Target intelligence / Profile preview

Acyl-Coenzyme A thioesterase 11 (ACOT11)

Target
ACOT11
Molecular classification
Enzyme, Acyl-CoA thioesterase, StAR-related lipid transfer (START) domain-containing protein
01

Overview

Acyl-Coenzyme A thioesterase 11 (ACOT11) is an enzyme encoded by the ACOT11 gene, primarily responsible for hydrolyzing medium- and long-chain fatty acyl-CoA esters into free fatty acids and coenzyme A. This activity regulates intracellular fatty acid and CoA pools, impacting lipid metabolism, energy expenditure, and membrane synthesis. ACOT11 contains a steroidogenic acute regulatory (StAR)-related lipid transfer (START) domain, allowing lipid sensing and transfer, and is particularly active in brown adipose tissue where it modulates fatty acid oxidation and lipid storage in response to cold exposure. Altered ACOT11 activity is implicated in metabolic diseases, cancer proliferation, and liver steatosis. The enzyme forms homodimers or higher order oligomers and is subject to regulation by post-translational modifications and lipid binding within its START domain. Alternative splicing creates distinct isoforms with tissue and functional specificity. There are no approved drugs targeting ACOT11, nor validated clinical biomarkers for its function.

Other names
STARD14BFITBFIT1KIAA0707THEATHEM1Acyl-CoA thioester hydrolase 11Adipose-associated thioesteraseBrown fat-inducible thioesterasePalmitoyl-coenzyme A thioesteraseStAR-related lipid transfer (START) domain-containing 14Thioesterase superfamily member 1
02

Mechanism of action

Enzymes hydrolyze long-chain fatty acyl-CoAs to free fatty acids and CoA, regulating intracellular fatty acid levels and supporting lipid storage or β-oxidation suppression. Drugs (or small molecules if validated in the future) would act as inhibitors or activators altering this enzymatic activity but none are documented in clinical use.

03

Biological functions

Hydrolysis of fatty acyl-CoA (especially medium- and long-chain fatty acyl-CoA)Lipid metabolism and energy homeostasis (regulation of acyl-CoA levels)Regulation of lipid droplet expansion, fatty acid re-esterification, and membrane synthesisModulation of energy expenditure, particularly in brown adipose tissue (BAT)
04

Disease associations

Obesity/metabolic dysfunctionCancer (supports cell proliferation via FA supply)Multiple acyl-CoA dehydrogenase deficiencyLeukoencephalopathy with vanishing white matterHepatic steatosis/metabolic dysfunction-associated steatotic liver disease (MASLD)
05

Safety considerations

There are no direct safety concerns listed for targeting ACOT11, but potential therapeutic challenges could include metabolic perturbations due to altered lipid metabolism, risk of fatty liver disease, or effects on energy expenditure
06

Interacting drugs

No direct drugs described as interacting with ACOT11 in the provided sources; current literature suggests a role in metabolism which may be indirectly influenced by drugs affecting lipid homeostasis, but no approved drugs specifically target ACOT11
07

Biomarkers

No clinically validated biomarkers for patient selection or efficacy monitoring are listed in current sources for ACOT11. Changes in expression (e.g., in brown fat or liver) may associate with metabolic disease risk, but are not established as primary biomarkers.

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