Researchers at the National Cancer Institute (NCI) have developed a novel method for identifying neoantigen reactive T cells and T cell receptors (TCRs), isolated from fresh tumors of common epithelial cancers. This highly specific and sensitive method allows rapid determination of the neoantigen reactive TCR sequences and can be very useful to translate this information into TCR-engineered T-cell populations for immunotherapy without the need to grow tumor infiltrating T-cells and expensive, time-consuming screening. The NCI seeks research co-development partners and/or licensees for this invention.
Investigators at the NCI discovered an Anti-TNF Induced Apoptosis (ATIA) protein, which protects cells against apoptosis. ATIA is highly expressed in glioblastoma and astrocytomas and its inhibition results in increased cell sensitivity to TNF-related apoptosis-inducing ligand induced cell death. The National Cancer Institute seeks parties interested in licensing or collaborative research to further develop, evaluate, or commercialize glioblastoma diagnostics and therapeutics.
Chimeric Antigen Receptors (CARs) are engineered proteins that can be used in a therapeutic capacity when expressed by an immune cell (e.g., a T cell). Specifically, CARs comprise a targeting domain (such as an antibody or binding fragment thereof) as well as domains that activate immune cells. By selecting a targeting domain that binds to a protein that is selectively expressed on a cancer cell, it is possible to target immune cells to the cancer cells. Upon binding to the target cell, the immune cells are activated, leading to the destruction of the cancer cell. This therapeutic approach holds great promise, as evidenced by the recent FDA-approval of CAR-T cell therapies, KYMRIAH and YESCARTA, both of which target CD19.
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.
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 Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) seek partners to collaborate on in vitro studies to validate these potential immunomodulators and to conduct in vivo studies in a murine cancer model to determine the effects of ligands (e.g., antibodies) to the proteins on the immune response to cancer cells. Preference will be given to responses received by March 31, 2016.
Researchers at the National Cancer Institute (NCI) developed compounds containing both a non-steroidal anti-inflammatory drug (NSAID) and a nitroxyl (HNO) -releasing agent that have significantly reduced toxicity, allowing their use for extended periods of time without severe side effects.The HNO-releasing moiety contained in this invention may expand the medical utility of NSAIDs. HNO releasing agents possess anticancer activity as well as good antioxidant properties, which has potential benefit for a variety of human diseases, including acute and chronic inflammation. NCI seeks parties to license or co-develop this technology.
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.
This licensing opportunity from the National Cancer Institute concerns the development of CARs comprising an antigen-binding fragment derived from the MGA271 antibody. The resulting CARs can be used in adoptive cell therapy treatment for neuroblastoma and other tumors that express CD276.
Researchers at the National Cancer Institute (NCI) developed novel analogs of the natural product schweinfurthins to treat neurofibromatosis type 1 (NF1). The compounds demonstrate effective growth inhibition in malignant peripheral nerve sheath tumor cell lines and mouse models of astrocytomas. Researchers seek licensing and/or co-development research collaboration opportunities to further develop the schweinfurthin analogs.
To improve the therapeutic effectiveness of PE-based immunotoxins through multiple rounds of drug administration, NIH inventors have sought to identify and remove the human B cell epitopes within PE. Previous work demonstrated that the removal of the murine B cell and T cell epitopes from PE reduced the immunogenicity of PE and resulted in immunotoxins with improved therapeutic activity. The National Cancer Institute's Laboratory of Molecular Biology seeks interested parties to co-develop and commercialize immunotoxins using toxin domains lacking human B cell epitopes.
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.
Investigators at the National Cancer Institute have discovered fluoroquinolone derivatives as specific Tdp1 inhibitors that could potentiate the pharmacological action of Top1 inhibitors currently used in cancer treatment.
Researchers at the National Cancer Institute (NCI) have developed peptidomimetic inhibitors that disrupt Polo-like kinase 1 (Plk1)-mediated protein interactions by targeting polo-box domain (PBD). The compounds are designed to selectively cause mitotic arrest in cancer cells with abnormal Plk1 expression. Researchers seek licensing and/or co-development research collaborations to further develop the inhibitors.
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.
Researchers at the National Cancer Institute’s Experimental Transplantation and Immunology Branch (NCI ETIB) developed a T Cell receptor that specifically targets the Kita-Kyushu Lung Cancer Antigen 1 (KK-LC-1) 52-60 epitope that is highly expressed by several common and aggressive epithelial tumor types.