SAN MATEO, Calif.--(BUSINESS WIRE)--#Clinicaltrials--Sagimet Biosciences, a clinical-stage biopharmaceutical company developing novel therapeutics targeting dysfunctional metabolic pathways, announced today that it will present additional Phase 2a data highlighting improved lipid composition and potential cardiovascular benefits of denifanstat in nonalcoholic steatohepatitis (NASH) patients. Denifanstat (formerly TVB-2640), the company’s lead product candidate, is an oral, selective, first-in-class fatty acid synthase (FASN) inhibitor. Data will be presented at the Keystone Symposia: Inter Organ Crosstalk in NASH, held August 7-10, 2022 in Whistler, British Columbia.
Presentation and poster details are as follows:
Title: Fatty Acid Synthase (FASN) Inhibitor, Denifanstat (TVB-2640), Changes Circulating Lipid Composition in NASH Patients
Presenter: Wen-Wei Tsai, Director, R&D, Sagimet Biosciences
Session/Track: NASH Therapeutics
Date and time: Poster session August 9, 7:30 pm PT; oral presentation August 10, 8 am PT, 2022.
Denifanstat’s unique mechanism of action directly targets the primary drivers of NASH by reducing excess liver fat (steatosis), decreasing inflammation and blunting fibrosis. Denifanstat is currently being evaluated in a Phase 2b liver biopsy-based clinical trial (“FASCINATE-2”) in NASH patients with moderate-to-severe fibrosis (Stage F2 or F3). Interim data are expected by the end of 2022, with paired-biopsy data expected in 2023. Additional information about FASCINATE-2 [NCT04906421] can be found at clinicaltrials.gov. Denifanstat is also being tested in a Phase 3 clinical trial for recurrent glioblastoma and a Phase 2 clinical trial for moderate to severe acne, both in China under exclusive license by Ascletis.
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 fatty acid synthase (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.