# 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