| Identification | Back Directory | [Name]
methyl 2-tetradecylglycidate | [CAS]
69207-52-9 | [Synonyms]
MCN-3716
NSC359682)
Methyl palmoxirate
Methyl parmoxirate
McN3716 (Methyl palmoxirate
methyl 2-tetradecylglycidate
2-Tetradecyloxiranecarboxylic acid methyl ester
2-Tetradecyloxirane-2-carboxylic acid methyl ester | [Molecular Formula]
C18H34O3 | [MDL Number]
MFCD00865479 | [MOL File]
69207-52-9.mol | [Molecular Weight]
298.46 |
| Chemical Properties | Back Directory | [Melting point ]
44-46 °C | [Boiling point ]
361.4±17.0 °C(Predicted) | [density ]
0.944±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
Soluble in DMSO | [form ]
Solid | [color ]
White to off-white |
| Hazard Information | Back Directory | [Uses]
Antidiabetic. | [in vivo]
Inhibition of brain mitochondrial β-oxidation by McN3716 (Methyl palmoxirate, MEP) significantly reduces the levels of all measured HETE and epoxytrienoic acids (EET), nonenzymatic auto-oxidative metabolites of ARA, by 23% to 44% and 32% to 50% compared with vehicle-injected rats, respectively, except for 15-HETE which was unaffected. There is a significant 34% reduction in the level of 6-keto-PGF1α, a byproduct of PGI2 (prostacyclin) in McN3716-treated rats. Similarly, the brain level of hydroxyeicosapentaenoic acids, nonenzymatic auto-oxidative metabolites of EPA, is reduced by 35% to 76% upon McN3716 treatment relative to vehicle[1]. | [storage]
Store at -20°C |
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