IVEVF - Inventiva announces a late breaker abstract and two additional abstracts on its lead compound lanifibranor at the AASLD The Liver Meeting® 2023 | Benzinga

• The phase II study led by Dr. Kenneth Cusi evaluating lanifibranor in patients with T2D and MASLD was selected as late breaker.
• Two additional scientific abstracts from the NATIVE Phase IIb clinical trial evaluating lanifibranor for the treatment of patients with NASH have been selected  for presentation. The two abstracts show:
  
  • the correlation between the increase of adiponectin under lanifibranor and the improvement of histological and serum markers of NASH severity both in terms of activity and fibrosis.
  • the improvement of liver histology and markers of cardiometabolic health in patients with NASH treated with lanifibranor, independent of PNPLA3 genotype.

Daix (France), Long Island City (New York, United States), November 6, 2023 – Inventiva (NASDAQ:IVA) (the "Company"), a clinical-stage biopharmaceutical company focused on the development of oral small molecule therapies for the treatment of nonalcoholic steatohepatitis (NASH) and other diseases with significant unmet medical needs, today announced that the phase II trial led by Dr. Cusi in patients with type two diabetes (T2D) has been accepted as late breaker, at the upcoming The Liver Meeting® 2023 hosted by the American Association for the Study of Liver Diseases on November 10-14, 2023 in Boston. In addition two other scientific abstracts have been selected for poster presentation.

The late breaker abstract "Lanifibranor reverses insulin resistance and improves glucose and lipid metabolism in patients with type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD)" presents results from a study sponsored by Dr. Cusi at the University of Florida, that evaluates the effect of lanifibranor on insulin resistance in the liver, muscle and adipose tissue, as well as its effect on intrahepatic triglyceride (IHTG) content in patients with T2D and Metabolic dysfunction associated steatotic liver disease (MASLD)¹.

The second abstract evaluates the correlation between adiponectin response with lanifibranor and the improvement of histological and serum markers of NASH severity, both in terms of disease activity and fibrosis. The change in adiponectin levels at end of treatment (categorized as unchanged, moderate or high increase) correlated positively to histological endpoints of NASH resolution and no worsening of fibrosis, improvement of fibrosis and no worsening of NASH, and NASH resolution and fibrosis improvement. The degree of adiponectin level increase correlated also with improvement of the NASH-CRN and SAF-Activity scores as well as with improvement of the individual components: steatosis, inflammation and ballooning. Lanifibranor-associated adiponectin increase also correlated with the improvement in histological fibrosis stage, pro-C3 levels and MACK-3 score. These data further support that adiponectin is a biomarker for the efficacy of lanifibranor treatment across the disease spectrum of NASH, from cardiometabolic health – as previously shown – to hepatic health. As a reminder, a 3.82 and 4.50 fold increase in adiponectin level were respectively reported in the 800mg arm and 1200mg arm during Inventiva's NATIVE Phase IIb clinical trial.

The third abstract evaluates the impact of the PNPLA3 variant I148M, which is strongly associated with risk for and the progression of NASH, on the histological and cardiometabolic response to lanifibranor. In a retrospective analysis of Inventiva's NATIVE Phase IIb clinical trial evaluating lanifibranor for the treatment of patients with NASH, histological and circulating marker responses were evaluated by PNPLA3 genotype subgroup. The response to lanifibranor treatment on the histological endpoints was similar across the three PNPLA3 genotype (II/IM/MM) despite a higher activity score measured at baseline in patients with MM genotype.
In addition, the improvement of cardiometabolic health markers (glycemic control, insulin, HOMA-IR, HsCRP, CAP and adiponectin) following treatment with lanifibranor was similar in the three PNPLA3 genotypes. These results demonstrate that the efficacy of lanifibranor on both liver histology and markers of cardiometabolic health appears to be independent of PNPLA3 status.

The details of the presentation are as follows:

Abstracts:

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