Triacsin C
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Triacsin C is an inhibitor of long fatty acyl CoA synthetase that has been isolated from Streptomyces aureofaciens.[1][2][3] It blocks β-cell apoptosis, induced by fatty acids (lipoapoptosis) in a rat model of obesity. In addition, it blocks the de novo synthesis of triglycerides, diglycerides, and cholesterol esters, thus interfering with lipid metabolism.[4]
In addition, triacsin C is a vasodilator.[1]
Inhibition of lipid metabolism reduces/removes lipid droplets from HuH7 cells.[5] In hepatitis C–infected HuH7 cells, this reduction/removal of lipid droplets by triacsin C correlates with a reduction in virion assembly and infectivity.[6]
General chemical description
Triacsin C belongs to a family of bacterial secondary metabolites all having an 11-carbon chain with a common N-hydroxytriazene moiety at the terminus. Due to the N-hydroxytriazene group, triacsin C has acidic properties and may be considered a polyunsaturated fatty acid analog. Script error: No such module "Unsubst".
Triacsin C was discovered by a group led by Keizo Yoshida in 1982 from a culture of the actinobacteria now known as Kitasatospora aureofaciens.[1]