The National Center for Complimentary and Integrative Health (NCCIH) seeks licensees and/or commercial partners to develop topical formulations of margaric acid to treat allodynia, neuropathy, and pain caused by chronic inflammation.
NCI seeks commercial partners to co-develop and/or license a novel method for isolation and construction of neoantigen-reactive T-cell receptors (TCRs) from peripheral blood lymphocytes (PBL).
NCI seeks commercial partners to co-develop and/or license a novel method to identify neoantigen reactive T cells and TCRs.
NCI seeks research co-development and/or potential licensees for a potential novel treatment for triple-negative breast cancer (TNBC) with acetalax (oxyphenisatin acetate).
Gel materials, particularly hydrogels, typically lose their mechanical strength and stiffness as they swell. This property limits their use in both biological (e.g., cartilage and ECM repair) and non-biological (e.g., sealant) applications. Innovative materials in both medical and non-medical application areas are sorely needed.
Due to the large degree of homology among dopamine D2-like receptors, discovering ligands capable of discriminating between the D2, D3, and D4 receptor subtypes remains a significant challenge. The development of subtype-selective pharmaceutical small molecules to activate (agonists) signals regulated by D2-like receptors has been especially difficult.
The NCI seeks research co-development partners and/or licensees for the development and commercialization of a diagnostic assay that detects sequence-specific (viral) RNA.
The National Cancer Institute (NCI) is actively seeking potential licensees and/or co-development research collaboration partners interested in advancing oxynitidine derivatives as novel inhibitors of topoisomerase IB (TOP1) and tyrosyl-DNA phosphodiesterase 1 (TDP1) for cancer treatment. These TOPI and TDP1 inhibitors, when administered together, demonstrate enhanced anti-tumor efficacy.
Programed Death-Ligand 1 (PD-L1, also known as B7-H1 or CD274) is a cell surface protein that binds to Programmed Cell Death Protein 1 (PD-1, also known as CD279). An imbalance in PD-1/PD-L1 activity contributes to cancer immune escape. PD-1 is expressed on the surface of antigen-stimulated T cells. The interaction between PD-L1 and PD-1 negatively regulates T cell-mediated immune responses. It has been suggested that disrupting the PD-L1/PD-1 signaling pathway can be used to treat cancers.