Etomoxir inhibits free fatty acid (FFA) oxidation by targeting the key enzyme CPT1. This inhibition is linked to the suppression of the direct interaction between P53 and Bax, as well as FAO-mediated mitochondrial ROS generation, as demonstrated in studies involving db/db mice^[3].

In experimental studies, rats injected with 20 mg/kg of Etomoxir daily for 8 days show a 44% decrease in cardiac CPT-I activity. This regimen does not affect blood glucose levels or general growth such as body mass or muscle mass in the hindlimbs, aligning with similar findings from other Etomoxir studies. Notably, Etomoxir treatment significantly increases both heart and liver mass by 11% in treated rats^[4].

Etomoxir irreversibly binds to the catalytic site of carnitine palmitoyltransferase-1 (CPT-1) on the outer mitochondrial membrane, inhibiting its activity and reducing fatty acid transport into mitochondria. Besides acting as a CPT-1 inhibitor, Etomoxir also functions as a peroxisomal proliferator in the liver, promoting DNA synthesis and liver growth, which suggests it might also act as a PPARalpha agonist^[1].

As a member of the oxirane carboxylic acid group, Etomoxir is recognized for its potential as a therapeutic for heart failure. Acute treatment with Etomoxir irreversibly inhibits CPT-1, leading to reduced mitochondrial fatty acid β-oxidation, accumulation of cytosolic fatty acids, and enhanced glucose oxidation. Extended exposure (24 hours) to Etomoxir affects the expression of various metabolic enzymes, indicating diverse metabolic impacts^[2].