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(R)-(+)-Etomoxir sodium salt

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

Etomoxir sodium salt

Size Price Availability Quantity
5mg USD 70  USD70 In stock
10mg USD 110  USD110 In stock
25mg USD 190  USD190 In stock
50mg USD 340  USD340 In stock
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Quality Control & Documentation
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.

Product Citations
Chemical Information
Molecular Weight 320.74
Formula C15H18ClNaO4
CAS Number 828934-41-4
Form Solid
Solubility (25°C) DMSO 45 mg/mL
Storage -20°C, protect from light, sealed
Conversion of different model animals based on BSA (PMID: 27057123)
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 Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 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 Compound A of 10 mg/kg.

References

[1] Li J, et al. Sci Rep. FFA-ROS-P53-mediated mitochondrial apoptosis contributes to reduction of osteoblastogenesis and bone mass in type 2 diabetes mellitus.

[2] Luiken JJ, et al. Biochem J. Etomoxir-induced partial carnitine palmitoyltransferase-I (CPT-I) inhibition in vivo does not alter cardiac long-chain fatty acid uptake and oxidation rates.

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