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April 4, 2013 /PRNewswire/ -- NewLink Genetics Corporation (NASDAQ: NLNK) is a biopharmaceutical company focused on discovering, developing and commercializing cancer therapeutics. The company today announced that preclinical data on one of its IDO pathway inhibitors,
NLG919, will be presented at the 2013 Annual Meeting of the American Association for Cancer Research (AACR) to be held
April 6-10 in
Washington, DC. The poster presentation will describe the benefits of targeting the IDO pathway with small molecule immunomodulatory drugs for the treatment of cancer.
NLG919 is in development as a potent IDO pathway inhibitor with desirable pharmacological properties.
(Poster #491): Sunday, April 7, 2013, 1:00 -5:00 PM, " NLG919, a novel indoleamine-2,3-dioxygenase (IDO)-pathway inhibitor drug candidate for cancer therapy," M. Mautino , Immunology 2: Vaccines, Immune Modulatory Agents, and Environment, Hall A-C, Poster Section 22, in The Washington Convention Center.
About inhibition of the IDO pathway
IDO pathway inhibitors are another class of immune check point inhibitors akin to the recently developed antibodies targeting CTLA-4 and PD-1 which represent a potential breakthrough approach to cancer therapy. The IDO pathway regulates immune response by suppressing T-cell function and enabling local tumor immune escape. Recent studies have demonstrated that the IDO pathway is active in many cancers, both within tumor cells as a direct defense against T-cell attack, and also within antigen presenting cells in tumor draining lymph nodes whereby this pathway promotes peripheral tolerance to tumor associated antigens (TAAs). When hijacked by developing cancers in this manner, the IDO pathway may facilitate the survival, growth, invasion and metastasis of malignant cells expressing TAAs that might otherwise be recognized and attacked by the immune system. NewLink has a number of active programs directed at synthesizing IDO pathway inhibitors. These small-molecule, anti-tolerogenic product candidates are intended to counteract this key mechanism by which tumors evade immune-mediated destruction.