Target intelligence / Profile preview

Acyl-CoA synthetase medium chain family member 1 (ACSM1)

Target
ACSM1
Molecular classification
Enzyme, Metabolic enzyme (CoA ligase; member of acyl-CoA synthetase superfamily), Mitochondrial protein
01

Overview

Acyl-CoA synthetase medium chain family member 1 (ACSM1) is a mitochondrial enzyme that catalyzes the activation of medium-chain fatty acids and certain carboxylate-containing xenobiotics, such as benzoate, by conjugating them to coenzyme A (CoA) in an ATP- or GTP-dependent reaction[4][5][7]. This process produces acyl-CoA esters, which are essential intermediates for subsequent metabolic pathways, including β-oxidation of fatty acids and detoxification of xenobiotics. ACSM1 also demonstrates in vitro activity with lipoic acid, although it lacks enantiomeric specificity and is not established as a physiological enzyme for lipoate metabolism[2]. The gene is primarily expressed in the mitochondria and plays a critical role in energy production from fatty acids[4][5]. Deficiencies or dysregulation of ACSM1 have been associated with certain cancers and may have broader roles in mitochondrial metabolic disorders, but its direct targeting by drugs or clinical use as a biomarker is not established in current literature[5][7].

Other names
MACS1BUCS1Xenobiotic/medium-chain fatty acid-CoA ligase HXM-BAcyl-coenzyme A synthetase ACSM1, mitochondrialMiddle-chain acyl-CoA synthetase 1Butyryl-coenzyme A synthetase 1Lipoate-activating enzymeBenzoate--CoA ligaseButyrate--CoA ligase 1Butyryl Coenzyme A synthetase 1
02

Mechanism of action

Drugs/substrates interact by providing acyl substrates or modulating fatty acid metabolism; ACSM1 catalyzes the conjugation of CoA to fatty acids/xenobiotics, enabling their metabolic breakdown or utilization. The physiologic activation of lipoate is controversial and not established as a drug mechanism.

03

Biological functions

Fatty acid activation (medium-chain fatty acids: e.g. C4–C10)Cellular metabolism (initiation of fatty acid β-oxidation)Activation of carboxylate-containing xenobiotics (such as benzoate)Lipoate activation (to form lipoyl-nucleoside monophosphate; though physiological relevance of this is debated)
04

Disease associations

Cancer (e.g. breast apocrine carcinoma)Metabolic disorders (potential role suggested in disorders of mitochondrial fatty acid oxidation)Other roles (possible involvement in diseases linked to mitochondrial metabolism; not strongly linked to inflammation or neurodegeneration in current consensus)
05

Safety considerations

As an endogenous metabolic enzyme, inhibition could theoretically impair fatty acid oxidation, but no therapeutic agents directly target ACSM1, so safety concerns are not established.Loss of function may contribute to mitochondrial dysfunction but is not associated with known adverse drug reactions.
06

Biomarkers

ACSM1 expression may be used as a metabolic biomarker (e.g. in cancer metabolism studies or mitochondrial disease research)No clinically established biomarkers associated with ACSM1 for patient selection or efficacy monitoring exist.

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