Product Name:N-Oleoylethanolamine CAS:111-58-0 MF:C20H39NO2 MW:325.53 EINECS:203-884-8 Mol File:111-58-0.mol Melting point:63-64 °C Boiling point:496.4±38.0 °C(Predicted) Density 0.915±0.06 g/cm3(Predicted) storage temp. −20°C pka14.49±0.10(Predicted) form White solid
Description N-Oleoylethanolamine is also a predominant NAE species in the injured rat brain, and it has also been found to be the major NAE species in a human brain that has suffered a hemispheric stroke. As early as 1975, N-oleoylethanolamine was synthesized as an inhibitor of ceramidase, the enzyme that degrades ceramide. Ceramide is involved in the regulation of apoptosis and cell proliferation. Cannabinoid-induced apoptosis in glioma cells is mediated via formation of ceramide. On a tentative basis, it can be suggested that anandamide-induced apoptosis may be aggravated by the presence of N-oleoylethanolamine because this leads to increased formation of ceramide. There are numerous studies in which N-oleoylethanolamine has been shown to facilitate the apoptosis-inducing effect of different compounds mediated via increased ceramide levels. However, it has also been reported that N-oleoylethanolamine decreases ceramide levels in JB6 P+ cells by an unknown mechanism. Recently, N-oleoylethanolamine has been shown to have a CB1-receptor-independent anorexic effect by inhibiting some intestinal neuronal functions in the rat, and it also causes vasodilation in rat mesenteric arterial segments by an unknown receptor mechanism. Whether these recently discovered biological effects of N-oleoylethanolamine are of significance for neuroprotection is not known, but it indicates that nonendocannabinoid NAEs are also bioactive molecules with potential for cerebral actions.
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