The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Section on Molecular Neurobiology seeks parties interested in licensing or collaborative research to further evaluate or commercialize specific rabbit monoclonal antibodies generated against the ErbB4 receptor (also known as HER4) that have been validated for specificity using tissue sections and extracts from ErbB4 knockout mice.
Researchers at the National Cancer Institute (NCI) have developed an engineered storage unit for frozen tissue, that provides a permanent base on which to mount tissue frozen in OCT and an enclosure for storage. The unit provides for chain-of-custody labeling and acts as an insulating container to protect the specimen. Other elements include devices for freezing the tissue to the base, as well as a holder for the base to facilitate cryosectioning. Application of the storage system allows a frozen tissue specimen to be moved between storage and cryosectioning without loss of label, deformation of tissue, or thermal alterations.
The National Cancer Institute's Cancer and Inflammation Program is seeking statements of capability or interest from parties interested in licensing monoclonal antibodies to IGF-1 and IGF-II for the treatment of cancer.
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). These 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.
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.
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.
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.
The National Eye Institute’s Ophthalmic Genetics and Visual Function Branch seeks partners to co-develop the protocol for iPSC to RPE differentiation and its use in clinical, screening and translational settings.
The National Institute of Child and Human Development seeks interested parties to further co-developa cell line with mutations in PRKAR1A, associated with tumor formation, for use a diagnostic or research tool.
Three anti-HIV proteins- the antiviral lectin cyanovirin, the antiviral lectin griffithsin, and the monoclonal antibody 2G12- have been successfully expressed in the same rice seed. The co-expression allows for a low cost, stable production method for a triple anti-HIV microbicide for the prevention of HIV. The National Cancer Institute (NCI) seeks licensees for the invention microbicide and production method.
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.