HMGCS1

Additional Preclinical Data on Denifanstat Published in Scientific Reports SAN MATEO, Calif.--(BUSINESS WIRE)--Sagimet Biosciences, a clinical-stage biopharmaceutical company developing novel therapeutics targeting dysfunctional metabolic pathways, announced today that it will present three abstracts at The Liver Meeting of the American Association for the Study of Liver Diseases (AASLD), taking place November 4-8, 2022, in Washington, DC. The presentations are focused on identifying non-invasive tests correlated with AI-based digital pathology to ultimately minimize unnecessary biopsies and serum profiling that reveals metabolic benefits of denifanstat, the company’s lead product candidate, in non-alcoholic steatohepatitis (NASH) patients. Additional Phase 2 biomarker data aimed at better identifying potential patient responders will also be presented. “Selecting patients for Phase 2b/3 NASH clinical trials currently requires liver biopsy, an invasive and costly procedure that is subject to variability that can result in a high rate of screen failures,” said Stephen Harrison, MD, visiting professor, University of Oxford, founder and chairman of Pinnacle Clinical Research. “Using AI-based digital pathology from the FASCINATE-2 study, we have identified readily available non-invasive tests that could help reduce the number of patients having unnecessary liver biopsies.” Separately, Sagimet announced the publication of preclinical data, “FASN Inhibition Targets Multiple Drivers of NASH by Reducing Steatosis, Inflammation and Fibrosis in Preclinical Models,” in the September 19, 2022, edition of Scientific Reports, an online peer-reviewed open access scientific journal published by Nature. Details for AASLD presentations are: ORAL PRESENTATION Abstract Title: "Correlation Between AI-based Digital Pathology and Non-invasive Tests (NITS) of NASH Fibrosis Stage: Baseline Data from the FASCINATE-2 Phase 2b Clinical Study of Denifanstat in Patients with F2/F3 NASH” Abstract Number: 99 Presenting Author: Stephen Harrison, MD, FAASLD, University of Oxford, Pinnacle Research Center Session Title: NASH Therapeutics and OMICs Date and Time: Sunday, November 6, 2022, 2:00-3:30 PM EST Presentation Time: 3:00 PM EST Location: Room 146, Walter E. Washington Convention Center LATE-BREAKING POSTER PRESENTATION Abstract Title: “Serum Proteomic Profiling Reveals that the Fatty Acid Synthase (FASN) Inhibitor Denifanstat Provides Metabolic Benefits via Increasing Fibroblast Growth Factor 19 (FGF-19) and Decreasing 3-Hydroxy-3-Methylglutaryl-COA Synthase 1 (HMGCS1) in NASH Patients” Abstract Number: 38967 Presenting Author: Wen-Wei Tsai, PhD, Director, R&D, Sagimet Biosciences Date and Time: Monday, November 7, 2022, 1:00 PM – 2:00 PM EST Location: Poster Hall, Walter E. Washington Convention Center POSTER PRESENTATION Abstract Title: “A Baseline Metabolomic Signature Predicts Liver Fat Response to Denifanstat (DFS), A First-in-class Fatty Acid Synthase (FASN) Inhibitor: Analysis in FASCINATE-1 and FASCINATE-2 Clinical Studies” Abstract Number: 2370 Presenting Author: Rohit Loomba, MD, FAASLD, University of California, San Diego, NAFLD Research Center, Division of Gastroenterology and Epidemiology Date and Time: Saturday, November 5, 2022, 1:00-2:00 PM EST Location: Poster Hall, Walter E. Washington Convention Center Denifanstat is an oral, once daily, selective, fatty acid synthase (FASN) inhibitor that directly targets three key NASH drivers by blocking accumulation of excess liver fat, reducing inflammation and blunting fibrosis. Sagimet recently completed patient enrollment of its FASCINATE-2 Phase 2b liver biopsy-based clinical trial with denifanstat in NASH patients and expects to report interim data in the fourth quarter of 2022. About Sagimet Biosciences Sagimet is a clinical-stage biopharmaceutical company developing novel therapeutics targeting dysfunctional metabolic pathways in diseases such as nonalcoholic steatohepatitis, certain cancers and acne. Sagimet compounds are designed to inhibit FASN, an enzyme involved in the production of fatty acids normally used for energy storage. In NASH, the activity of FASN enzyme is upregulated, resulting in excess accumulation of liver fat, inflammation, and fibrosis. FASN dysregulation has also been implicated in multiple cancers with lipogenic phenotypes.