Name | (R)-2-(6-(4-chlorophenoxy)hexyl)oxirane-2-carboxylate sodium salt |
Synonyms | ANTI-EAPII Etomoxir(Nasalt) Anti-eapii (ttrap) Etomoxir hydrate sodium (+)-ETOMOXIR (SODIUM SALT) (+)-etomoxir sodium hydrate (+)-Etomoxir hydrate sodium salt (+)-Etomoxir hydrate sodium salt R(+)-2-[6-(4-Chlorophenoxy)hexyl]-oxirane-2-carboxylic (R)-2-(6-(4-chlorophenoxy)hexyl)oxirane-2-carboxylate sodium salt sodium (2R)-2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate hydrate (R)-(+)-2-[6-(4-Chlorophenoxy)hexyl]-oxirane-2-carboxylic acid sodium salt r(+)-2-[6-(4-chlorophenoxy)hexyl]-oxirane-2-carboxylic acid sodium salt hydrate R(+)-2-[6-(4-Chlorophenoxy)hexyl]-oxirane-2-carboxylic acid hydrate sodium salt |
CAS | 828934-41-4 |
InChI | InChI=1/C15H19ClO4.Na.H2O/c16-12-5-7-13(8-6-12)19-10-4-2-1-3-9-15(11-20-15)14(17)18;;/h5-8H,1-4,9-11H2,(H,17,18);;1H2/q;+1;/p-1/t15-;;/m1../s1 |
InChIKey | WENJLJJSJDAJDN-QCUBGVIVSA-M |
Molecular Formula | C15H20ClNaO4 |
Molar Mass | 322.76 |
Solubility | H2O: freely soluble |
Appearance | White solid |
Color | white |
Storage Condition | Inert atmosphere,2-8°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO may be stored at -20°C for up to 1 month. |
In vitro study | Etomoxir is also a direct agonist of PPAR alpha. Etomoxir binds irreversibly to the catalytic site of the CPT-1. Inhibits CPT-1 activity and upregulates fatty acid oxidase activity. The effect of Etomoxir on transcription can be attributed to 1. Changes in energy metabolism, increased utilization of glucose; 2. Activation of PPAR α. Etomoxir reduces the production of proinflammatory cytokines by MOG-specific T cells and promotes their apoptosis. Etomoxir reduces its oxygen consumption rate and ATP, NADPH production in the pediatric glioblastoma cell line sf188. |
In vivo study | Similar to other known PPAR α agonists, Etomoxir has a protective effect against ischemia/reperfusion injury in the kidney. Etomoxir was developed for the treatment of non-insulin-dependent diabetes. In rat hearts perfused with fatty acids (independent of changes in long-chain acylcarnitine levels),etomoxir accelerates functional repair by increasing glucose utilization. Chronic treatment of rats with etomoxir increased SR Ca2 -ATPase activity, calcium ion absorption rate, number of active Ca2 pump E ~ P, SERCA2 protein and SERCA2 mRNA abundance in their hearts. Low doses of etomoxir have a specific effect on the systolic and diastolic rates of the overloaded heart. In the liver, Etomoxir can promote the proliferation of oxidase bodies, enhance DNA synthesis and liver growth. Etomoxir-treated mice reduced the infiltration of immune cells in the central nervous system, with only a small number of macrophages, activated microglia or T cells, and reduced inflammation and demyelination. Etomoxir inhibits fatty acid oxidation, prolongs the lifespan of syngeneic glioblastoma mice and slows their tumor growth. Etomoxir delayed the onset and development of glioma. Etomoxir has been clinically studied in Phase I/II for the treatment of moderate congestive heart failure. The current trial was terminated because 4 patients (226 trial participants) had high levels of liver transaminases after the drug, the risk of this side effect is such that the potential therapeutic effect of this drug is rejected. |
Hazard Symbols | Xn - Harmful |
Risk Codes | 22 - Harmful if swallowed |
UN IDs | UN 2811 6.1/PG 3 |
WGK Germany | 3 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 3.118 ml | 15.588 ml | 31.177 ml |
5 mM | 0.624 ml | 3.118 ml | 6.235 ml |
10 mM | 0.312 ml | 1.559 ml | 3.118 ml |
5 mM | 0.062 ml | 0.312 ml | 0.624 ml |