of A Novel D3 Dopamine Receptor-selective Agonist

# data[].attributes.field_technology_names[]
Identification Of A Novel D3 Dopamine Receptor-selective Agonist

# data[].attributes.field_technology_owners[]
NCATS - NCGC, NINDS, University of Kansas, University of North Carolina, Chapel Hill

# data[].attributes.field_technology_owners[]
NCATS - NCGC, NINDS, Northeastern University, University of North Carolina, Chapel Hill

# data[].attributes.title
Astrocyte Differentiation of Neural Stem Cells with StemPro Embryonic Stem Cell Serum Free Medium for Research and Potential Therapeutic Use

# data[].attributes.body.value
This technology includes an innovative method for differentiating astrocytes from neural stem cells (NSCs). The process involves using Life Technologies StemPro embryonic stem cell serum-free medium to initially guide NSCs towards a neuronal lineage. Over a period of 28-35 days, as the cells are continually passaged, neurons gradually die off, leading to the proliferation of astrocytes. By the end of this differentiation protocol, approximately 70% of the cells exhibit markers characteristic of mature astrocytes, specifically GFAP. Additionally, this method allows for the astrocytes to be frozen at early stages and later thawed to continue their differentiation into the astrocyte lineage. This technology stands out from previous methods by significantly enhancing the efficiency and speed of astrocyte derivation. The potential applications of this technology are extensive, including facilitating research into astrocyte development mechanisms and providing a scalable way to produce astrocytes for potential clinical applications in cellular replacement therapies for brain and spinal cord injuries.

# data[].attributes.body.processed
This technology includes an innovative method for differentiating astrocytes from neural stem cells (NSCs). The process involves using Life Technologies StemPro embryonic stem cell serum-free medium to initially guide NSCs towards a neuronal lineage. Over a period of 28-35 days, as the cells are continually passaged, neurons gradually die off, leading to the proliferation of astrocytes. By the end of this differentiation protocol, approximately 70% of the cells exhibit markers characteristic of mature astrocytes, specifically GFAP. Additionally, this method allows for the astrocytes to be frozen at early stages and later thawed to continue their differentiation into the astrocyte lineage. This technology stands out from previous methods by significantly enhancing the efficiency and speed of astrocyte derivation. The potential applications of this technology are extensive, including facilitating research into astrocyte development mechanisms and providing a scalable way to produce astrocytes for potential clinical applications in cellular replacement therapies for brain and spinal cord injuries.

# data[].attributes.field_collaboration_description.value
We are seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology.

# data[].attributes.field_collaboration_description.processed
We are seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology.

# data[].attributes.field_commercial_applications.value
The technology holds promise for advancing research in astrocyte development and could be pivotal in cellular replacement therapies for treating brain and spinal cord injuries.

# data[].attributes.field_commercial_applications.processed
The technology holds promise for advancing research in astrocyte development and could be pivotal in cellular replacement therapies for treating brain and spinal cord injuries.

# data[].attributes.field_competitive_advantages.value
This astrocyte differentiation technology offers a competitive advantage by enabling the efficient and rapid generation of mature astrocytes, surpassing previous methods in both speed and efficacy.

# data[].attributes.field_competitive_advantages.processed
This astrocyte differentiation technology offers a competitive advantage by enabling the efficient and rapid generation of mature astrocytes, surpassing previous methods in both speed and efficacy.

# data[].attributes.field_licensingcontact_hrefs[]
vlado.knezevic@nih.gov?subject=Web Inquiry on [TAB-4568] Astrocyte Differentiation of Neural Stem Cells with StemPro Embryonic Stem Cell Serum Free Medium for Research and Potential Therapeutic Use&body=Please send me information about technology [TAB-4568] Astrocyte Differentiation of Neural Stem Cells with StemPro Embryonic Stem Cell Serum Free Medium for Research and Potential Therapeutic Use.

# data[].attributes.field_licensingcontact_htmls[]
Knezevic, Vladimir
vlado.knezevic@nih.gov

# data[].attributes.field_licensing_contacts[].value
Knezevic, Vladimir
vlado.knezevic@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Knezevic, Vladimir
vlado.knezevic@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
vlado.knezevic@nih.gov?subject=Web Inquiry on [TAB-4568] Astrocyte Differentiation of Neural Stem Cells with StemPro Embryonic Stem Cell Serum Free Medium for Research and Potential Therapeutic Use&body=Please send me information about technology [TAB-4568] Astrocyte Differentiation of Neural Stem Cells with StemPro Embryonic Stem Cell Serum Free Medium for Research and Potential Therapeutic Use.

# data[].attributes.field_technology_names[]
Astrocyte Differentiation Of Neural Stem Cells With StemPro Embryonic Stem Cell Serum Free Medium

# data[].attributes.field_technology_owners[]
Buck Institute for Research on Aging, NIAMS

# data[].attributes.title
Novel Dopamine Receptor Ligands As Therapeutics For Central Nervous System Disorders

# data[].attributes.body.value
Summary:

The National Institute on Drug Abuse's Medications Discovery Research Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize 4-phenylpiperazine derivatives as dopamine D3 selective ligands.

Description of Technology:

The dopamine D3 receptor subtype is a member of the dopamine D2 subclass of receptors.  These receptors have been implicated in a number of CNS disorders, including psychostimulant abuse, psychosis and Parkinson's disease.  Compounds that bind with high affinity and selectivity to D3 receptors can not only provide important tools with which to study the structure and function of this receptor subtype, but may also have therapeutic potential in the treatment of numerous psychiatric and neurologic disorders.

The 4-phenylpiperazine derivatives are an important class of dopamine D3 selective ligands.  However, due to their highly lipophilic nature, these compounds suffer from solubility problems in aqueous media and reduced bioavailability.  To address this problem, a process was designed to introduce functionality into the carbon chain linker of these compounds.  Compared to currently available dopamine D3 receptor ligands, the resulting compounds show improved pharmacological properties and D3 selectivities but due to their more hydrophilic nature, these derivatives are predicted to have improved water solubility and bioavailability.

R&D Status: Pre-clinical discovery

Further R&D Needed:

Evaluate selected compounds in animal models of drug abuse, psychosis, obesity and Parkinson''s disease

Design and synthesize novel, functionalized analogs using both classical and computational drug design to improve D3 receptor affinity and selectivity

Evaluate compounds for binding in D3 and D2 receptor expressing cell lines and in in vitro functional assays

Correlate in vitro binding affinities with in vivo function in rats and monkeys and evaluate compounds in knockout mice models

Pursue PET and SPECT imaging agents by radiolabel of D3 ligands and evaluation in rats and non-human primates.

IP Status:  PCT Application PCT/US2007/071412 filed 6/17/2007

Potential Commercial Applications:

Therapeutics for a variety of psychiatric and neurologic disorders

Research tools to study D3 receptor structure and function

Competitive Advantages:

Improved pharmacological properties and selectivity over existing dopamine D3 receptor ligands.

Hydrophilic nature likely to lead to improved water solubility and bioavailability

# data[].attributes.body.processed
Summary:

The National Institute on Drug Abuse's Medications Discovery Research Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize 4-phenylpiperazine derivatives as dopamine D3 selective ligands.

Description of Technology:

The dopamine D3 receptor subtype is a member of the dopamine D2 subclass of receptors.  These receptors have been implicated in a number of CNS disorders, including psychostimulant abuse, psychosis and Parkinson's disease.  Compounds that bind with high affinity and selectivity to D3 receptors can not only provide important tools with which to study the structure and function of this receptor subtype, but may also have therapeutic potential in the treatment of numerous psychiatric and neurologic disorders.

The 4-phenylpiperazine derivatives are an important class of dopamine D3 selective ligands.  However, due to their highly lipophilic nature, these compounds suffer from solubility problems in aqueous media and reduced bioavailability.  To address this problem, a process was designed to introduce functionality into the carbon chain linker of these compounds.  Compared to currently available dopamine D3 receptor ligands, the resulting compounds show improved pharmacological properties and D3 selectivities but due to their more hydrophilic nature, these derivatives are predicted to have improved water solubility and bioavailability.

R&D Status: Pre-clinical discovery

Further R&D Needed:

Evaluate selected compounds in animal models of drug abuse, psychosis, obesity and Parkinson''s disease

Design and synthesize novel, functionalized analogs using both classical and computational drug design to improve D3 receptor affinity and selectivity

Evaluate compounds for binding in D3 and D2 receptor expressing cell lines and in in vitro functional assays

Correlate in vitro binding affinities with in vivo function in rats and monkeys and evaluate compounds in knockout mice models

Pursue PET and SPECT imaging agents by radiolabel of D3 ligands and evaluation in rats and non-human primates.

IP Status:  PCT Application PCT/US2007/071412 filed 6/17/2007

Potential Commercial Applications:

Therapeutics for a variety of psychiatric and neurologic disorders

Research tools to study D3 receptor structure and function

Competitive Advantages:

Improved pharmacological properties and selectivity over existing dopamine D3 receptor ligands.

Hydrophilic nature likely to lead to improved water solubility and bioavailability

# data[].attributes.field_inventor_companies[]
University of North Texas Health Science Center

# data[].attributes.field_licensingcontact_hrefs[]
merissa.baxter@nih.gov?subject=Web Inquiry on [TAB-4205] Novel Dopamine Receptor Ligands As Therapeutics For Central Nervous System Disorders&body=Please send me information about technology [TAB-4205] Novel Dopamine Receptor Ligands As Therapeutics For Central Nervous System Disorders.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Baxter, Merissa
merissa.baxter@nih.gov

# data[].attributes.field_licensing_contacts[].value
Baxter, Merissa
merissa.baxter@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Baxter, Merissa
merissa.baxter@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
merissa.baxter@nih.gov?subject=Web Inquiry on [TAB-4205] Novel Dopamine Receptor Ligands As Therapeutics For Central Nervous System Disorders&body=Please send me information about technology [TAB-4205] Novel Dopamine Receptor Ligands As Therapeutics For Central Nervous System Disorders.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2007/071412
Filed on 2007-06-15
Status: Expired

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Patent Cooperation Treaty
(PCT) PCT/US2007/071412
Filed on 2007-06-15
Status: Expired

# data[].attributes.field_patents[].value
US Patent 8,748,608
Filed on 2010-06-25
Status: Issued

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US Patent 8,748,608
Filed on 2010-06-25
Status: Issued

# data[].attributes.field_patents[].value
Australia
National Stage 2007354861
Filed on 2007-06-15
Status: Issued

# data[].attributes.field_patents[].processed
Australia
National Stage 2007354861
Filed on 2007-06-15
Status: Issued

# data[].attributes.field_patents[].value
Canada
National Stage 2690789
Filed on 2012-03-20
Status: Issued

# data[].attributes.field_patents[].processed
Canada
National Stage 2690789
Filed on 2012-03-20
Status: Issued

# data[].attributes.field_patents[].value
US
Divisional (DIV) 14/266,076
Filed on 2014-04-30
Status: Abandoned

# data[].attributes.field_patents[].processed
US
Divisional (DIV) 14/266,076
Filed on 2014-04-30
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2007/071412
Filed on 2007-06-15
Status: Expired

# data[].attributes.field_patent_htmls[]
US Patent 8,748,608
Filed on 2010-06-25
Status: Issued

# data[].attributes.field_patent_htmls[]
Australia
National Stage 2007354861
Filed on 2007-06-15
Status: Issued

# data[].attributes.field_patent_htmls[]
Canada
National Stage 2690789
Filed on 2012-03-20
Status: Issued

# data[].attributes.field_patent_htmls[]
US
Divisional (DIV) 14/266,076
Filed on 2014-04-30
Status: Abandoned

# data[].attributes.field_patent_titles[]
4-Phenylpiperazine Derivatives With Functionalized Linkers as Dopamine D3 Receptor Selective Ligands and Methods Of Use

# data[].attributes.field_patent_titles[]
4-Phenylpiperazine Derivatives With Functionalized Linkers As Dopamine D3 Receptor Selective Ligands And Methods of Use

# data[].attributes.field_patent_titles[]
4-Phenylpiperazine Derivatives With Functionalized Linkers as Dopamine D3 Receptor Selective Ligands and Methods Of Use

# data[].attributes.field_patent_titles[]
4-Phenylpiperazine Derivatives With Functionalized Linkers as Dopamine D3 Receptor Selective Ligands and Methods Of Use

# data[].attributes.field_patent_titles[]
4-Phenylpiperazine Derivatives With Functionalized Linkers As Dopamine D3 Receptor Selective Ligands And Methods of Use

# data[].attributes.field_technology_names[]
4-Phenylpiperazine Derivatives With Functionalized Linkers As Dopamine D3 Receptor Selective Ligands With Drug Abuse Therapeutic Potential

# data[].attributes.field_technology_owners[]
National Institute on Drug Abuse (NIDA), University of North Texas Health Science Center

# data[].attributes.title
Novel Chemoattractant-Based Toxins To Improve Vaccine Immune Responses for Cancer and Infectious Diseases

# data[].attributes.body.value
Description of Technology:

Cancer is one of the leading causes of death in United States and it is estimated that there will be more than half a million deaths caused by cancer in 2009.  A major drawback of the current chemotherapy-based therapeutics is the cytotoxic side-effects associated with them.  Thus there is a dire need to develop new therapeutic strategies with fewer side-effects.  Immunotherapy has taken a lead among the new therapeutic approaches.  Enhancing the innate immune response of an individual has been a key approach for the treatment against different diseases such as cancer and infectious diseases.

This technology involves the generation of novel chemoattractant toxins that deplete the T regulatory cells (Treg) or other immunosuppressive or hyperactivated cells locally.  Treg controls activation of immune responses by suppressing the induction of adaptive immune responses, particularly T cell responses.  Immunosuppressive cells such as tumor infiltrating macrophages, regulatory T cells, regulatory B cells, or NKT and other cells down regulate antitumor immune responses.  The chemoattractant toxins consist of a toxin moiety fused with a chemokine receptor ligand, such as chemokines and various chemoattractants, that enables specific targeting and delivery to the regulatory cells. This technology is advantageous over the more harmful antibodies and chemicals that are currently used for the systemic depletion of regulatory cells.  The current technology can be used therapeutically in a variety of ways.  They can be used together with vaccines to increase efficacy of the vaccine for the treatment of cancer, and can be used to locally deplete Treg, Bregs, or other immuno suppressive cells to induce cytolytic cell responses at the tumor site or to eliminate chronic infectious diseases such as HIV and tuberculosis.

Development Status:
The technology is currently in the pre-clinical stage of development.

Potential Commercial Applications:

New chemoattractant-based toxins targeted towards Treg cells.

New chemoattractant-based toxins targeted towards immunosuppressive B cells, NKT and macrophages.

New chemoattractant based toxins targeted towards local depletion of hyperactivated CD4 T cells to treat autoimmune diseases.

Chemoattractant-based toxins depleting Treg cells or other immunosuppressive cells causing enhanced vaccine immune responses.

Novel immunotherapy by increasing vaccine efficacy against cancer and infectious diseases.

# data[].attributes.body.processed
Description of Technology:

Cancer is one of the leading causes of death in United States and it is estimated that there will be more than half a million deaths caused by cancer in 2009.  A major drawback of the current chemotherapy-based therapeutics is the cytotoxic side-effects associated with them.  Thus there is a dire need to develop new therapeutic strategies with fewer side-effects.  Immunotherapy has taken a lead among the new therapeutic approaches.  Enhancing the innate immune response of an individual has been a key approach for the treatment against different diseases such as cancer and infectious diseases.

This technology involves the generation of novel chemoattractant toxins that deplete the T regulatory cells (Treg) or other immunosuppressive or hyperactivated cells locally.  Treg controls activation of immune responses by suppressing the induction of adaptive immune responses, particularly T cell responses.  Immunosuppressive cells such as tumor infiltrating macrophages, regulatory T cells, regulatory B cells, or NKT and other cells down regulate antitumor immune responses.  The chemoattractant toxins consist of a toxin moiety fused with a chemokine receptor ligand, such as chemokines and various chemoattractants, that enables specific targeting and delivery to the regulatory cells. This technology is advantageous over the more harmful antibodies and chemicals that are currently used for the systemic depletion of regulatory cells.  The current technology can be used therapeutically in a variety of ways.  They can be used together with vaccines to increase efficacy of the vaccine for the treatment of cancer, and can be used to locally deplete Treg, Bregs, or other immuno suppressive cells to induce cytolytic cell responses at the tumor site or to eliminate chronic infectious diseases such as HIV and tuberculosis.

Development Status:
The technology is currently in the pre-clinical stage of development.

Potential Commercial Applications:

New chemoattractant-based toxins targeted towards Treg cells.

New chemoattractant-based toxins targeted towards immunosuppressive B cells, NKT and macrophages.

New chemoattractant based toxins targeted towards local depletion of hyperactivated CD4 T cells to treat autoimmune diseases.

Chemoattractant-based toxins depleting Treg cells or other immunosuppressive cells causing enhanced vaccine immune responses.

Novel immunotherapy by increasing vaccine efficacy against cancer and infectious diseases.

# data[].attributes.field_licensingcontact_hrefs[]
darackn@mail.nih.gov?subject=Web Inquiry on [TAB-4403] Novel Chemoattractant-Based Toxins To Improve Vaccine Immune Responses for Cancer and Infectious Diseases&body=Please send me information about technology [TAB-4403] Novel Chemoattractant-Based Toxins To Improve Vaccine Immune Responses for Cancer and Infectious Diseases.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

# data[].attributes.field_licensingcontact_htmls[]
Guyton, Nicole
darackn@mail.nih.gov

# data[].attributes.field_licensing_contacts[].value
Guyton, Nicole
darackn@mail.nih.gov

# data[].attributes.field_licensing_contacts[].processed
Guyton, Nicole
darackn@mail.nih.gov

# data[].attributes.field_licensing_contacts_uris[]
darackn@mail.nih.gov?subject=Web Inquiry on [TAB-4403] Novel Chemoattractant-Based Toxins To Improve Vaccine Immune Responses for Cancer and Infectious Diseases&body=Please send me information about technology [TAB-4403] Novel Chemoattractant-Based Toxins To Improve Vaccine Immune Responses for Cancer and Infectious Diseases.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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US
Provisional (PRV) 60/722,675
Filed on 2005-09-30
Status: Abandoned

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US
Provisional (PRV) 60/722,675
Filed on 2005-09-30
Status: Abandoned

# data[].attributes.field_patents[].value
Patent Cooperation Treaty
(PCT) PCT/US2006/038195
Filed on 2006-09-28
Status: Expired

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Patent Cooperation Treaty
(PCT) PCT/US2006/038195
Filed on 2006-09-28
Status: Expired

# data[].attributes.field_patents[].value
Australia
National Stage 2006297126
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patents[].processed
Australia
National Stage 2006297126
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patents[].value
Canada
National Stage 2624662
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patents[].processed
Canada
National Stage 2624662
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patents[].value
European Patent
National Stage 06825277.4
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patents[].processed
European Patent
National Stage 06825277.4
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patents[].value
US Patent 8,795,674
Filed on 2008-03-28
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 8,795,674
Filed on 2008-03-28
Status: Issued

# data[].attributes.field_patents[].value
European Patent
Divisional (DIV) 6825277.4
Filed on 2006-09-28
Status: Administratively Closed

# data[].attributes.field_patents[].processed
European Patent
Divisional (DIV) 6825277.4
Filed on 2006-09-28
Status: Administratively Closed

# data[].attributes.field_patents[].value
US Patent 9,605,044
Filed on 2014-06-24
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 9,605,044
Filed on 2014-06-24
Status: Issued

# data[].attributes.field_patents[].value
US Patent 10,300,115
Filed on 2017-01-11
Status: Issued

# data[].attributes.field_patents[].processed
US Patent 10,300,115
Filed on 2017-01-11
Status: Issued

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 60/722,675
Filed on 2005-09-30
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Patent Cooperation Treaty
(PCT) PCT/US2006/038195
Filed on 2006-09-28
Status: Expired

# data[].attributes.field_patent_htmls[]
Australia
National Stage 2006297126
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patent_htmls[]
Canada
National Stage 2624662
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patent_htmls[]
European Patent
National Stage 06825277.4
Filed on 2006-09-28
Status: Abandoned

# data[].attributes.field_patent_htmls[]
US Patent 8,795,674
Filed on 2008-03-28
Status: Issued

# data[].attributes.field_patent_htmls[]
European Patent
Divisional (DIV) 6825277.4
Filed on 2006-09-28
Status: Administratively Closed

# data[].attributes.field_patent_htmls[]
US Patent 9,605,044
Filed on 2014-06-24
Status: Issued

# data[].attributes.field_patent_htmls[]
US Patent 10,300,115
Filed on 2017-01-11
Status: Issued

# data[].attributes.field_patent_titles[]
METHODS AND COMPOSITIONS FOR MODULATING IMMUNE TOLERANCE

# data[].attributes.field_patent_titles[]
Chemoattractant-based Toxins Which Deplete T Regulatory Cells To Improve Vaccine Immune Responses For Cancer And Other Clinically Relevant Diseases

# data[].attributes.field_patent_titles[]
Chemoattractant-based Toxins Which Deplete T Regulatory Cells To Improve Vaccine Immune Responses For Cancer And Other Clinically Relevant Diseases

# data[].attributes.field_patent_titles[]
Chemoattractant-based Toxins Which Deplete T Regulatory Cells To Improve Vaccine Immune Responses For Cancer And Other Clinically Relevant Diseases

# data[].attributes.field_patent_titles[]
Chemoattractant-based Toxins Which Deplete T Regulatory Cells To Improve Vaccine Immune Responses For Cancer And Other Clinically Relevant Diseases

# data[].attributes.field_patent_titles[]
METHODS AND COMPOSITIONS FOR MODULATING IMMUNE TOLERANCE

# data[].attributes.field_patent_titles[]
Chemoattractant-based Toxins Which Deplete T Regulatory Cells To Improve Vaccine Immune Responses For Cancer And Other Clinically Relevant Diseases

# data[].attributes.field_patent_titles[]
Methods and Compositions for Modulating Immune Tolerance

# data[].attributes.field_patent_titles[]
Methods and Compositions for Modulating Immune Tolerance

# data[].attributes.field_publications[].value
R Schiavo et al. Chemokine receptor targeting efficiently directs antigens to MHC class I pathways and elicits antigen-specific CD8+ T-cell responses. Blood 2006 Jun 15; 107(12):4597-4605.

# data[].attributes.field_publications[].processed
R Schiavo et al. Chemokine receptor targeting efficiently directs antigens to MHC class I pathways and elicits antigen-specific CD8+ T-cell responses. Blood 2006 Jun 15; 107(12):4597-4605.

# data[].attributes.field_publications[].value
D Baatar, P Olkhanud, D Newton, K Sumitomo, A Biragyn. CCR4-expressing T cell tumors can be specifically controlled via delivery of toxins to chemokine receptors. J Immunol. 2007 Aug 1;179(3):1996-2004.

# data[].attributes.field_publications[].processed
D Baatar, P Olkhanud, D Newton, K Sumitomo, A Biragyn. CCR4-expressing T cell tumors can be specifically controlled via delivery of toxins to chemokine receptors. J Immunol. 2007 Aug 1;179(3):1996-2004.

# data[].attributes.field_publications[].value
M Coscia, A Biragyn. Cancer immunotherapy with chemoattractant peptides. Semin Cancer Biol. 2004 Jun; 14(3):209-218.

# data[].attributes.field_publications[].processed
M Coscia, A Biragyn. Cancer immunotherapy with chemoattractant peptides. Semin Cancer Biol. 2004 Jun; 14(3):209-218.

# data[].attributes.field_publications[].value
D Baatar, P Olkhanud, K Sumitomo, D Taub, R Gress, A Biragyn. Human peripheral blood T regulatory cells (Tregs), functionally primed CCR4+ Tregs and unprimed CCR4- Tregs, regulate effector T cells using FasL. J Immunol. 2007 Apr 15;178(8):4891-4900.

# data[].attributes.field_publications[].processed
D Baatar, P Olkhanud, K Sumitomo, D Taub, R Gress, A Biragyn. Human peripheral blood T regulatory cells (Tregs), functionally primed CCR4+ Tregs and unprimed CCR4- Tregs, regulate effector T cells using FasL. J Immunol. 2007 Apr 15;178(8):4891-4900.

# data[].attributes.field_technology_names[]
Chemoattractant-based Toxins Which Deplete T Regulatory Cells To Improve Vaccine Immune Responses For Cancer And Other Clinically Relevant Diseases

# data[].attributes.field_technology_owners[]
National Institute on Aging (NIH/NIA), University of Tokyo

# data[].attributes.title
RP2 and RPGR Vectors For Treating X-linked Retinitis Pigmentosa

# data[].attributes.body.value
X-linked forms of retinitis pigmentosa (XLRP) are relatively severe blinding disorders, resulting from progressive photoreceptor dysfunction primarily caused by mutations in RPGR or RP2 gene.

This technology is poised to advance RPGR or RP2 gene therapy to clinical stage using AAV8 or AAV9 vector carrying human full-length RPGR or RP2-coding sequence.  The investigators have performed a wide dose range study over 18-months and found it to preserve rod and/or cone function as evidenced by ERG and/or OCT, optomotor tests. Morphologically, the treatment preserved rod and cone viability, and corrected mistrafficking of cone opsin and/or rhodopsin. The therapeutic effect was also achieved in advanced disease stage. The broad treatment window and long-lasting therapeutic effects make the RPGR and RP2 gene therapy attractive for clinical development.

This technology is available for licensing, or the NEI research team will entertain potential collaborations that will advance this technology through the remaining preclinical stage toward IND development under a CRADA or a license combined with a CRADA project.

This patented treatment of albinism has not been approved by the U.S. Food and Drug Administration (FDA), and currently there is no active clinical trial to assess this albinism therapy benefit. However, if you are interested in participating in a future or upcoming NIH clinical trial on albinism, please contact NIH clinical coordinator, Ms. Ellaine Galindez-Balut (ellaine.galindez-balut@nih.gov), for helpful information. Thank you.

Competitive Advantages:

Pre-clinical dose efficacy study done

RPGR and RP2 available in both AAV-8 and AAV-9 vectors.

Preclinical data to show that treatment at advanced age also shows remarkable preservation of retinal structure and function.

Commercial Applications:

Use in gene therapy to prevent or cure XLRP

Preserving cone and/or rod function, restoring ERG and protein in the retina, increasing photoreceptor numbers, decrease in retinal detachments

Improving quality of life, visual acuity, ability to drive and independent living

# data[].attributes.body.processed
X-linked forms of retinitis pigmentosa (XLRP) are relatively severe blinding disorders, resulting from progressive photoreceptor dysfunction primarily caused by mutations in RPGR or RP2 gene.

This technology is poised to advance RPGR or RP2 gene therapy to clinical stage using AAV8 or AAV9 vector carrying human full-length RPGR or RP2-coding sequence.  The investigators have performed a wide dose range study over 18-months and found it to preserve rod and/or cone function as evidenced by ERG and/or OCT, optomotor tests. Morphologically, the treatment preserved rod and cone viability, and corrected mistrafficking of cone opsin and/or rhodopsin. The therapeutic effect was also achieved in advanced disease stage. The broad treatment window and long-lasting therapeutic effects make the RPGR and RP2 gene therapy attractive for clinical development.

This technology is available for licensing, or the NEI research team will entertain potential collaborations that will advance this technology through the remaining preclinical stage toward IND development under a CRADA or a license combined with a CRADA project.

This patented treatment of albinism has not been approved by the U.S. Food and Drug Administration (FDA), and currently there is no active clinical trial to assess this albinism therapy benefit. However, if you are interested in participating in a future or upcoming NIH clinical trial on albinism, please contact NIH clinical coordinator, Ms. Ellaine Galindez-Balut (ellaine.galindez-balut@nih.gov), for helpful information. Thank you.

Competitive Advantages:

Pre-clinical dose efficacy study done

RPGR and RP2 available in both AAV-8 and AAV-9 vectors.

Preclinical data to show that treatment at advanced age also shows remarkable preservation of retinal structure and function.

Commercial Applications:

Use in gene therapy to prevent or cure XLRP

Preserving cone and/or rod function, restoring ERG and protein in the retina, increasing photoreceptor numbers, decrease in retinal detachments

Improving quality of life, visual acuity, ability to drive and independent living

# data[].attributes.field_licensingcontact_hrefs[]
ricquita.pollard@nih.gov?subject=Web Inquiry on [TAB-4110] RP2 and RPGR Vectors For Treating X-linked Retinitis Pigmentosa&body=Please send me information about technology [TAB-4110] RP2 and RPGR Vectors For Treating X-linked Retinitis Pigmentosa.&cc=michael.salgaller@nih.gov, tdiaz@mail.nih.gov

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Pollard, Ricquita
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# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors For Treating X-linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 AND RPGR VECTORS FOR TREATING X-LINKED RETINITIS PIGMENTOSA

# data[].attributes.field_patent_titles[]
RP2 AND RPGR VECTORS FOR TREATING X-LINKED RETINITIS PIGMENTOSA

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_patent_titles[]
RP2 and RPGR Vectors for Treating X-Linked Retinitis Pigmentosa

# data[].attributes.field_publications[].value
Wu Z, et al. A long-term efficacy study of gene replacement therapy for RPGR-associated retinal degeneration

# data[].attributes.field_publications[].processed
Wu Z, et al. A long-term efficacy study of gene replacement therapy for RPGR-associated retinal degeneration

# data[].attributes.field_publications[].value
Zhang H, et al. Mistrafficking of prenylated proteins causes retinitis pigmentosa 2.

# data[].attributes.field_publications[].processed
Zhang H, et al. Mistrafficking of prenylated proteins causes retinitis pigmentosa 2.

# data[].attributes.field_publications[].value
Li L, et al. Ablation of the X-linked retinitis pigmentosa 2 (Rp2) gene in mice results in opsin mislocalization and photoreceptor degeneration

# data[].attributes.field_publications[].processed
Li L, et al. Ablation of the X-linked retinitis pigmentosa 2 (Rp2) gene in mice results in opsin mislocalization and photoreceptor degeneration

# data[].attributes.field_publications[].value
Mookherjee S, et al. Long-term rescue of cone photoreceptor degeneration in retinitis pigmentosa 2 (RP2)-knockout mice by gene replacement therapy

# data[].attributes.field_publications[].processed
Mookherjee S, et al. Long-term rescue of cone photoreceptor degeneration in retinitis pigmentosa 2 (RP2)-knockout mice by gene replacement therapy

# data[].attributes.field_related_inventions[].processed
E-162-2016

# data[].attributes.field_related_inventions[].processed
E-164-2014

# data[].attributes.field_technology_names[]
Novel Gene Therapy Vectors For Treating X-linked Retinitis Pigmentosa Caused Bymutations In RPGR And/or RP2 Genes

# data[].attributes.title
Replication-Competent VSV–BDBV Vaccine for Rapid Prevention and Post- Exposure Protection Against Bundibugyo Virus

# data[].attributes.body.value
Bundibugyo virus (BDBV) is one of several ebolaviruses that cause Ebola virus disease (EVD). Sporadic outbreaks continue to occur in Central Africa, highlighting the need for effective vaccines that provide rapid protection.

Researchers at NIAID’s Laboratory of Virology developed a vaccine against BDBV using vesicular stomatitis virus (VSV) to carry the BDBV surface glycoprotein (GP), a key target of the immune response, to BDBV. The team also created the DNA plasmid pATX– VSVDG–BDBV GP, a circular DNA molecule used to produce the vaccine virus in cell culture. Subsequent laboratory studies confirmed that the vaccine could be produced in cells and express the BDBV glycoprotein as intended. This design stimulates both early immune defenses and longer- lasting immune responses against BDBV. The BDBV glycoprotein may also facilitate delivery of the vaccine to antigen-presenting cells, including monocytes, macrophages, and dendritic cells, which play a central role in initiating antiviral immune responses.

In nonhuman primate studies, a single intramuscular dose of the vaccine protected animals from disease within 3 days of vaccination, supporting further development of the vaccine for rapid protection and post-exposure use. The licensable materials include both the recombinant rVSV–BDBV vaccine and the corresponding DNA plasmid to support further development, manufacturing, and outbreak response.

This technology is available for licensing for commercial development in accordance with 35 U.S.C. 209 and 37 CFR part 404, as well as for further development and evaluation under a research collaboration.

# data[].attributes.body.processed
Bundibugyo virus (BDBV) is one of several ebolaviruses that cause Ebola virus disease (EVD). Sporadic outbreaks continue to occur in Central Africa, highlighting the need for effective vaccines that provide rapid protection.

Researchers at NIAID’s Laboratory of Virology developed a vaccine against BDBV using vesicular stomatitis virus (VSV) to carry the BDBV surface glycoprotein (GP), a key target of the immune response, to BDBV. The team also created the DNA plasmid pATX– VSVDG–BDBV GP, a circular DNA molecule used to produce the vaccine virus in cell culture. Subsequent laboratory studies confirmed that the vaccine could be produced in cells and express the BDBV glycoprotein as intended. This design stimulates both early immune defenses and longer- lasting immune responses against BDBV. The BDBV glycoprotein may also facilitate delivery of the vaccine to antigen-presenting cells, including monocytes, macrophages, and dendritic cells, which play a central role in initiating antiviral immune responses.

In nonhuman primate studies, a single intramuscular dose of the vaccine protected animals from disease within 3 days of vaccination, supporting further development of the vaccine for rapid protection and post-exposure use. The licensable materials include both the recombinant rVSV–BDBV vaccine and the corresponding DNA plasmid to support further development, manufacturing, and outbreak response.

This technology is available for licensing for commercial development in accordance with 35 U.S.C. 209 and 37 CFR part 404, as well as for further development and evaluation under a research collaboration.

# data[].attributes.field_collaboration_description.value
The National Institute of Allergy and Infectious Diseases is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology. For collaboration opportunities, please contact Terrence Joyce at 301–761– 7235, or terrence.joyce@nih.gov.

# data[].attributes.field_collaboration_description.processed
The National Institute of Allergy and Infectious Diseases is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology. For collaboration opportunities, please contact Terrence Joyce at 301–761– 7235, or terrence.joyce@nih.gov.

# data[].attributes.field_commercial_applications.value
Leverages existing rVSV platforms, potentially reducing development and scale-up risk in manufacturing.

Emergency vaccination programs, including vaccination of close contacts and surrounding communities during BDBV outbreaks.

Pre-exposure vaccination for healthcare workers, laboratory personnel, outbreak-response teams, and others at increased risk of BDBV exposure.

Post-exposure use and related development programs for BDBV and other filovirus countermeasures.

# data[].attributes.field_commercial_applications.processed
Leverages existing rVSV platforms, potentially reducing development and scale-up risk in manufacturing.

Emergency vaccination programs, including vaccination of close contacts and surrounding communities during BDBV outbreaks.

Pre-exposure vaccination for healthcare workers, laboratory personnel, outbreak-response teams, and others at increased risk of BDBV exposure.

Post-exposure use and related development programs for BDBV and other filovirus countermeasures.

# data[].attributes.field_competitive_advantages.value
VSV vectors replicate transiently, producing rapid strong innate immune activation and early antibody responses. Recent nonhuman primate studies showed complete protection within 3 days after a single vaccination, which is exceptionally rapid for an Ebola vaccine platform.

Proven viral platform built on the same rVSV technology as the licensed Ebola vaccine Ervebo, providing clinical and regulatory familiarity.

Designed to provide rapid protection with a single intramuscular dose, simplifying use during outbreak response.

May stimulate both early immune defenses and longer-lasting immune responses against BDBV.

Ideal for ring vaccinations by supporting rapid immunization of contacts and contacts-of-contacts to help contain outbreaks.

Includes the BDBV glycoprotein, which may direct the vaccine to immune cells like monocytes, macrophages, and dendritic cells involved in activating antiviral responses.

Available for licensing as both the recombinant rVSV–BDBV vaccine and the DNA plasmid construct used to produce it.

# data[].attributes.field_competitive_advantages.processed
VSV vectors replicate transiently, producing rapid strong innate immune activation and early antibody responses. Recent nonhuman primate studies showed complete protection within 3 days after a single vaccination, which is exceptionally rapid for an Ebola vaccine platform.

Proven viral platform built on the same rVSV technology as the licensed Ebola vaccine Ervebo, providing clinical and regulatory familiarity.

Designed to provide rapid protection with a single intramuscular dose, simplifying use during outbreak response.

May stimulate both early immune defenses and longer-lasting immune responses against BDBV.

Ideal for ring vaccinations by supporting rapid immunization of contacts and contacts-of-contacts to help contain outbreaks.

Includes the BDBV glycoprotein, which may direct the vaccine to immune cells like monocytes, macrophages, and dendritic cells involved in activating antiviral responses.

Available for licensing as both the recombinant rVSV–BDBV vaccine and the DNA plasmid construct used to produce it.

# data[].attributes.field_licensingcontact_hrefs[]
terrence.joyce@nih.gov?subject=Web Inquiry on [TAB-5138] Replication-Competent VSV–BDBV Vaccine for Rapid Prevention and Post- Exposure Protection Against Bundibugyo Virus&body=Please send me information about technology [TAB-5138] Replication-Competent VSV–BDBV Vaccine for Rapid Prevention and Post- Exposure Protection Against Bundibugyo Virus.

# data[].attributes.field_licensingcontact_htmls[]
Joyce, Terrence
terrence.joyce@nih.gov

# data[].attributes.field_licensing_contacts[].value
Joyce, Terrence
terrence.joyce@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Joyce, Terrence
terrence.joyce@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
terrence.joyce@nih.gov?subject=Web Inquiry on [TAB-5138] Replication-Competent VSV–BDBV Vaccine for Rapid Prevention and Post- Exposure Protection Against Bundibugyo Virus&body=Please send me information about technology [TAB-5138] Replication-Competent VSV–BDBV Vaccine for Rapid Prevention and Post- Exposure Protection Against Bundibugyo Virus.

# data[].attributes.field_publications[].value
O’Donnell, KL, et al., "A single-dose Bundibugyo virus vaccine protects macaques within 3 days", bioRxiv. Published online June 15, 2026. doi:10.64898/2026.06.14.732188.

# data[].attributes.field_publications[].processed
O’Donnell, KL, et al., "A single-dose Bundibugyo virus vaccine protects macaques within 3 days", bioRxiv. Published online June 15, 2026. doi:10.64898/2026.06.14.732188.

# data[].attributes.field_technology_names[]
Vesicular stomatitis virus-based vaccine against Bundibugyo virus (VSV-BDBV)

# data[].attributes.field_technology_owners[]
National Institute of Allergy and Infectious Diseases (NIAID/NIH), NIAID - DIR, RML

# data[].attributes.title
48-Position Custom Deep Well Plate For In Vitro Equilibrium Dialysis at a 1:1 Sample to Buffer Volume Ratio

# data[].attributes.body.value
CDC scientists have developed a new design for a multi-well dialysis microplate for equilibrium dialysis. The unique design accommodates a 1:1 buffer to sample ratio and provides additional room at the base of the well to enable optimal cartridge immersion and analyte diffusion. The microplate is readily adaptable into existing automated analytical systems and meets the criteria of American National Standards Institute (ANSI). The microplate is designed for measuring blood or other biological fluid samples over a wide range of sample volumes and may be used in a high throughput manner. Use of the microplate has been shown to reduce errors, while increasing accuracy, precision, and sensitivity.

Thus far, the microplate has been successfully used for free testosterone measurement. The microplate may also be used for measuring other analytes and has the potential to be used in both clinical and research settings.

# data[].attributes.body.processed
CDC scientists have developed a new design for a multi-well dialysis microplate for equilibrium dialysis. The unique design accommodates a 1:1 buffer to sample ratio and provides additional room at the base of the well to enable optimal cartridge immersion and analyte diffusion. The microplate is readily adaptable into existing automated analytical systems and meets the criteria of American National Standards Institute (ANSI). The microplate is designed for measuring blood or other biological fluid samples over a wide range of sample volumes and may be used in a high throughput manner. Use of the microplate has been shown to reduce errors, while increasing accuracy, precision, and sensitivity.

Thus far, the microplate has been successfully used for free testosterone measurement. The microplate may also be used for measuring other analytes and has the potential to be used in both clinical and research settings.

# data[].attributes.field_collaboration_description.value
The CDC-NICHD is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the multi-well dialysis microplate. For collaboration opportunities, please contact: Madhavi Sriram nxu2@cdc.gov; TTO@cdc.gov.

# data[].attributes.field_collaboration_description.processed
The CDC-NICHD is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the multi-well dialysis microplate. For collaboration opportunities, please contact: Madhavi Sriram nxu2@cdc.gov; TTO@cdc.gov.

# data[].attributes.field_commercial_applications.value
Diagnostics: Meets the criteria of American National Standards Institute (ANSI).

Research Materials.

# data[].attributes.field_commercial_applications.processed
Diagnostics: Meets the criteria of American National Standards Institute (ANSI).

Research Materials.

# data[].attributes.field_competitive_advantages.value
Diagnostics: Dialysis microplate for measuring free hormone analytes such as free testosterone, free thyroxine (FT4), triiodothyronine, as well as measuring unbound drugs such as dolutegravir in diagnostic or research settings.

Public Health: Use of the dialysis microplate to provide dialysis testing services for customers.

# data[].attributes.field_competitive_advantages.processed
Diagnostics: Dialysis microplate for measuring free hormone analytes such as free testosterone, free thyroxine (FT4), triiodothyronine, as well as measuring unbound drugs such as dolutegravir in diagnostic or research settings.

Public Health: Use of the dialysis microplate to provide dialysis testing services for customers.

# data[].attributes.field_licensingcontact_hrefs[]
dawn.taylor-mulneix@nih.gov?subject=Web Inquiry on [TAB-5096] 48-Position Custom Deep Well Plate For In Vitro Equilibrium Dialysis at a 1:1 Sample to Buffer Volume Ratio&body=Please send me information about technology [TAB-5096] 48-Position Custom Deep Well Plate For In Vitro Equilibrium Dialysis at a 1:1 Sample to Buffer Volume Ratio.

# data[].attributes.field_licensingcontact_htmls[]
Taylor-Mulneix, Dawn
dawn.taylor-mulneix@nih.gov

# data[].attributes.field_licensing_contacts[].value
Taylor-Mulneix, Dawn
dawn.taylor-mulneix@nih.gov

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Taylor-Mulneix, Dawn
dawn.taylor-mulneix@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
dawn.taylor-mulneix@nih.gov?subject=Web Inquiry on [TAB-5096] 48-Position Custom Deep Well Plate For In Vitro Equilibrium Dialysis at a 1:1 Sample to Buffer Volume Ratio&body=Please send me information about technology [TAB-5096] 48-Position Custom Deep Well Plate For In Vitro Equilibrium Dialysis at a 1:1 Sample to Buffer Volume Ratio.

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Provisional (PRV) 63/551,965
Filed on 2024-02-09
Status: Expired

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US
Provisional (PRV) 63/551,965
Filed on 2024-02-09
Status: Expired

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Patent Cooperation Treaty
(PCT) PCT/US2025/014980
Filed on 2025-02-07
Status: Expired

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Patent Cooperation Treaty
(PCT) PCT/US2025/014980
Filed on 2025-02-07
Status: Expired

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National Stage None
Filed on None
Status: In Preparation

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Provisional (PRV) 63/551,965
Filed on 2024-02-09
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Filed on 2025-02-07
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National Stage None
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# data[].attributes.field_technology_names[]
48-Position Custom Deep Well Plate For In Vitro Equilibrium Dialysis at a 1:1 Sample to Buffer Volume Ratio

# data[].attributes.title
Next generation MRI platform Signal Amplification by Reversible Exchange (SABRE) hyperpolarization

# data[].attributes.body.value
Hyperpolarized magnetic resonance imaging (MRI) is an emerging molecular imaging method for metabolic imaging for detecting cancer, cardiovascular disease, stroke, and traumatic brain injury and monitoring therapy with no Gadolinium or Iron. Available for licensing and commercial development is a patent estate covering a perfluorinated single amplification by reversible exchange (SABRE) catalyst for generating MRI agents that includes a d-block element and a perfluorinated ligand hyperpolarized substrate comprising a 1/2 spin nucleus or nuclei using the perfluorinated SABRE catalysts, and isolating the resulting hyperpolarized substrate for administration. The invention also provides methods for separating a hyperpolarized substrate from the SABRE catalyst and/or hyperpolarized SABRE catalyst complex containing a heavy metal. These changes can be observed in patients in real time with a specialized MRI approach called hyperpolarization. By transiently changing the nuclear spin of naturally occurring intermediates in cellular energy production, the metabolic fate can be observed with greater than 10,000-fold sensitivity. Current methods of hyperpolarization require expensive machines with limited throughput.

# data[].attributes.body.processed
Hyperpolarized magnetic resonance imaging (MRI) is an emerging molecular imaging method for metabolic imaging for detecting cancer, cardiovascular disease, stroke, and traumatic brain injury and monitoring therapy with no Gadolinium or Iron. Available for licensing and commercial development is a patent estate covering a perfluorinated single amplification by reversible exchange (SABRE) catalyst for generating MRI agents that includes a d-block element and a perfluorinated ligand hyperpolarized substrate comprising a 1/2 spin nucleus or nuclei using the perfluorinated SABRE catalysts, and isolating the resulting hyperpolarized substrate for administration. The invention also provides methods for separating a hyperpolarized substrate from the SABRE catalyst and/or hyperpolarized SABRE catalyst complex containing a heavy metal. These changes can be observed in patients in real time with a specialized MRI approach called hyperpolarization. By transiently changing the nuclear spin of naturally occurring intermediates in cellular energy production, the metabolic fate can be observed with greater than 10,000-fold sensitivity. Current methods of hyperpolarization require expensive machines with limited throughput.

# data[].attributes.field_commercial_applications.value
MRI imaging

Hyperpolarization

Infusion Device for imaging reagents

Cancer diagnostics

Cardiovascular disease diagnostics

# data[].attributes.field_commercial_applications.processed
MRI imaging

Hyperpolarization

Infusion Device for imaging reagents

Cancer diagnostics

Cardiovascular disease diagnostics

# data[].attributes.field_competitive_advantages.value
High Sensitivity: Over 10,000-fold sensitivity improvement.

Cost Efficiency: Avoids expensive hyperpolarization machines.

Metal-Free Imaging: No gadolinium or iron required.

Real-Time Monitoring: Enables immediate observation of metabolic changes.

# data[].attributes.field_competitive_advantages.processed
High Sensitivity: Over 10,000-fold sensitivity improvement.

Cost Efficiency: Avoids expensive hyperpolarization machines.

Metal-Free Imaging: No gadolinium or iron required.

Real-Time Monitoring: Enables immediate observation of metabolic changes.

# data[].attributes.field_inventor_companies[]
National Heart, Lung, and Blood Institute (NHLBI)

# data[].attributes.field_licensingcontact_depts[]
Office of Technology Transfer and Development

# data[].attributes.field_licensingcontact_hrefs[]
shmilovm@nih.gov?subject=Web Inquiry on [TAB-5034] Next generation MRI platform Signal Amplification by Reversible Exchange (SABRE) hyperpolarization&body=Please send me information about technology [TAB-5034] Next generation MRI platform Signal Amplification by Reversible Exchange (SABRE) hyperpolarization.

# data[].attributes.field_licensingcontact_htmls[]
Shmilovich, Michael
shmilovm@nih.gov

# data[].attributes.field_licensing_contacts[].value
Shmilovich, Michael
shmilovm@nih.gov

# data[].attributes.field_licensing_contacts[].processed
Shmilovich, Michael
shmilovm@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
shmilovm@nih.gov?subject=Web Inquiry on [TAB-5034] Next generation MRI platform Signal Amplification by Reversible Exchange (SABRE) hyperpolarization&body=Please send me information about technology [TAB-5034] Next generation MRI platform Signal Amplification by Reversible Exchange (SABRE) hyperpolarization.

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National Stage 23707534.6
Filed on 2024-07-23
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National Stage 21741941.5
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China Patent (CN) 62025104551.9
Filed on 2025-03-11
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Hong Kong
China Patent (CN) 62025104551.9
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European patent (EP) 23721501.7
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US
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European Patent
National Stage 23707534.6
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Status: Pending

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Israel
National Stage 315942
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US
National Stage 18/854,462
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European Patent
National Stage 23721501.7
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Status: Pending

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National Stage 294365
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National Stage 21741941.5
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Israel
National Stage 294464
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Status: Issued

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US
National Stage 17/793,089
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Status: Pending

# data[].attributes.field_patent_htmls[]
Hong Kong
China Patent (CN) 62025104551.9
Filed on 2025-03-11
Status: Abandoned

# data[].attributes.field_patent_htmls[]
France
European patent (EP) 23721501.7
Filed on 2024-11-06
Status: Pending

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Germany
European patent (EP) 23721501.7
Filed on 2024-11-06
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European patent (EP) 23721501.7
Filed on 2024-11-06
Status: Pending

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European patent (EP) 23721501.7
Filed on 2024-11-06
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European patent (EP) 23721501.7
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# data[].attributes.field_patent_titles[]
TEMPERATURE CYCLING METHOD FOR HYPERPOLARIZATION OF TARGET MOLECULES AND CONTRAST AGENTS USING PARAHYDROGEN

# data[].attributes.field_patent_titles[]
TEMPERATURE CYCLING METHOD FOR HYPERPOLARIZATION OF TARGET MOLECULES AND CONTRAST AGENTS USING PARAHYDROGEN

# data[].attributes.field_patent_titles[]
TEMPERATURE CYCLING METHOD FOR HYPERPOLARIZATION OF TARGET MOLECULES AND CONTRAST AGENTS USING PARAHYDROGEN

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
PREPARATION OF ISOTOPICALLY LABELED KETOGLUTARATES AND METHODS OF HYPERPOLARIZATION THROUGH SIGNAL AMPLIFICATION BY REVERSIBLE EXCHANGE (SABRE)

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

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INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

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REAL-TIME MONITORING OF IN VIVO FREE RADICAL SCAVENGERS THROUGH HYPERPOLARIZED N-ACETYL CYSTEINE ISOTOPES

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REAL-TIME MONITORING OF IN VIVO FREE RADICAL SCAVENGERS THROUGH HYPERPOLARIZED N-ACETYL CYSTEINE ISOTOPES

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REAL-TIME MONITORING OF IN VIVO FREE RADICAL SCAVENGERS THROUGH HYPERPOLARIZED N-ACETYL CYSTEINE ISOTOPES

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REAL-TIME MONITORING OF IN VIVO FREE RADICAL SCAVENGERS THROUGH HYPERPOLARIZED N-ACETYL CYSTEINE ISOTOPES

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REAL-TIME MONITORING OF INVIVO FREE RADICAL SCAVENGERS THROUGH HYPERPOLARIZED N-ACETYL CYSTEINE ISOTOPES

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Isotopes Of Alpha Ketoglutarate And Related Compounds For Hyperpolarized MRI Imaging

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ISOTOPES OF ALPHA KETOGLUTARATE AND RELATED COMPOUNDS FOR HYPERPOLARIZED IMAGING

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ISOTOPES OF ALPHA KETOGLUTARATE AND RELATED COMPOUNDS FOR HYPERPOLARIZED IMAGING

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ISOTOPES OF ALPHA KETOGLUTARATE AND RELATED COMPOUNDS AND THEIR USE IN HYPERPOLARIZED IMAGING

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ISOTOPES OF ALPHA KETOGLUTARATE AND RELATED COMPOUNDS AND THEIR USE IN HYPERPOLARIZED IMAGING

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INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_patent_titles[]
INFUSION DEVICE FOR THE PREPARATION AND DELIVERY OF MRI PROBES

# data[].attributes.field_publications[].value
Ettedgui J, 2024

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Ettedgui J, 2024

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Hong D, 2023

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Hong D, 2023

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Schmidt AB, 2022

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Schmidt AB, 2022

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Adelabu I, 2022

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Adelabu I, 2022

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Adelabu I, 2022

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Adelabu I, 2022

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AbuSalim JE, 2021

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AbuSalim JE, 2021

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Miura N, 2021

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Miura N, 2021

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Chapman B, 2021

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Chapman B, 2021

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Yamamoto K, 2021

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Yamamoto K, 2021

# data[].attributes.field_technology_names[]
Synthesis Of Iridium SABRE Catalysts Containing Heavy Perfluorinated Carbon Chains For Its Facile Removal And Delivery Of Metal-free Hyperpolarized Contrast Agents Such As Pyruvate

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Preparation Of Deuterated 12C, 13C-ketoglutarate (1-13C-3-D2-4-D-512C Ketoglutarate) And Methods To Hyperpolarization Using SABRE-Signal Amplification By Reversible Exchange

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TEMPERATURE CYCLING METHOD FOR HYPERPOLARIZATION OF TARGET MOLECULES AND CONTRAST AGENTS USING PARAHYDROGEN

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INFUSION DEVICE FOR THE USE OF HYPERPOLARIZED MRI PROBES PREPARED BY FLUOROUS CATALYZED SABRE

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Real-time Monitoring Of In Vivo Free Radical Scavengers Through Hyperpolarized [1-13C] N-acetyl Cysteine

# data[].attributes.field_technology_names[]
Isotopes Of Alpha Ketoglutarate And Related Compounds For Hyperpolarized MRI Imaging

# data[].attributes.field_technology_owners[]
National Heart, Lung, and Blood Institute (NHLBI), NCI

# data[].attributes.field_technology_owners[]
National Heart, Lung, and Blood Institute (NHLBI), NCI

# data[].attributes.field_technology_owners[]
National Heart, Lung, and Blood Institute (NHLBI)

# data[].attributes.field_technology_owners[]
National Heart, Lung, and Blood Institute (NHLBI), NCI

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National Heart, Lung, and Blood Institute (NHLBI), NCI

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National Cancer Institute (NCI), National Heart, Lung, and Blood Institute (NHLBI), National Heart, Lung, and Blood Institute (NHLBI), Radiation Biology Branch

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In research settings, visualization of  tumors or tumor cells is often done using either bioluminescence or fluorescence.  However, both of these methods have shortcomings: bioluminescence is not sensitive enough to sort individual tumor cells, and fluorescence cannot be used effectively to view internal tumors and is best used with surface tumors.

Researchers at NCI developed twelve lentiviral vectors that express both fluorescent and luminescent markers as a single fusion protein under various gene promoters.  By combining the two reporters into a single fusion protein, the tumor can be visualized within the animal as well as sorted from non-tumor cells for post-necropsy experiments.  The advantage of bioluminescent visualization allows for in vivo experiments that more closely simulate the biological development of tumors in organs, rather than at the skin surface. Additionally, since twelve different vectors with different gene promoters were constructed, they can be tested in individual tumor models to find the best vector for visualizing that particular tumor cell line. The vectors are able to sustain long-term expression of both visualization markers, depending on the cell type and promoter in each vector.

Competitive Advantages:

The bioluminescent marker allows for effective visualization of deep (non-surface) tumors in mice

The fluorescence label permits efficient sorting of tumor cells from normal (non-labeled) cells after tumors are excised from the mice

The vectors allow in vivo experiments that more closely simulate the biological development of tumors in organs rather than at surface of skin

The vectors sustain long-term expression

Commercial Applications:

Useful for experiments in which both in vivo and in vitro analysis is desired

For screening cancer cell lines and in tumor models for reporter gene activity

Useful in drug development

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In research settings, visualization of  tumors or tumor cells is often done using either bioluminescence or fluorescence.  However, both of these methods have shortcomings: bioluminescence is not sensitive enough to sort individual tumor cells, and fluorescence cannot be used effectively to view internal tumors and is best used with surface tumors.

Researchers at NCI developed twelve lentiviral vectors that express both fluorescent and luminescent markers as a single fusion protein under various gene promoters.  By combining the two reporters into a single fusion protein, the tumor can be visualized within the animal as well as sorted from non-tumor cells for post-necropsy experiments.  The advantage of bioluminescent visualization allows for in vivo experiments that more closely simulate the biological development of tumors in organs, rather than at the skin surface. Additionally, since twelve different vectors with different gene promoters were constructed, they can be tested in individual tumor models to find the best vector for visualizing that particular tumor cell line. The vectors are able to sustain long-term expression of both visualization markers, depending on the cell type and promoter in each vector.

Competitive Advantages:

The bioluminescent marker allows for effective visualization of deep (non-surface) tumors in mice

The fluorescence label permits efficient sorting of tumor cells from normal (non-labeled) cells after tumors are excised from the mice

The vectors allow in vivo experiments that more closely simulate the biological development of tumors in organs rather than at surface of skin

The vectors sustain long-term expression

Commercial Applications:

Useful for experiments in which both in vivo and in vitro analysis is desired

For screening cancer cell lines and in tumor models for reporter gene activity

Useful in drug development

# data[].attributes.field_licensingcontact_htmls[]
Freel, Rose
rose.freel@nih.gov

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Freel, Rose
rose.freel@nih.gov

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Freel, Rose
rose.freel@nih.gov

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Day CP, et al. Lentivirus-mediated bifunctional cell labeling for in vivo melanoma study.

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Day CP, et al. Lentivirus-mediated bifunctional cell labeling for in vivo melanoma study.

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Lentiviral Vectors For Long-term In Vivo Expression Of Dual Luorescence/luminescence Reporters

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Characterization of novel pan anti-HLA antibodies that block LILR inhibitory receptors and activate anti-tumor immunity

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Cancer immunotherapy has transformed treatment for some patients, but many tumors still do not respond well to current options, including checkpoint inhibitors. Researchers at NIAID’s Laboratory of Immune System Biology (LISB) have developed new antibodies designed to help the immune system fight tumors. These lab-made antibodies, called pan-anti-HLA monoclonal antibodies, block signals that can limit immune cell activity.

These signals are part of a pathway that regulates immune responses. In this pathway, inhibitory receptors in the leukocyte immunoglobulin-like receptor (LILR) family, found on many immune cells like natural killer (NK) cells and T cells, act like a brake when they interact with molecules called MHC-I. The antibodies are designed to block this interaction and release that brake. Earlier studies showed that antibodies targeting this interaction could activate both innate immunity, the body’s first line of defense, and adaptive immunity, the part of the immune system that builds more targeted responses and immune memory.

The new pan anti-HLA antibodies 3C10 and 15B1 block LILR interactions by binding to a different site on MHC-I than previously developed antibodies DX17 and W6/32. They also bind more than 50 times better and activate human NK and T cells for tumor control. To support development of next-generation checkpoint therapies, researchers will further evaluate the 3C10 and 15B1 antibodies in animal and tissue-based models.

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Cancer immunotherapy has transformed treatment for some patients, but many tumors still do not respond well to current options, including checkpoint inhibitors. Researchers at NIAID’s Laboratory of Immune System Biology (LISB) have developed new antibodies designed to help the immune system fight tumors. These lab-made antibodies, called pan-anti-HLA monoclonal antibodies, block signals that can limit immune cell activity.

These signals are part of a pathway that regulates immune responses. In this pathway, inhibitory receptors in the leukocyte immunoglobulin-like receptor (LILR) family, found on many immune cells like natural killer (NK) cells and T cells, act like a brake when they interact with molecules called MHC-I. The antibodies are designed to block this interaction and release that brake. Earlier studies showed that antibodies targeting this interaction could activate both innate immunity, the body’s first line of defense, and adaptive immunity, the part of the immune system that builds more targeted responses and immune memory.

The new pan anti-HLA antibodies 3C10 and 15B1 block LILR interactions by binding to a different site on MHC-I than previously developed antibodies DX17 and W6/32. They also bind more than 50 times better and activate human NK and T cells for tumor control. To support development of next-generation checkpoint therapies, researchers will further evaluate the 3C10 and 15B1 antibodies in animal and tissue-based models.

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The National Institute of Allergy and Infectious Diseases is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology. For collaboration opportunities, please contact Yogikala Prabhu at 202-365-4785, or yogikala.prabhu@nih.gov

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The National Institute of Allergy and Infectious Diseases is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this technology. For collaboration opportunities, please contact Yogikala Prabhu at 202-365-4785, or yogikala.prabhu@nih.gov

# data[].attributes.field_commercial_applications.value
An antibody-based cancer immunotherapy that helps release immune “brakes” on tumor-fighting cells

A next-generation checkpoint therapy that could be used alone or with other immunotherapies, including CAR-T or CAR-NK cells

A potential immune-based treatment strategy for chronic infections such as TB, HIV, and hepatitis B or C

# data[].attributes.field_commercial_applications.processed
An antibody-based cancer immunotherapy that helps release immune “brakes” on tumor-fighting cells

A next-generation checkpoint therapy that could be used alone or with other immunotherapies, including CAR-T or CAR-NK cells

A potential immune-based treatment strategy for chronic infections such as TB, HIV, and hepatitis B or C

# data[].attributes.field_competitive_advantages.value
Target a broad immune “brake” pathway rather than just individual LILR receptors

Bind to a different site on MHC-I and does so over 50 times more strongly than earlier antibodies

Activates human natural killer (NK) cells and T cells for tumor control

Builds on earlier findings showing that blocking this pathway can trigger anti-tumor immune responses

# data[].attributes.field_competitive_advantages.processed
Target a broad immune “brake” pathway rather than just individual LILR receptors

Bind to a different site on MHC-I and does so over 50 times more strongly than earlier antibodies

Activates human natural killer (NK) cells and T cells for tumor control

Builds on earlier findings showing that blocking this pathway can trigger anti-tumor immune responses

# data[].attributes.field_licensingcontact_hrefs[]
yogikala.prabhu@nih.gov?subject=Web Inquiry on [TAB-5136] Characterization of novel pan anti-HLA antibodies that block LILR inhibitory receptors and activate anti-tumor immunity&body=Please send me information about technology [TAB-5136] Characterization of novel pan anti-HLA antibodies that block LILR inhibitory receptors and activate anti-tumor immunity.

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Prabhu, Yogikala
yogikala.prabhu@nih.gov

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Prabhu, Yogikala
yogikala.prabhu@nih.gov

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Prabhu, Yogikala
yogikala.prabhu@nih.gov

# data[].attributes.field_licensing_contacts_uris[]
yogikala.prabhu@nih.gov?subject=Web Inquiry on [TAB-5136] Characterization of novel pan anti-HLA antibodies that block LILR inhibitory receptors and activate anti-tumor immunity&body=Please send me information about technology [TAB-5136] Characterization of novel pan anti-HLA antibodies that block LILR inhibitory receptors and activate anti-tumor immunity.

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US
Provisional (PRV) 64/053,946
Filed on 2026-04-30
Status: Pending

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US
Provisional (PRV) 64/053,946
Filed on 2026-04-30
Status: Pending

# data[].attributes.field_patent_htmls[]
US
Provisional (PRV) 64/053,946
Filed on 2026-04-30
Status: Pending

# data[].attributes.field_patent_titles[]
ANTI-PAN HLA ANTIBODIES THAT BLOCK LILRB AND ACTIVATE IMMUNE CELLS

# data[].attributes.field_technology_names[]
Characterization of novel pan anti-HLA antibodies that block LILR inhibitory receptors and activate anti-tumor immunity