Date: 2016-04-16
Type of information: Presentation of results at a congress
phase: preclinical
Announcement: presentation of results at The International Liver Congress 2016 in Barcelona, Spain.
Company: Gilead Sciences (USA - CA)
Product: GS-9674
Action
mechanism: farnesoid X receptor agonist. GS-9674 is a selective, non-steroidal agonist of the Farnesoid X receptor (FXR), a nuclear hormone receptor that is highly expressed in the gastrointestinal tract and liver. FXR is the primary regulator of bile acid synthesis and plays important roles in glucose and lipid metabolism.
Disease: NASH (non-alcoholic steatohepatitis)
Therapeutic area: Liver diseases - Hepatic diseases
Country:
Trial details:
Latest
news: * On April 16, 2016, Gilead Sciences announced data supporting the development of GS-9674 for the treatment of nonalcoholic steatohepatitis (NASH). The data were presented in oral and poster sessions at The International Liver Congress 2016 in Barcelona, Spain. GS-9674 is a selective, non-steroidal agonist of the Farnesoid X receptor (FXR), a nuclear hormone receptor that is highly expressed in the gastrointestinal tract and liver. FXR is the primary regulator of bile acid synthesis and plays important roles in glucose and lipid metabolism. Results from two preclinical studies selected for oral presentation highlight the therapeutic efficacy of GS-9674 in animal models of NASH. In a Gilead-led study, a diet-induced obesity model demonstrated that mice administered GS-9674 had reduced hepatic steatosis and fibrosis, as well as serum levels of cholesterol, ALT and AST compared with untreated animals (Oral PS-066). In a second study, presented by Philipp Schwabl, MD, and led by Michael Trauner, MD, both of the Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria, rats were administered sodium nitrate and fed a choline-deficient, high-fat diet for 10 weeks that resulted in cirrhosis and portal hypertension. Data demonstrate that GS-9674 treatment had dose-dependent anti-fibrotic effects and lowered portal pressure (Oral PS-058). The results of these pre-clinical studies support the evaluation of GS-9674 in patients with NASH following completion of an ongoing Phase 1 study.
