Search Technologies

The National Cancer Institute (NCI) has a novel mouse model of autoimmunity based on chronic interferon-gamma expression (ARE-Del). This mouse can be used as an in vivo model to study female-biased autoimmune diseases, including: Systemic Lupus Erythematosus, Primary Biliary Cholangitis, and Ovarian Failure Syndrome.

The Hippo signaling pathway is one of the most frequently altered pathways in human cancer. Researchers at the National Cancer Institute (NCI) have developed a genetically encoded peptide inhibitor of the Hippo signaling pathway members YAP1/TAZ-TEAD, to dissect and study the specific TEAD-downstream regulatory gene expression networks of cell proliferation, tissue homeostasis, and stem cell functions in different cell types and pathologies. The DNA construct encoding this inhibitor may be delivered to cells using lentivirus, adenovirus, or adeno-associated virus, and is a valuable research tool. NCI seeks licensees for this peptide inhibitor and the encoding DNA construct.

Recent research has demonstrated that neoantigen-specific T-cell receptors (TCRs) can be isolated from a cancer patient’s lymphocytes. These TCRs may be used to engineer populations of tumor-reactive T cells for cancer immunotherapies. Obtaining sequences of these functional TCRs is a critical initial step in preparing this type of personalized cancer treatment; however, current methods are time-consuming and labor-intensive. Scientists at the National Cancer Institute (NCI) have developed a rapid and robust method of isolating the sequences of mutation-specific TCRs to alleviate these issues; they seek licensing and/or co-development research collaborations for the development of a method for isolating the sequences of tumor-reactive TCRs. For collaboration opportunities, please contact Steven A. Rosenberg, M.D., Ph.D. at sar@nih.gov.

The National Cancer Institute seeks licensees for a model used to study molecular mechanisms and/or signaling pathways involved in tumorigenesis, angiogenesis and metastasis of breast cancer and its response to therapy.

Researchers at the National Cancer Institute (NCI) have developed a bioluminescent MB49-luciferase bladder cancer cell line that can be used in preclinical studies to evaluate anti-cancer agents in bladder cancer. NCI seeks parties to non-exclusively license this research material.

The National Institute of Child Health & Human Development (NICHD), Program in Genomics of Differentiation, seeks interested parties to further co-develop small molecule inhibitors of RNase H1, especially in regards to genome instability, transcription, and translation.

Scientists at the National Cancer Institute (NCI) have developed the Cytokine Signaling Analyzer (CytoSig), a software-based platform that provides both a database of target genes modulated by cytokines and a predictive model of cytokine signaling cascades from transcriptomic profiles. NCI seeks collaborators or licensees to advance the development of CytoSig for research, target discovery, or as a Clinical Decision Support System (CDSS).

Hibernation in mammals is a seasonal state of metabolic suppression and dormancy characterized by a decrease in body temperature to survive extreme environmental stresses. A new Induced Pluripotent Stem Cell (iPSC) line has been established from the neural precursor cells of wild type thirteen-lined ground squirrel (Spermophilus tridecemlineatus), a small mammalian hibernator with unique metabolic adaptations for coping with cold and restricted food supply. This ground squirrel iPSC line can be differentiated into many different cell types for hibernation studies, disease modeling, and drug screening for neuronal injuries or other diseases.

Pulmonary surfactant plays a critical role in preventing alveolar collapse by decreasing surface tension at the alveolar air-liquid interface. Surfactant deficiency contributes to the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), common disorders that can afflict patients of all ages and carry a mortality rate greater than 25%. Excess surfactant leads to pulmonary alveolar proteinosis. NCI investigators created a G-protein coupled receptor GPR116 mutant mouse model and showed that GPR116 plays a previously unexpected, essential role in maintaining normal surfactant levels in the lung. The National Cancer Institute seeks partners interested in collaborative research to license surfactant modulating agents for the treatment of surfactant related lung disorders.