Tuberculosis (TB) is an infectious disease that typically affects the lungs. Current therapies include a panel of antibiotics given over a range of 6-9 months. As a result of the expense of treatment, the extended timeframe needed for effective treatment, and the scarcity of medicines in some developing countries, patient compliance with TB treatment is very low and results in multi-drug resistant TB (MDR-TB). There remains a need for a faster, more effective treatment for TB. NCI researchers seek licensing and/or co-development of peptide inhibitors of STAT3 and IL-10 developed to treat bacterial infections such as tuberculosis. See aslo: NIH inventions E-164-2007 and E-167-2010
IFN-gamma and IL-10 are cytokine signaling molecules that play fundamental roles in inflammation, cancer growth and autoimmune diseases. Unfortunately, there are no specific inhibitors of IFN-gamma or IL-10 on the market to date. The National Cancer Institute seeks parties interested in licensing or collaborative research to co-develop selective IL-10 and IFN-gamma peptide inhibitors.
The National Cancer Institute (NCI) seeks licensing and/or co-development research collaborations for a polymeric drug delivery platform that targets scavenger receptor A1 (SR-A1), a receptor highly expressed in macrophages, monocytes, mast cells, dendritic cells (myeloid lineages), and endothelial cells. The platform delivers various immunomodulatory therapeutic cargo including small molecule drugs, therapeutic peptides, and vaccines, to the lymphatic system and myeloid/antigen presenting cell (APC) sub-populations.
This technology provides improved processes for production and purification of nucleic acid-containing compositions, such as non-naturally occurring viruses, for example, recombinant polioviruses that can be employed as oncolytic agents. Some of the improved processes relate to improved processes for producing viral DNA template.
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.