肉碱棕榈酰转移酶I（CPT1）抑制剂，(R)-(+)-Etomoxir sodium salt 是 Etomoxir sodium salt 的 R 型异构体。Etomoxir 是一种有效的肉碱棕榈酰转移酶 (carnitine palmitoyltransferase-I，CPT-1) 抑制剂。

中文名称 
(R)-(+)-Etomoxir sodium salt
中文别名 
(2R)-2-[6-(4-氯苯氧基)己基]环氧乙烷甲酸钠;(R)-(+)-乙莫克舍钠盐;钠 (r)-2-(6-(4-氯苯氧基)己基)环氧乙烷-2-羧酸;SODIUM (R)-2-(6-(4-CHLOROPHENOXY)HEXYL)OXIRANE-2-CARBOXYLATE;(R)-2-(6-(4-氯苯氧基)己基)环氧乙烷-2-羧酸钠盐
英文名称 
(R)-(+)-Etomoxir sodium salt
英文别名 
2-Oxiranecarboxylicacid, 2-[6-(4-chlorophenoxy)hexyl]-, sodium salt (1:1), (2R)-;(+)-Etomoxir (sodium salt);(+)-Etomoxir sodium salt;(R)-(+)-Etomoxir sodium salt;(R)-2-(6-(4-chlorophenoxy)hexyl)oxirane-2-carboxylate sodium salt or (R)-Etomoxir sodium salt;ANTI-EAPII (TTRAP);SODIUM (R)-2-(6-(4-CHLOROPHENOXY)HEXYL)OXIRANE-2-CARBOXYLATE;sodium (S)-2-(6-(4-chlorophenoxy)hexyl)oxirane-2-carboxylate;sodium,(2R)-2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate
Cas No. 
828934-41-4
分子式 
C15H18O4Cl-.Na+
分子量 
320.74
包装储存 
-20°C, protect from light, stored under nitrogen
*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
生物活性 
Etomoxir((R)-(+)-Etomoxir) sodium salt is an irreversible inhibitor of carnitine palmitoyltransferase 1a (CPT-1a), inhibits fatty acid oxidation (FAO) through CPT-1a and inhibits palmitate β-oxidation in human, rat and guinea pig.
性状 
Solid
IC50 & Target[1][2] 
CPT-1a
体外研究(In Vitro) 
Etomoxir mediates differential metabolic channeling of fatty acid and glycerol precursors into cardiolipin in H9c2 cells.
Etomoxir does not affect the activities of the cardiolipin biosynthetic and remodeling enzymes but causes a reduction in [1-C]palmitic acid or [1-C]oleic acid incorporation into cardiolipin.
Etomoxir increases [1,3-H]glycerol incorporation into cardiolipin. The mechanism is a 33% increase in glycerol kinase activity, which produces an increased glycerol flux through the de novo pathway of cardiolipin biosynthesis.
Medlife has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay
Cell Line:    Rat heart H9c2 myoblastic cells
Concentration:    1-80 μM
Incubation Time:    2 hours
Result:    Reduced the incorporation of [1-14C]fatty acids into CL and PtdGro in H9c2 cardiac myoblast cells but did not affect total incorporation of radioactivity into these cells.
体内研究(In Vivo) 
Etomoxir significantly inhibits the decrease of bone mineral density (BMD) and bone breaking strength in db/db and high fat (HF)-fed mice and suppresses the reduction of BMSCs-differentiated osteoblasts. 
Etomoxir inhibits the increase of mitochondrial ROS generation in db/db and HF-fed mice and osteoblasts.
Etomoxir-induced partial carnitine palmitoyltransferase-I (CPT-I) inhibition in vivo does not alter cardiac long-chain fatty acid uptake and oxidation rates
Medlife has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:    80 male C57BLKS/J lar-Lepr mice
Dosage:    1?mg/kg
Administration:    Intraperitoneally injected; twice every week
Result:    Serum alkaline phosphatase was increased in db/db mice, which event was significantly suppressed by Etomoxir. Serum level of osteocalcin, a marker of bone formation, was reduced in db/db mice and Etomoxir markedly inhibited the reduction of osteocalcin. Serum tartrate-resistant acid phosphatase was elevated in db/db mice which phenomenon was significantly suppressed by Etomoxir.
Animal Model:    Rats
Dosage:    20 mg/kg
Administration:    Injected daily; for 8 days
Result:    Etomoxir-treated rats displayed a 44% reduced cardiac CPT-I activity.
运输条件 
Room temperature or refrigerated transportation.
储存方式 
-20°C, protect from light, stored under nitrogen
*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
参考文献 
[1]. Roddy S OConnor, et al. The CPT1a inhibitor, etomoxir induces severe oxidative stress at commonly used concentrations.Sci Rep. 2018 Apr 19;8(1):6289.  [Information]
[2]. Fred Y Xu,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.  [Information]
[3]. Jun Li, 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.  [Information]
[4]. Joost J F P Luiken, 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.  [Information]

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