Scientists at NIH have identified 7 new agonist epitopes of the MUC-1 tumor associated antigen. Compared to their native epitope counterparts, peptides reflecting these agonist epitopes have been shown to enhance the generation of human tumor cells, which in turn have a greater ability to kill human tumor cells endogenously expressing the native MUC-1 epitope.
The National Cancer Institute is seeking statements of capability or interest from parties interested in collaborative research to co-develop antibody-based therapeutic against MERS-CoV, including animal studies, cGMP manufacturing, and clinical trials.
The National Eye Institute (NEI) seeks research co-development partners and/or licensees for gene therapy for CRX retinopathies such as Leber congenital amaurosis, retinitis pigmentosa, and cone-rod dystrophy.
The National Cancer Institute's Cancer and Inflammation Program is seeking statements of capability or interest from parties interested in licensing therapeutic agents that generate Nitroxyl (HNO) in physiological media.
The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for small molecules that inhibit histone lysine demethylases (KDMs). These compounds may be effective therapeutics for Rhabdomyosarcoma (RMS) and other cancers.
Researchers at the NCI seek licensing and/or co-development research collaborations for an anti-viral polypeptide, Griffithsin, and its antiviral use against Hepatitis C, Severe Acute Respiratory Syndrome (SARS), H5N1, or Ebola.
Researchers at NCI developed a rabbit monoclonal antibody that recognizes the marker for CD133 and is useful in pharmacodynamic testing to inform targeted anti-cancer chemotherapy development and clinical monitoring. CD133 is a cell surface glycoprotein used as a marker and expressed in stem cells such as hematopoietic stem cells, endothelial progenitor cells and neural stem cells. The NCI seeks collaborative co-development or licensing partners for this technology.
The National Cancer Institute (NCI) and the National Institute of Child Health and Human Development (NICHD) seek research co-development partners and/or licensees for an antiviral treatment that can target SARS-Cov-2 replication in Covid-19 patients.
Investigators at the National Cancer Institute''s Vaccine Branch have found that beta-mannosylceramide (Beta-ManCer) promotes immunity in an IFN-gamma independent mechanism and seek statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize beta-ManCer.
Researchers at the National Cancer Institute (NCI) have developed an invention consisting of hydrocarbon stapled peptides that disrupt the linear ubiquitin-chain assembly complex (LUBAC), which is involved in NF-κB signaling. These peptides can be used as a therapeutic in the treatment of the activated B cell-like (ABC) subtype of diffuse large B cell lymphoma (DLBCL), a type of non-Hodgkin’s lymphoma, as well as inflammatory diseases. The NCI seeks licensing and/or co-development research collaborations for inhibitors of NF-κB signaling and/or treatment of ABC DLBCL, as well as inflammatory diseases.
The proto-oncogene c-Myc is deregulated and overexpressed in ~70% of all cancers. Thus, c-Myc is an attractive therapeutic target. Beyond cancer, Myc is also a positive effector of tissue inflammation, and its function has been implicated in the pathophysiology of heart failure. Researchers at the National Cancer Institute (NCI) developed novel small molecules that target c-Myc at the transcriptional level, thus enabling a potential pan-cancer therapeutic. Specifically, these compounds stabilize the transcription repressing quadruplex in the c-Myc gene promoter region. The National Cancer Institute seeks parties interested in licensing or collaborative research to co-develop these therapeutic targets.'
Chk2 is a protein kinase activated in response to DNA double strand breaks. In normal tissues, Chk2 phosphorylates and thereby activates substrates that induce programmed cell death, or apoptosis, via interactions with p53, E2F1, PML proteins. In cancer tissues, where apoptosis is suppressed, Chk2 phosphorylates and inactivates cell cycle checkpoints (via interactions with Cdc25, phosphatases and Brca1 proteins), which allows cancer cells to repair and tolerate DNA damage. Hence, Chk2 inhibitors would be expected to protect normal tissues by reducing apoptosis, and to sensitize cancer cells to DNA-targeted agents.
The National Cancer Institute seeks licensees for small molecule inhibitors of Chk2 for the treatment of cancer.
The National Cancer Institute’s Surgery Branch seeks partners interested in collaborative research to co-develop adoptive transfer of tumor infiltrating leukocytes (TIL) for cancers other than melanoma.