Roidipedia.Compound reference & reporting
06 AUG 2026
CompoundsResearch chemical Etomoxir
Research chemicalResearch chemicalMetabolic modulatorCPT-1 inhibitor

Etomoxir

Also known as Etomoxir sodium salt · B 807-27

An irreversible carnitine palmitoyltransferase-1 (CPT-1) inhibitor developed as a metabolic drug for diabetes and heart failure. Clinical development was halted after unacceptable hepatotoxicity. It is now used almost exclusively as a laboratory tool to block fatty-acid oxidation in research.

01 Overview

Etomoxir irreversibly inhibits CPT-1, the enzyme that shuttles long-chain fatty acids into mitochondria, thereby blocking beta-oxidation and forcing reliance on glucose. It was investigated for type 2 diabetes and chronic heart failure on the metabolic-shift rationale shared with perhexiline and trimetazidine.

The ERGO trial in heart failure was terminated early because of hepatotoxicity (elevated transaminases), ending clinical development. Etomoxir persists as a widely used experimental probe of fatty-acid oxidation in immunometabolism and cancer-metabolism research, though even that use is complicated by off-target effects at high concentrations. It has no approved human indication.

02 Mechanism

Irreversibly inhibits carnitine palmitoyltransferase-1 (CPT-1), blocking mitochondrial fatty-acid uptake and beta-oxidation, shifting metabolism toward glucose.

03 Dosing

TierDoseRouteNotes
Historic trial dose80 mg/dayOralDose used in the terminated ERGO heart-failure trial; not a recommendation.

04 Effects

EffectMagnitudeEvidence
Blocks fatty-acid oxidationReliably suppresses beta-oxidation, the basis for its use as a laboratory tool.Preclinical
Metabolic shift to glucose oxidationPreclinically improves cardiac efficiency, but human benefit was never established.Preclinical

05 Side effects

EffectSeverityFrequencyEvidenceCountermeasures
Cardiac hypertrophy (preclinical)Animal studies raised concern for maladaptive cardiac hypertrophy with chronic CPT-1 blockade.ModeratePreclinical signalPreclinical
HepatotoxicityElevated liver transaminases led to early termination of the ERGO trial.SevereTrial-terminatingClinical

07 References

Etomoxir for the treatment of chronic heart failure (ERGO trial)European Journal of Heart Failure, 2007
Etomoxir off-target effects on complex I of the respiratory chainCell Metabolism, 2018

08 Discussion0 comments

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This page is reference information, not medical advice. Doses and protocols are documented as they appear in the clinical literature and in practice — describing them is not a recommendation to use them. Countermeasures listed here are not a substitute for a physician. Legal status varies by jurisdiction and changes.