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.
This technology consists of highly specific rabbit monoclonal antibodies reactive with phosphorylated tyrosine located at amino acid 1235 in the human MET sequence. Binding to this pYl235 residue is independent of the phosphorylation of other tyrosines in the vicinity (1230 and 1234), does not cross-react with these nearby phosphotyrosine residues, and does not occur when Y1235 is unphosphorylated. Researchers at the NCI seek licensing and/or co-development research collaborations to commercialize and develop a companion diagnostic for selective MET 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.
Engineered bacterial spores can provide many useful functions such as the treatment of infections, use as an adjuvant for the delivery of vaccines, and the enzymatic degradation of environmental pollutants. Researchers at the National Cancer Institute’s Laboratory of Molecular Biology have developed a novel, synthetic spore husk-encased lipid bilayer (SSHEL) particle that is uniquely suited for a variety of these functions. NCI seeks partners to license and/or co-develop this technology toward commercialization.
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 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.
Researchers at the National Cancer Institute (NCI) have developed nucleic-acid-based nanoparticle that can be adapted for RNA interference (RNAi), molecular imaging, or a combination thereof. The invention nanoparticles can be used as therapeutics in the treatment of cancer, whichthe NCI seeks parties to license or co-develop.
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.
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.
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.
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.
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.