Inventiva announces two scientific presentations at the EASL International Liver Congress 2024

• The first abstract demonstrates that the improvements of MACK-3, a diagnostic test for metabolic dysfunction-associated steatohepatitis, parallel the histological response to lanifibranor therapy in patients with MASH/NASH, in the NATIVE Phase IIb clinical trial.
• The second abstract brings additional evidence supporting the role of intrahepatic vascular alterations in the development of MASLD-related portal hypertension and the progression to MASH and highlights the potential of lanifibranor in addressing the different components of MASH disease including vascular alterations.

Daix (France), Long Island City (New York, United States), May 22, 2024 – Inventiva (Euronext Paris and Nasdaq: IVA), a clinical-stage biopharmaceutical company focused on the development of oral small molecule therapies for the treatment of metabolic dysfunction-associated steatohepatitis (“MASH”), also known as non-alcoholic steatohepatitis (“NASH”), and other diseases with significant unmet medical needs, today announced that two scientific abstracts have been selected for poster presentation at the upcoming International Liver Congress 2024 hosted by the European Association for the Study of the Liver (EASL) on June 5-8, 2024 in Milan, Italy.

The first abstract evaluates the correlation of the response of the biomarker algorithm MACK-3 with the improvement of liver histology as well as markers of cardiometabolic health with lanifibranor treatment. MACK-3 is composed of HOMA-IR, AST and CK-18 and has been validated against histology as a diagnostic marker for active MASH/NASH with fibrosis. The authors demonstrated that the decrease in MACK-3 value at the end of a 24 week-treatment period was significantly higher among the patients treated with lanifibranor which were qualified as responders for the histological endpoints of “MASH/NASH resolution and fibrosis improvement”, “Fibrosis improvement without worsening of MASH/NASH” and “MASH/NASH resolution without fibrosis worsening, compared to patients treated with lanifibranor but qualified as non-responders for the endpoints. Similar results were observed for improvement of NAS, SAF, and individual liver lesions: steatosis, lobular inflammation, and ballooning. MACK-3 improvement correlated as well as with increase of adiponectin levels and decrease of Pro-C3, a circulating marker of fibrogenesis, following therapy with lanifibranor. These results warrant additional study to evaluate MACK-3 as a potential marker for the evaluation of a treatment response to lanifibranor.