MetaVia Presents Pre-Clinical Data on DA-1241 Demonstrating Additive Hepatoprotective Effects in Combination With Efruxifermin at the ADA's 85th Scientific Session | MTVA Stock News

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Jun 21, 2025
  • MetaVia's (MTVA, Financial) pre-clinical study shows DA-1241 combined with Efruxifermin achieved a 94% response rate in improving NAFLD activity score.
  • The combination therapy demonstrated significant reductions in inflammatory and fibrotic markers, with some markers showing up to 88% improvement.
  • DA-1241 was weight-neutral, highlighting the potential for a comprehensive MASH treatment strategy independent of weight loss.

MetaVia Inc. (MTVA), a biotechnology company focused on cardiometabolic diseases, has unveiled promising pre-clinical data on its novel G-Protein-Coupled Receptor 119 agonist, DA-1241. Presented at the American Diabetes Association's 85th Scientific Sessions, the study demonstrated that combining DA-1241 with Efruxifermin (EFX), a fibroblast growth factor 21 analogue, results in enhanced hepatoprotective effects when tested in a metabolic dysfunction-associated steatohepatitis (MASH) mouse model.

The 12-week study evidenced that 94% of mice subjected to the combination therapy achieved at least a 2-point improvement in their non-alcoholic fatty liver disease (NAFLD) activity score. Analysis showed notable reductions in inflammatory markers with TNF? decreasing by 58%, CXCL10 by 56%, CCL2 by 77%, and galectin-3 by 87%. Fibrotic markers also saw remarkable reductions, with type 1 collagen ?1 down by 72%, ?-SMA by 59%, and TIMP1 by 88%.

While EFX alone induced a 17% reduction in body weight, DA-1241 maintained a weight-neutral profile, and the combination therapy's effects were independent of weight reduction. The data suggests potential for DA-1241 to be utilized as part of a combination strategy in addressing the complex pathology of MASH, offering therapeutic benefits that extend beyond weight management.

These outcomes underscore the mechanistic synergy between DA-1241 and Efruxifermin, potentially offering a robust approach to targeting multiple disease pathways in MASH through complementary mechanisms of action.

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