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Acyl-CoA synthetase medium-chain family member 2B (ACSM2B) is a mitochondrial enzyme highly expressed in human liver, catalyzing the activation of medium-chain fatty acids and various xenobiotic carboxylic acids (such as benzoate and salicylate) into their respective acyl-CoA derivatives[1][5][7]. This activation is the first and essential step in mitochondrial β-oxidation and in the glycine conjugation pathway, a detoxification function critical for homeostasis of coenzyme A and glycine[1][3][7]. ACSM2B plays a major role at the intersection of energy metabolism and detoxification of dietary and drug-derived compounds. Genetic variation or altered expression of ACSM2B influences susceptibility to metabolic syndromes, drug responses (notably to nonsteroidal anti-inflammatory drugs), and may serve as a marker for metabolic and hepatocellular disease processes[1][4][6].
Drugs are conjugated to CoA by ACSM2B, forming acyl-CoA derivatives to facilitate β-oxidation or detoxification (e.g., enabling glycine conjugation for urinary excretion)[1][5]
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