Target intelligence / Profile preview

Elongation of very long chain fatty acids protein 7 (ELOVL7)

Target
ELOVL7
Molecular classification
Enzyme, Transferase (acyl transferase/3-keto acyl-CoA synthase), Endoplasmic-reticulum membrane protein
01

Overview

Elongation of very long chain fatty acids protein 7 (ELOVL7) is an integral membrane enzyme, localized to the endoplasmic reticulum, that catalyzes the first and rate-limiting condensation step in the elongation cycle of long and very long chain fatty acids (VLCFAs) by adding two carbons per round, especially favoring C18 acyl-CoA substrates[1][2][3][4][5]. ELOVL7 forms an essential part of the biosynthetic machinery for ceramides, sphingolipids, and other complex lipids vital for diverse cellular functions such as membrane integrity, signaling, and nerve myelination[2][4]. Dysfunction or mutation leads to several human diseases, including hereditary neurodegenerative disorders and metabolic syndromes, and the enzyme has been implicated in carcinogenesis and other pathologies where VLCFA dysregulation is a risk factor[2][4]. Although no approved targeted therapeutics exist, structural studies support the feasibility of selective inhibition, and ELOVL7 is considered a promising drug target in conditions involving toxic VLCFA accumulation[2][4].

Other names
Very long chain fatty acid elongase 7ELOVL FA elongase 7FLJ235633-keto acyl-CoA synthase ELOVL7Very long chain 3-ketoacyl-CoA synthase 7Very long chain 3-oxoacyl-CoA synthase 7ELOVL family member 7
02

Mechanism of action

Inhibition or modulation of ELOVL7 may reduce synthesis of very long chain fatty acids and their incorporation into complex lipids; candidate inhibitors would act by blocking the first, rate-limiting condensation reaction of fatty acid elongation[2][4].

03

Biological functions

Fatty acid elongationVery long chain fatty acid biosynthetic processLipid metabolismSynthesis of membrane lipids and lipid mediators
04

Disease associations

Cancer (including prostate and gynecological cancer)Spinocerebellar ataxia (types 38 and 34)Parkinson’s disease (early-onset forms)Metabolic diseases (e.g., insulin resistance, hepatic steatosis)X-linked adrenoleukodystrophy (via VLCFA accumulation)
05

Safety considerations

Potential consequences of modulating ELOVL7 include impaired synthesis of essential membrane lipids, possible neurotoxicity, or peripheral organ dysfunction due to altered lipid composition.
06

Interacting drugs

No approved drugs listed as direct ELOVL7 modulators; chemical matter and tool compounds with potential binding have been identified, but are not currently sufficient for cellular or functional studies[4].
07

Biomarkers

Very long chain fatty acid levels (especially C26:0 and related species) in plasma or tissues can serve as biomarkers for disorders stemming from ELOVL7 dysfunction or inhibition[4].

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