(R)-Etomoxir sodium salt

SKU: orb1221747

Description

(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.

Key Properties

• CAS Number: 828934-41-4
• MW: 320.74
• Purity: >98% (HPLC)
• Formula: C₁₅H₁₈ClO₄.Na
• SMILES: [Na+].[O-]C(=O)[C@@]1(CCCCCCOc2ccc(Cl)cc2)CO1
• Target: P450
• Solubility: H2O : 80 mg/mL 249.42 mM

Bioactivity

• 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. 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.
• 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. 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.

Storage & Handling

• Storage: Storage temperature: -20°C. Stability: ≥ 2 years
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

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

Quick Database Links

Gene Symbol

P450