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 (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 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''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.
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.
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.
Adoptive T Cell Therapy (ACT) has proven to effectively treat established tumors. This treatment consists of harvesting Tumor Infiltrated Lymphocytes (TIL) which specifically recognize cancer, expanding the tumor-specific TIL in vitro, and then reinfusing these cells into the patient for treatment. Both these lymphocytes and their T cell receptors (TCR) are valuable for cancer immunotherapy. Inventors from the National Cancer Institute (NCI) have developed an improved method to identify tumor-specific TCRs by reprogramming TIL into stem cells. This invention is available to license further development.
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.
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.