On April 3, 2018 Reata Pharmaceuticals, Inc. (Nasdaq:RETA) (Reata or Company), a clinical-stage biopharmaceutical company, reported the upcoming presentation of preclinical data for its novel RORγt inverse agonist RTA 1701 at the Annual Meeting of the American Association of Immunologists in Austin, Texas on May 6-7, 2018 (Press release, Reata Pharmaceuticals, APR 3, 2018, View Source;p=RssLanding&cat=news&id=2340738 [SID1234525163]). RTA 1701 is the lead product candidate from Reata’s proprietary series of RORγt inverse agonists for the potential treatment of a broad range of autoimmune, inflammatory, and fibrotic diseases. RTA 1701 is an orally-bioavailable, RORγt-selective, inverse agonist that demonstrates strong efficacy in rodent disease models. RTA 1701 potently suppresses production of IL-17A, a clinically important cytokine, in human immune cells and when dosed orally to non-human primates.
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Reata will present key preclinical data characterizing RTA 1701 in the following sessions:
Dulubova et al., "RTA 1701 is an orally-bioavailable, potent, and selective RORγt inhibitor that suppresses Th17 differentiation in vitro and is efficacious in mouse models of autoimmune disease." May 6, 2:30 pm CT.
Reisman et al., "RTA 1701 is an oral RORγt inhibitor that suppresses the IL-17A response in non-human primates." May 7, 2:30 pm CT.
"Our data with RTA 1701, and especially our primate proof-of-concept experiments, are highly encouraging," said Keith Ward, Ph.D., Reata’s Chief Development Officer. "We believe that a high, unmet need remains for patients with autoimmune and inflammatory disorders, and that RTA 1701 represents a promising small molecule development candidate in these indications." RTA 1701 was discovered by Reata, who holds global rights for the asset.
Reata plans to continue the development of RTA 1701 with a first-in-human study in 2018 that includes evaluation of IL-17A suppression with initial results expected by 1H19.
About RORγt
RORγt is the key transcription factor that orchestrates the differentiation of Th17 cells and drives production of key pro-inflammatory cytokines, including IL-17A. Aberrant IL-17A signaling has been implicated in many diseases, including chronic inflammatory and autoimmune diseases such as rheumatoid arthritis, psoriasis, inflammatory bowel disease, multiple sclerosis, and many others. Therefore, suppression of activity of RORγt via an inverse agonist such as RTA 1701 has the potential for broad activity across multiple therapeutic areas of high, unmet medical need.