Firsocostat | Allosteric acetyl-CoA carboxylase inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $75.00 | ||
| 25 mg | $235.00 |
Firsocostat (1434635-54-7) is a 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
References/Citations:
- Harriman et al. (2016), Acetyl-CoA carboxylase inhibition by ND-630 reduces hepatic steatosis, improves insulin sensitivity, and modulates dyslipidemia in rats; Proc. Nat. Acad. Sci. USA, 113 E1796
- Looma et al. (2018), GS-0976 Reduces Hepatic Steatosis and Fibrosis Markers in Patients With Nonalcoholic Fatty Liver Disease; Gastroenterology, 155 1463
- Bates et al. (2020), Acetyl-CoA carboxylase inhibition disrupts metabolic reprogramming during hepatic stellate cell activation; J. Hepatol., 73 896
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
Firsocostat (1434635-54-7) is a 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
References/Citations:
- Harriman et al. (2016), Acetyl-CoA carboxylase inhibition by ND-630 reduces hepatic steatosis, improves insulin sensitivity, and modulates dyslipidemia in rats; Proc. Nat. Acad. Sci. USA, 113 E1796
- Looma et al. (2018), GS-0976 Reduces Hepatic Steatosis and Fibrosis Markers in Patients With Nonalcoholic Fatty Liver Disease; Gastroenterology, 155 1463
- Bates et al. (2020), Acetyl-CoA carboxylase inhibition disrupts metabolic reprogramming during hepatic stellate cell activation; J. Hepatol., 73 896
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Focus Biomolecules • Plymouth Meeting, PA USA • 1-855-FOCUS21
Focus Biomolecules
Plymouth Meeting, PA USA
1-855-FOCUS21
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