Etomoxir sodium salt

Etomoxir sodium salt ((R)-Etomoxir sodium salt) 是一种肉碱棕榈酰转移酶 1a (CPT-1a) 抑制剂,通过抑制 CPT-1a 可抑制脂肪酸氧化,并抑制人、大鼠和豚鼠中棕榈酸酯的氧化。

CAS号

828934-41-4

分子式

C15H18ClO4.Na

主要靶点

Apoptosis|Others

仅限科研使用

Cat No : CM06721

Print datasheet

Synonyms

(R)-(+)-乙莫克舍钠盐|(R)-Etomoxir sodium salt|Na salt|Etomoxir



产品信息

(R)-Etomoxir sodium salt is R-form of Etomoxir. Etomoxir is a potent inhibitor of carnitine palmitoyltransferase-I (CPT-1).

CAS号 828934-41-4
分子式 C15H18ClO4.Na
主要靶点 Apoptosis|Others
主要通路 其他|凋亡
分子量 320.74
纯度 99.39%, 此纯度可做参考,具体纯度与批次有关系,可咨询客服
储存条件 Powder: -20°C for 3 years | In solvent: -80°C for 1 year
别名 (R)-(+)-乙莫克舍钠盐|(R)-Etomoxir sodium salt|Na salt|Etomoxir

体内活性

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[3]. 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 [4].

体外活性

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 a peroxisomal proliferator, increasing DNA synthesis and liver growth. Thus, etomoxir, in addition to being a CPT1 inhibitor could be considered as a PPARalpha agonist[1]. Etomoxir is a member of the oxirane carboxylic acid carnitine palmitoyltransferase 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 enzymes [2].

溶解度

H2O:15.59mM,DMSO:199.5 mM

参考文献

1.Rupp H, et al. The use of partial fatty acid oxidation inhibitors for metabolic therapy of angina pectoris and heart failure. Herz. 2002 Nov;27(7):621-36.
2.Xu FY, et al. Etomoxir mediates differential metabolic channeling of fatty acid and glycerol precursors into cardiolipin in H9c2 cells. J Lipid Res. 2003 Feb;44(2):415-23.
3.Li J, et al. FFA-ROS-P53-mediated mitochondrial apoptosis contributes to reduction of osteoblastogenesis and bone mass in type 2 diabetes mellitus. Sci Rep. 2015 Jul 31;5:12724.
4.Luiken JJ, et al. Etomoxir-induced partial carnitine palmitoyltransferase-I (CPT-I) inhibition in vivo does not alter cardiac long-chain fatty acid uptake and oxidation rates. Biochem J. 2009 Apr 15;419(2):447-55.

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
=
×
×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
×
=
×
C1   V1   C2   V2