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Our lead drug candidate, denifanstat, is an oral, once-daily pill and selective FASN inhibitor in development for the treatment of metabolic dysfunction-associated steatohepatitis (MASH), acne and select forms of cancer.
Our second FASN inhibitor, TVB-3567, is a potent and selective small molecule FASN inhibitor in development for acne.
FASN inhibition for the treatment of MASH The critical role of FASN overactivity in MASH makes it an attractive target for drug therapy.
Our FASN inhibitor, denifanstat, targets multiple drivers of MASH by reducing steatosis, inflammation and fibrosis.
MASH: A growing epidemic MASH is an aggressive form of metabolic dysfunction-associated steatotic liver disease (MASLD), 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, MASH is a growing epidemic that affected more than 265 million people worldwide in 2019.
There are few approved treatments for non-cirrhotic MASH (stages F1, F2 and F3 fibrosis) and no approved treatments for cirrhotic MASH (F4).
We believe FASN inhibition may offer a meaningful therapeutic solution for this unmet need.
The therapeutic potential of our FASN inhibitor, denifanstat, stems from its differentiated mechanism of action directly targeting the three key drivers of MASH pathogenesis: steatosis, inflammation, and fibrosis.
Phase 2b FASCINATE-2 clinical trial of denifanstat in MASH Denifanstat met all primary and multiple secondary endpoints in the Phase 2b FASCINATE-2 clinical trial evaluating denifanstat in 168 biopsy-confirmed MASH patients with stage F2 or F3 fibrosis compared to placebo at week 52.
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Explanatory Note Reflecting the change in disease nomenclature from non-alcoholic fatty liver disease (NAFLD) to metabolic dysfunction-associated steatotic liver disease (MASLD) and from nonalcoholic steatohepatitis (NASH) to metabolic dysfunction-associated steatohepatitis (MASH), we are using MASLD and MASH throughout this document other than when referring to titles of publications or other activities that utilized the term NAFLD or NASH.
Our lead drug candidate, denifanstat, is an oral, once-daily pill and selective FASN inhibitor in development for the treatment of metabolic dysfunction-associated steatohepatitis (MASH), formerly known as nonalcoholic steatohepatitis (NASH).
Denifanstat has been studied in over 740 people to date in our clinical trials, including our Phase 2 FASCINATE-1 and Phase 2b FASCINATE-2 clinical trials.
In January 2024, we announced positive topline results from the Phase 2b FASCINATE-2 clinical trial evaluating denifanstat in 168 biopsy-confirmed MASH patients with stage F2 or F3 fibrosis compared to placebo at week 52.
The Phase 2b FASCINATE-2 clinical trial achieved statistically significant results on primary and multiple secondary endpoints at week 52 in MASH patients in the modified intention to treat (mITT) population, including: The primary endpoints of 2-point reduction in NAS (NAFLD Activity Score) without worsening of fibrosis (denifanstat 52% vs.
placebo 20%, p=0.0003), and MASH resolution without worsening of fibrosis with 2-point reduction in NAS (denifanstat 36% vs.
Multiple secondary endpoints of fibrosis improvement by 1 stage with no worsening of MASH (denifanstat 41% vs.
placebo 18%, p=0.0102), MASH resolution with no worsening of fibrosis (denifanstat 38% vs.
placebo 16%, p=0.0043), and a greater proportion of MRI-derived proton density fat fraction (MRI-PDFF) 30% responders relative to placebo (denifanstat 65% vs.
Denifanstat showed also statistical significance in fibrosis improvement as measured by an artificial intelligence (AI) digital pathology-based qFibrosis assessment.