Commentary
In this review, J. L. Fraile et al. (University of Aberdeen, UK) have performed an exhaustive review of the current therapeutic landscape (drug classes, biologics vs small molecules, and target molecules) for NASH.
Regarding lanifibranor, the authors stated, “it’s an oral small molecule that activates all three PPAR isoforms, inducing anti-fibrotic, anti-inflammatory and other beneficial metabolic changes in the body, and delivers these outcomes by decreasing triglyceride levels and increasing high-density lipoprotein cholesterol levels and insulin sensitisation.”
Lanifibranor “is the only pan-PPAR agonist in clinical development for NASH.” The 24-week Phase 2b NATIVE clinical trial “demonstrated that the higher dose used in this study (1200 mg per day) reduced by at least two points the steatosis activity fibrosis (SAF) score (SAF is a measure that combines the degree of hepatocellular inflammation and cellular ballooning) with no worsening of fibrosis (primary endpoint). The study also met secondary endpoints with the same dose, which included resolution of NASH with no worsening of fibrosis and improvement of fibrosis without worsening of NASH.”
