The National Cancer Institute (NCI) seeks research co-development partners or licensees for antisense oligonucleotides that reduce cancer cell migration and invasion. These are expected to be therapeutic against metastatic cancer.
Researchers at the NCI have developed immunologically active peptides of NGEP that activate cytotoxic lymphocytes to effectively kill prostate cancer cells. These peptides can be applied to multiple immunotherapy strategies to treat and prevent prostate cancer.
Novel thalidomide analogs and their use as immunomodulatory agents are disclosed in this invention by scientists at the National Institute on Aging (NIA). These therapeutic compounds could reduce chronic systemic and central nervous system inflammation. The NIA seeks licensing or co-development partners to commercialize this technology.
The National Cancer Institute's Laboratory of Experimental Immunology, Cancer Inflammation Program, seeks parties interested in collaborative research to co-develop, evaluate, or commercialize the use of certain cucurbatacins or withanolides in combination with pro-apoptotic agonists of TRAIL death receptors for cancer therapy.
A considerable effort has been devoted to identifying and targeting specific extracellular cancer markers using antibody based therapies. However, diminished access to new cancer cell surface markers has limited the development of corresponding antibodies. NCI Technology Transfer Center is seeking to license cancer immunotherapy using virus-like particles.
The National Eye Institute (NEI) seek research co-development or licensees for advancing AAV8/9-based therapies for X-linked forms of retinitis pigmentosa (XLRP) caused by mutations in RPGR (retinitis pigmentosa GTPase regulator) or RP2 (retinitis pigmentosa 2) gene.
There is a need to develop compounds that can sensitize cancer cells to apoptosis inducing ligands, such as poly I:C and TRAIL. In collaboration with the University of Arizona, NCI investigators discovered a series of compounds in the withanolide family that synergistically enhance the response of cancer cells to treatment with an apoptosis-inducing ligand. The NCI seeks licensing and/or co-development research collaborations for development of withanolide E analogues 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.'
A library of novel compounds that selectively bind the dopamine D3 receptor have been designed and characterized extensively. In vivo rodent studies indicate selected lead molecules may be useful to treat drug addiction/dependence.
There is a marked increase in immunosuppressive myeloid progenitors and myeloid cells in tumors and at metastatic tissue sites, rendering these types of cells useful in cancer therapeutics, especially after genetic modifications that improve their anti-tumor properties further. The National Cancer Institute (NCI) seeks research co-development or licensing partners to further develop genetically engineered myeloid cells (GEMys) for use in cancer immunotherapy.
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 NCI have developed a vaccine technology that stimulates the immune system to selectively destroy metastasizing cells. Stimulation of T cells with the Brachyury peptide promote a robust immune response and lead to targeted lysis of invasive tumor cells. NCI seeks licensing or co-development of this invention.
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 an invention describing compounds that bind and alter the nuclear copy number of a long non-coding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), with the proposed consequence of inducing slower tumor growth and a reduction in metastasis. The NCI seeks licensing and/or co-development research collaborations for novel small molecule antagonists targeting MALAT1 lncRNA as anticancer agents.
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 (NCI) Vaccine Branch, seeks research co-development or licenses for a novel method of improving HIV vaccine efficacy by activating Ras signaling. Upregulating the Ras pathway can improve an HIV patient’s immune response to anti-retroviral vaccines.
The Section on Translational Neuroscience of NICHD seeks parties interested in licensing and/or collaborative research to co-develop this therapeutic management of Menkes Disease and related copper transport disorders.