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(R)-(+)-Etomoxir sodium salt

Cat. No. M9075
(R)-(+)-Etomoxir sodium salt Structure
Synonym:

Etomoxir sodium salt

Size Price Availability
10mg USD 150 4-7 Days
50mg USD 580 4-7 Days
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Quality Control
  • Current batch:
  • Purity >98%
  • COA
  • MSDS
Biological Activity

Etomoxir is a potent inhibitor of carnitine palmitoyltransferase-I (CPT-1). 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. (R)-(+)-Etomoxir sodium salt is R-form of Etomoxir sodium salt. 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. Etomoxir has also been identified as a direct agonist of PPARα.

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Chemical Information
Molecular Weight 320.74
Formula C15H18ClNaO4
CAS Number 828934-41-4
Purity >98%
Solubility Water: ≥ 30 mg/mL warming
Storage at -20°C
References

FFA-ROS-P53-mediated mitochondrial apoptosis contributes to reduction of osteoblastogenesis and bone mass in type 2 diabetes mellitus.
Li J, et al. Sci Rep. 2015 Jul 31;5:12724. PMID: 26226833.

Etomoxir-induced partial carnitine palmitoyltransferase-I (CPT-I) inhibition in vivo does not alter cardiac long-chain fatty acid uptake and oxidation rates.
Luiken JJ, et al. Biochem J. 2009 Apr 15;419(2):447-55. PMID: 19138173.

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