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We are a clinical-stage biopharmaceutical company developing novel therapeutics called fatty acid synthase (FASN) inhibitors that target dysfunctional metabolic pathways in diseases resulting from the overproduction of the fatty acid, palmitate. Our lead drug candidate, denifanstat, is an oral, once-daily pill and selective FASN inhibitor in development for the treatment of nonalcoholic steatohepatitis (NASH), for which there are no treatments currently approved in the United States or Europe. Denifanstat has been studied in over 600 people to date and we are currently testing it in our FASCINATE-2 Phase 2b trial in NASH. The interim results, which were presented at the American Association for the Study of Liver Diseases (AASLD) meeting in November 2022, showed statistically significant improvements across key markers of disease in patients treated with denifanstat, including an approximately 34% reduction in liver fat and 67% responder rate (defined as reduction in liver fat by 30% or more) at 26 weeks as compared to baseline. These interim results are consistent with earlier findings from our FASCINATE-1 Phase 2 trial, which achieved its primary endpoint (relative change from baseline in liver fat at 12 weeks) and key secondary endpoint (percentage of subjects with at least a 30% reduction in liver fat at 12 weeks) at the once-daily 50mg dose. Improvements in liver fat were also observed at the 25mg dose (not statistically significant) and at the 75mg dose (not placebo controlled). Together, these results strengthen our belief that the topline liver biopsy results we expect to announce in the first quarter of 2024 will directly show improvement in disease. However, interim clinical trial results may not be indicative of future results. Additionally, our precision medicine approach is core to our development strategy in NASH, and includes the application of pharmacodynamic and predictive biomarkers to confirm target engagement and clinical response in patients treated with denifanstat. We are also evaluating the promise of FASN inhibition, beyond NASH, in additional disease areas in which dysregulation of fatty acid metabolism also plays a key role, including in acne and certain forms of cancer. We believe that denifanstat is differentiated among treatments in development for NASH: • Integral role of FASN in three key drivers of NASH. FASN is a key enzyme in de novo lipogenesis (DNL), the biochemical pathway responsible for production of palmitate resulting in excess liver fat buildup in NASH It is also directly involved in inflammation and fibrosis. • Comprehensive improvements across biomarkers. Our clinical trial data to date have shown that denifanstat at the 50mg once daily dose level improves non- invasive biomarkers of NASH across liver fat, inflammation, and fibrosis— three major drivers of disease—and biomarkers of cardiometabolic health. • Rigorous development strategy. Our denifanstat program began with in-house discovery of a proprietary portfolio of FASN inhibitors, followed by a comprehensive demonstration of activity in preclinical models, FASN inhibition in human clinical trials and improvement of critical biomarkers of NASH and has been generally well tolerated in the FASCINATE-1 trial at 25mg and 50mg dose levels once daily. We are currently focused on evaluating efficacy in the FASCINATE-2 Phase 2b clinical trial of biopsy-confirmed NASH patients. Introduction to NASH NASH is an aggressive form of nonalcoholic fatty liver disease (NAFLD), a condition where an abnormal buildup of excess fat (known as steatosis) occurs in the liver unrelated to the consumption of alcohol. According to a study published in 2023, NASH is a growing epidemic that affected more than 265 million people worldwide in 2019 and for which there are currently no approved treatments in the United States or Europe. It is often associated with insulin resistance, type 2 diabetes, cardiovascular disease, and an increase in overall mortality. Left untreated, damage to the liver can lead to cirrhosis or liver cancer, potentially making liver transplantation necessary. Our lead drug candidate—denifanstat Denifanstat, formerly known as TVB-2640, an oral, once-daily pill, is our selective FASN inhibitor currently being developed for the treatment of NASH. Denifanstat was selected from our library of over 1,200 internally-discovered and wholly owned FASN inhibitors that were identified through a rigorous medicinal chemistry and preclinical development effort. Denifanstat was advanced into clinical development based on its convenient oral administration, high selectivity for FASN, and excellent pharmacokinetic and pharmaceutical properties, including restricted penetration of the blood-brain barrier. Following a robust translational research program that demonstrated FASN inhibition reduced liver fat and decreased inflammation and fibrosis in multiple preclinical models, as well as a proof-of-mechanism clinical trial that demonstrated denifanstat’s ability to inhibit hepatic DNL in humans, we embarked on two Phase 2 clinical trials in patients with NASH: FASCINATE-1 and FASCINATE-2. Across indications, denifanstat has been studied in over 600 people to date. The FASCINATE-1 trial examined multiple doses of denifanstat, ranging from 25mg to 75mg daily, administered for 12 weeks compared to placebo in 142 patients in the United States and China. Denifanstat caused a rapid and robust reduction in liver fat that was statistically significant in the 50mg cohort, as well as improvements in inflammatory, fibrotic and cardiometabolic components of the disease. Denifanstat at dose levels of 25mg or 50mg once daily was generally well tolerated in these diverse populations. Based on the totality of the data, we selected the 50mg dose for further study. The FASCINATE-2 trial has enrolled 168 subjects with biopsy confirmed NASH with moderate to advanced fibrosis (F2-F3) at baseline. These patients are being dosed with 50mg of denifanstat or placebo for one year. In November 2022, we announced results from a planned interim analysis of non-invasive tests (NITs) from a subset of patients and tolerability as of the data cut-off date of the interim analysis. At the end of dosing, a follow-up biopsy will be taken to evaluate the direct impact of the drug on disease at week 52. Topline liver biopsy results are expected in the first quarter of 2024. Recently, we presented interim analysis results from NITs, also known as biomarkers, from 52 of the earliest patients enrolled in the FASCINATE-2 trial after they completed 26 weeks of dosing. These interim results were consistent with the conclusions of the FASCINATE-1 trial in this more advanced population of NASH patients. In this interim cohort, 67% of patients treated with denifanstat reduced their liver fat by 30% or more, and 45% of these responders reduced their liver fat by 50% or more. Third-party studies have shown that NASH patients qualifying as responders are much more likely to have improved liver histology than patients who do not achieve this goal. Denifanstat also showed a statistically significant decrease of 16.5 U/L (p<0.05), or a 25% decrease, in levels of ALT, which is a marker of hepatic inflammation and damage, and a statistically significant decrease of 0.34 (p<0.05) in enhanced liver fibrosis (ELF) score (Figure A). Decreases in ELF score suggest reduced levels of fibrosis. In addition to decreases in LDL-cholesterol, these improvements across biomarkers of liver fat, inflammation and fibrosis are consistent with those seen in the earlier FASCINATE-1 trial. --- Results from FASCINATE-1 and -2 will enable us to design the pivotal Phase 3 program for denifanstat in NASH. In March 2021, we received fast track designation for denifanstat for the treatment of NASH. This allows us to work expeditiously with the U.S. Food and Drug Administration (FDA) to align on the design of this program. NASH remains an under-diagnosed and under-served disease, often due to lack of access to sophisticated or specialized equipment. Our precision medicine approach is central to our development strategy for denifanstat in NASH. This includes the development of blood-based pharmacodynamic drug response biomarkers, such as tripalmitin, to confirm FASN inhibition and pathway engagement by denifanstat. We are also developing blood-based predictive biomarker tests using metabolomics and single nucleotide polymorphisms (SNPs) to more easily identify patients at risk and likely to benefit from treatment. We will continue to validate these tests with the biomarker and liver biopsy results from the ongoing FASCINATE-2 clinical trial and anticipate developing complementary diagnostic tools to benefit patients, clinicians and payors. We were incorporated in Delaware in December 2006 under the name 3-V Biosciences, Inc., and changed our name to Sagimet Biosciences Inc. in August 2019. Our principal executive offices are located at 155 Bovet Road, Suite 303, San Mateo, California.
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