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The National Cancer Institute (NCI) seeks licensing and/or co-development of an adoptive cellular therapeutic modality that targets CCR4, which is overexpressed in certain lymphoid malignancies as well as solid tumors.

Cancer therapies that specifically target Glypican 2 (GPC2) are strong therapeutic candidates for pediatric patients with neuroblastoma and other GPC2 expressing cancers. The inventors at the National Cancer Institute (NCI) have developed and isolated two new antibodies that target GPC2 (CT3 and CT5) that are available for licensing and co-development.

The National Cancer Institute (NCI) seeks licensing or co-development for a novel human antibody against tumor necrosis factor receptor type 2 (TNFR2) for cancer immunotherapy.

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.

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 (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.

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 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.'

Researchers at the NCI have developed a method of improving the immune response in cancer immunotherapy by exploiting in the role of the Linker Adapted for T-Cell Signaling (LAT) molecule. The LAT molecular can enhance signaling through TCRs, thus, improving a patient’s own immune response to cancer or infectious diseases.