Catalog No. size PriceQuantity
M6565-2 2mg solid $114
M6565-10 10mg solid $452



Product Information:

R-(+)-ETOMOXIR is an irreversible inhibitor of carnitine palmitoyltransferase-1 (CPT-1) on the outer face of the inner mitochondrial membrane. This prevents the formation of acyl carnitines, a step that is necessary for the transport of fatty acyl chains from the cytosol into the intermembrane space of the mitochondria. This step is essential to the production of ATP from fatty acid oxidation. Etomoxir has also been identified as a direct agonist of PPARα.


Chemical Formula: C17H23ClO4


Exact Mass: 326.1285


Molecular Weight: 326.82


Elemental Analysis: C, 62.48; H, 7.09; Cl, 10.85; O, 19.58





B 807-54



B 80754





Chemical Name: 

Ethyl (2R)-2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate


InChi Key: 



InChi Code: InChI=1S/C17H23ClO4/c1-2-20-16(19)17(13-22-17)11-5-3-4-6-12-21-15-9-7-14(18)8-10-15/h7-10H,2-6,11-13H2,1H3/t17-/m1/s1


Smiles Code:




Technical Data:


Appearance: Solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: Soluble in DMSO

Shelf Life: >3 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001


In Vitro

Etomoxir binds irreversibly to the catalytic site of CPT-1 inhibiting its activity, but also upregulates fatty acid oxidation enzymes. Etomoxir is developed as an inhibitor of the mitochondrial carnitine palmitoyltransferase-1 (CPT-1) located on the outer mitochondrial membrane. Etomoxir, in the liver can act as peroxisomal proliferator, increasing DNA synthesis and liver growth. Thus, etomoxir, in addition of being a CPT1 inhibitor could be considered as a PPARalpha agonist. Etomoxir is a member of the oxirane carboxylic acid carnitine palmitoyl transferase I inhibitors and has been suggested as a therapeutic agent for the treatment of heart failure. Acute Etomoxir treatment irreversibly inhibits the activity of carnitine palmitoyltransferase I. As a result, fatty acid import into the mitochondria and β-oxidation is reduced, whereas cytosolic fatty acid accumulates and glucose oxidation is elevated. Prolonged incubation (24 h) with Etomoxir produces diverse effects on the expression of several metabolic enzyme.


In Vivo

Etomoxir is an inhibitor of free fatty acid (FFA) oxidation-related key enzyme CPT1. P53 interacts directly with Bax, which is inhibited by Etomoxir, further confirming the direct interaction of P53 and Bax, and the involvement of FAO-mediated mitochondrial ROS generation in db/db mice. Rats are injected daily with Etomoxir, a specific CPT-I inhibitor, for 8 days at 20 mg/kg of body mass. Etomoxir-treated rats display a 44% reduced cardiac CPT-I activity. The treatment of Lewis rats for 8 days with 20 mg/kg Etomoxir does not alter blood glucose, which is in line with comparable etomoxir-feeding studies. Similarly, Etomoxir feeding does not affect general growth characteristics such as gain in body mass, nor does it affect hindlimb muscle mass. However, heart mass and liver mass are both significantly increased by 11% in Etomoxir-treated rats.





  1. Yao H, Gong J, Peterson AL, Lu X, Zhang P, Dennery PA. Fatty Acid Oxidation Protects Against Hyperoxia-Induced Endothelial Cell Apoptosis and Lung Injury in Neonatal Mice. Am J Respir Cell Mol Biol. 2018 Dec 20. doi: 10.1165/rcmb.2018-0335OC. [Epub ahead of print] PubMed PMID: 30571144.


  1. Zhuang W, Lian G, Huang B, Du A, Gong J, Xiao G, Xu C, Wang H, Xie L. CPT1 regulates the proliferation of pulmonary artery smooth muscle cells through the AMPK-p53-p21 pathway in pulmonary arterial hypertension. Mol Cell Biochem. 2018 Dec 3. doi: 10.1007/s11010-018-3480-z. [Epub ahead of print] PubMed PMID: 30511343.


  1. Xu A, Wang B, Fu J, Qin W, Yu T, Yang Z, Lu Q, Chen J, Chen Y, Wang H. Diet-induced hepatic steatosis activates Ras to promote hepatocarcinogenesis via CPT1α. Cancer Lett. 2019 Feb 1;442:40-52. doi: 10.1016/j.canlet.2018.10.024. Epub 2018 Oct 26. PubMed PMID: 30401637.


Products are for research use only. Not for human use.

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