Potent (IC50 = 1.7 nM ACC1, 2.6 nM ACC2) allosteric protein-protein interaction inhibitor of acetyl-CoA carboxylase (ACC).1 It interacts with the ACC phosphopeptide acceptor and dimerization site to inhibit enzymatic activity resulting in decreased fatty acid synthesis and stimulation of fatty acid oxidation. It reduced hepatic steatosis, improves insulin sensitivity, reduces weight gain, and favorably affects dyslipidemia in rats. Firsocostat decreased hepatic steatosis and fibrosis markers in patients with nonalcoholic fatty liver disease.2 Directly impairs profibrinogenic activity of hepatic stellate cells (HSC) via prevention of induction of glycolysis and oxidative phosphorylation during HSC activation.3
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