Target intelligence / Profile preview

Acyl-CoA synthetase medium-chain family member 2B (ACSM2B)

Target
ACSM2B
Molecular classification
Enzyme, Ligase (specifically acyl-CoA synthetase), Mitochondrial protein
01

Overview

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].

Other names
Acyl-coenzyme A synthetase ACSM2B, mitochondrialACSM2BACSM2HYST1046HXMAAcyl-CoA synthetase medium-chain family member 2Middle-chain acyl-CoA synthetase 2BXenobiotic/medium-chain fatty acid-CoA ligase HXM-ABenzoate–CoA ligaseButyrate–CoA ligase 2BButyryl-coenzyme A synthetase 2B
02

Mechanism of action

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]

03

Biological functions

Fatty acid activation (medium-chain)Xenobiotic carboxylic acid conjugationMitochondrial β-oxidationGlycine conjugation pathway (detoxification)Energy metabolism
04

Disease associations

Metabolic disorders (including metabolic syndrome and insulin resistance traits)Drug-induced toxicity (including altered NSAID response)Hepatocellular carcinoma (differential regulation in cancer context)[6]Obesity-related traits[3]
05

Safety considerations

Genetic polymorphisms or altered expression may predispose to metabolic dysfunction or increased sensitivity to drug toxicity (especially with xenobiotic carboxylic acids, such as NSAIDs)[1][4]
06

Interacting drugs

Benzoic acid/benzoate

1 more in the full profile.

07

Biomarkers

Potential biomarker for hepatic metabolic activityVariants/MRNA expression as biomarkers for susceptibility to metabolic disorders or drug-induced toxicity; differential expression in liver and kidney disease states[1][2][4]

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