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Triacsin C is a fungal metabolite that acts as a competitive inhibitor of acyl-CoA synthetase, preventing conversion of fatty acids to fatty acyl-CoA. Triacsin C inhibits synthesis of triacylglycerol (TAG), diacylglycerol (DAG), cholesterol esters, and phospholipids. Triacsin C increases NO synthesis and eNOS activity, inducing vasodilatory activity and enhancing relaxation of aortic rings.
| Cas No. | 76896-80-5 |
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| Purity | ≥95% |
| Formula | C11H17N3O |
| Formula Wt. | 207.27 |
| IUPAC Name | N-[(E)-[(2E,4E,7E)-undeca-2,4,7-trienylidene]amino]nitrous amide |
| Melting Point | 102-104°C |
| Appearance | White to off white powder |
| Store Temp | 4°C |
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| Ship Temp | Ambient |
| MSDS | |
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| Info Sheet |
Gauthier MS, Miyoshi H, Souza SC, et al. AMP-activated protein kinase is activated as a consequence of lipolysis in the adipocyte: potential mechanism and physiological relevance. J Biol Chem. 2008 Jun 13;283(24):16514-24. PMID: 18390901.
Weis MT, Crumley JL, Young LH, et al. Inhibiting long chain fatty Acyl CoA synthetase increases basal and agonist-stimulated NO synthesis in endothelium. Cardiovasc Res. 2004 Aug 1;63(2):338-46. PMID: 15249192.
Igal RA, Wang P, Coleman RA. Triacsin C blocks de novo synthesis of glycerolipids and cholesterol esters but not recycling of fatty acid into phospholipid: evidence for functionally separate pools of acyl-CoA. Biochem J. 1997 Jun 1;324 ( Pt 2):529-34. PMID: 9182714.