| CAS NO: | 828934-41-4 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 2mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 250mg | 电议 |
| 500mg | 电议 |
| Molecular Weight (MW) | 320.74 |
|---|---|
| Formula | C15H18ClO4.Na |
| CAS No. | 828934-41-4 |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: 64 mg/mL (199.5 mM) |
| Water: 64 mg/mL (199.5 mM) | |
| Ethanol: 13 mg/mL (40.5 mM) | |
| Other info | Chemical Name: (2R)-2-[6-(4-chlorophenoxy)hexyl]-2-oxiranecarboxylic acid monosodium salt SMILES Code: O=C([C@]1(CCCCCCOC2=CC=C(Cl)C=C2)OC1)[O-].[Na+] |
| Synonyms | Etomoxir sodium; B 807-54; B807-54; B-807-54; B 80754; B80754; B-80754; |
| In Vitro | In vitro activity: Etomoxir has also been identified as a direct agonist of PPARα. Etomoxir is a compound that binds irreversibly to the catalytic site of CPT-1 inhibiting its activity, but also upregulates fatty acid oxidation enzymes. Transcriptional effects of etomoxir could be due to 1. shift in energy metabolism with increased glucose utilization and 2. PPARalpha activation. Etomoxir reduces pro-inflammatory cyokine production and increases apoptosis of MOG specific T cells. Etomoxir has been shown to decrease oxygen consumption rates (OCRs) and impair ATP and NADPH production in the pediatric glioblastoma cell line SF188. Cell Assay: C57BL/6 mice are immunized with 200 μg MOG35-55 peptide s.c., and 14 days later splenocytes are isolated and cultured at a concentration of 6×106 cells/ml in DMEM containing high (4.5 g/L) or low (1 g/L) glucose, 10% FBS 50 μg/ml MOG peptide, and 25 ng/ml IL-12 (R&D systems, Minneapolis, MN) in the presence of vehicle or 100 μM etomoxir. 72 hours later cells are harvested for APO-BrdU staining and supernatants collected for IL-4, IL-17 and IFN-γ ELISA. (MOG:myelin oligodendrocyte glycoprotein). |
|---|---|
| In Vivo | Etomoxir has a protective action on the ischemia/reperfusion injury of the kidney similarly to an established PPARalpha agonist. It has been developed for treating non-insulindependent diabetes mellitus. Etomoxir increases the functional recovery of fatty acid perfused ischemic rat hearts which is unrelated to changes in levels of long-chain acylcarnitines and is attributed to an increased glucose use. A chronic treatment of rats with etomoxir increases the SR Ca2+-ATPase activity, the Ca2+ uptake rate, the number of active Ca2+ pumps E~P, the SERCA2 protein and the SERCA2 mRNA abundance of the heart. At a low dosage, etomoxir has a selective influence on the rate of contraction and relaxation of overloaded hearts. Etomoxir, in the liver can act as peroxisomal proliferator, increasing DNA synthesis and liver growth. Etomoxir-treated mice displays a reduced immune cell infiltration in the CNS with few macrophages, activated microglia, or T cells present. Etomoxir reduces inflammation and demyelination in the CNS of treated mice. Inhibition of fatty acid oxidation by etomoxir prolongs survival time in a syngeneic mouse model of malignant glioma and slow tumor growth. Emergence and progression of glioma are delayed upon treatment with the investigational drug etomoxir. Etomoxir has already been tested in phase I/II clinical trials for treating moderate congestive heart failure; this trial is discontinued because 4 patients (of 226 taking the drug) developed unacceptably high liver transaminase levels upon treatment, and the risk of such drastic side effects is deemed sufficient to negate the potential benefit of this drug for these patients. |
| Animal model | C57BL6/J mice |
| Formulation & Dosage | Dissolved in water; 15 mg/kg; i.p,. injection |
| References | Herz. 2002 Nov;27(7):621-36; Sci Rep. 2011;1:79; Neuro Oncol. 2017 Jan;19(1):43-54. |
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