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.
The National Cancer Institute (NCI) and the National Institute of Child Health and Human Development (NICHD) seek research co-development partners and/or licensees for an antiviral treatment that can target SARS-Cov-2 replication in Covid-19 patients.
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.
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.
The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) is seeking parties interested in co-development or licensing a substrate reduction therapy for Smith-Lemli-Opitz Syndrome (SLOS) and other diseases which have a secondary Niemann-Pick type C disease like cellular phenotype.
The Office of the Director, National Cancer Institute is seeking statements of capability or interest from parties interested in collaborative research (using the Cooperative Research and Development Agreement (CRADA) or Material Transfer Agreement (MTA) to further develop, evaluate, or commercialize the software for accurate segmentation of cell nuclei and FISH signals in tissue sections. Collaborators working in the field of quantitative and automated pathology may be interested.
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.
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 National Cancer Institute (NCI) have developed single domain human CD4 proteins to inhibit HIV-1 entry and improved human domain antibodies against HIV-1. Fusion proteins comprising the single domain CD4 and HIV-1 antibody can be used to effectively neutralize HIV-1 in vitro. Researchers seek licensing for development of these antibody-based therapeutics for the treatment of HIV-1.
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 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.
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.
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). 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) 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.