(R)-Etomoxir sodium salt

Research use only, not for human use.

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

(R)-Etomoxir sodium salt is R-form of Etomoxir. Etomoxir is a potent inhibitor of carnitine palmitoyltransferase-I (CPT-1).(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 [1-14C]palmitic acid or [1-14C]oleic acid incorporation into cardiolipin.Etomoxir increases [1,3-3H]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.(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.

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 [1-14C]palmitic acid or [1-14C]oleic acid incorporation into cardiolipin.Etomoxir increases [1,3-3H]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. 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.

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 Animal Model:80 male C57BLKS/J lar-Leprdb/db 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.

(R)-(+)-Etomoxir (sodium salt)

Metabolic Enzyme/Protease

P450

CPT-1

Metabolic Disease

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828934-41-4

320.74

C15H18ClO4.Na

>98% (HPLC)

H2O : 80 mg/mL 249.42 mM

[Na+].[O-]C(=O)[C@@]1(CCCCCCOc2ccc(Cl)cc2)CO1

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(-20℃)

With Ice Pack

≥ 2 years