| Identification | More | [Name]
N-Oleoylethanolamine | [CAS]
111-58-0 | [Synonyms]
N-[2,6-BIS(1-METHYLETHYL)PHENYL]-9Z-OCTADECENAMIDE
ODA
OLEIC ACID-2,6-DIISOPROPYL ANILIDE
N-(2-hydroxyethyl)-,(Z)-9-Octadecenamide
Oleoylmonoethanolamide
OLEAMIDE MEA
9-Octadecenamide, N-(2-hydroxyethyl)-, (9Z)-
(Z)-N-(2-hydroxyethyl)octadec-9-enamide
LSUREMONOETHANOLAMID
Oleyl monoethanolamide
N-(2-Hydroxyethyl)oleamide
N-(cis-9-Octadecenoyl)ethanolamine
N-Oleoylethanolamine
OEA
N-(cis-9-Octadecenoyl)ethanolamine, N-(Hydroxyethyl)oleamide, OEA, oleoylethanolamide
(Z)-N-(2-Hydroxyethyl)-9-octadecenamide
AM-3101
N-(2-Hydroxyethyl)oleic amide | [EINECS(EC#)]
203-884-8 | [Molecular Formula]
C30H51NO | [MDL Number]
MFCD08059579 | [Molecular Weight]
441.73 | [MOL File]
111-58-0.mol |
| Chemical Properties | Back Directory | [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
| [solubility ]
Soluble in DMSO (up to 25 mg/ml) or in Ethanol (up to 35 mg/ml) | [form ]
White solid | [pka]
14.49±0.10(Predicted) | [color ]
White | [Stability:]
Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 1 month. | [Cosmetics Ingredients Functions]
VISCOSITY CONTROLLING
ANTISTATIC
SURFACTANT - FOAM BOOSTING | [Cosmetic Ingredient Review (CIR)]
Oleoyl Ethanolamide (111-58-0) | [InChI]
InChI=1S/C20H39NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-20(23)21-18-19-22/h9-10,22H,2-8,11-19H2,1H3,(H,21,23)/b10-9- | [InChIKey]
BOWVQLFMWHZBEF-KTKRTIGZSA-N | [SMILES]
C(NCCO)(=O)CCCCCCC/C=C\CCCCCCCC | [LogP]
6.406 (est) | [CAS DataBase Reference]
111-58-0(CAS DataBase Reference) | [EPA Substance Registry System]
111-58-0(EPA Substance) |
| Hazard Information | Back Directory | [Description]
Oleoyl ethanolamide (OEA) is an analog of the endocannabinoid AEA found in brain tissue and in chocolate.1 It is one of the long chain fatty acid ethanolamides that accumulates rapidly in infarcted tissue,2 but its biosynthesis is reduced in the intestine of rats following food deprivation.3 OEA is an endogenous, potent agonist for PPARα, exhibiting an EC50 value of 120 nM in a transactivation assay.4 Systemic administration of OEA suppresses food intake and reduces weight gain in rats (10 mg/kg intraperitoneally) and PPARα wild-type mice, but not in PPARα knockout mice.3,4 These data indicate that OEA regulates food intake by a PPARα-mediated mechanism. | [Uses]
N-?Oleoylethanolamide is an agonist of peroxisome proliferator-activated receptor-α (PPAR-?α). N-?Oleoylethanolamide generates an intestinal signal that stimulates central dopamine activity establishing a link between caloric-?homeostatic and hedonic-?homeostatic controllers. Oleoylethanolamide has been implicated as the molecular mechanism associated with gastric bypass success. N-?Oleoylethanolamide is a selective GPR55 agonist. | [Application]
N-Oleoyl Ethanolamide has been used to study its effects on glucagon-like peptide (GLP)-1RA-mediated anorectic signaling and weight loss. | [Definition]
ChEBI: An N-(long-chain-acyl)ethanolamine that is the ethanolamide of oleic acid. The monounsaturated analogue of the endocannabinoid anandamide | [Biosynthesis]
Oleoylethanolamide (OEA) is produced by the small intestine following feeding in two steps. First an N-acyl transferase (NAT) activity joins the free amino terminus of phosphatidylethanolamine (PE) to the oleoyl group (one variety of acyl group) derived from sn-1-oleoyl-phosphatidylcholine, which contains the fatty acid oleic acid at the sn-1 position. This produces an N-acylphosphatidylethanolamine, which is then split (hydrolyzed) by N-acyl phosphatidylethanolamine-specific phospholipase D (NAPE-PLD) into phosphatidic acid and OEA. The biosynthesis of OEA and other bioactive lipid amides is modulated by bile acids. | [Biological Functions]
N-Oleoyl Ethanolamide 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-Oleoyl Ethanolamide 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-Oleoyl Ethanolamide because this leads to increased formation of ceramide. There are numerous studies in which N-Oleoyl Ethanolamide 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-Oleoyl Ethanolamide decreases ceramide levels in JB6 P+ cells by an unknown mechanism. Recently, N-Oleoyl Ethanolamide 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-Oleoyl Ethanolamide are of significance for neuroprotection is not known, but it indicates that nonendocannabinoid NAEs are also bioactive molecules with potential for cerebral actions. | [General Description]
Oleoylethanolamide (OEA) is an endogenous?fatty acid?ethanolamine. Small intestine cells, adipose tissues, neurons and astrocytes produces OEA. | [Biological Activity]
Lipid mediator and analog of anandamide (N-(2-Hydroxyethyl)-5Z,8Z,11Z,14Z-eicosatetraenamide ) that is involved in peripheral regulation of feeding. Selective GPR55 agonist (EC 50 values are 0.44, >30 and >30 μ M at GPR55, CB 1 and CB 2 respectively) and PPAR α agonist (EC 50 = 120 nM). Induces satiety through activation of PPAR α and is also a ceramidase inhibitor. Also endogenous agonist at the GPR119 receptor. | [Biochem/physiol Actions]
Oleoylethanolamide (OEA) is a lipid mediator, which helps to control various biological functions, like food intake. It modulates the gene expression in the small intestine. OEA has the ability to initiate several receptors, such as cannabinoid receptor type 1 (CB1), peroxisome proliferator-activated receptors (PPARs) and?G protein-coupled receptor 119 (GPR119). | [Enzyme inhibitor]
This endocannabinoid-related metabolite (FW = 325.54 g/mol; CAS 111- 58-0; Symbol: NOE and OEA; Soluble in Ethanol, Chloroform, or Methanol) is widely employed to inhibit acid and neutral ceramidases (IC50 ~ 500 μM) that cleave fatty acids from ceramide, producing sphingosine (SPH), which is then enzymatically phosphorylated to form the receptorsensed metabolite, sphingosine-1-phosphate, or S1P. NOE also inhibits the glucosylation of naturally occurring ceramides. In CHP-100 neuroepithelioma cells treated with N-hexanoylsphingosine (C6-Cer; 30 μM), NOE affected only marginally short-chain glucocerebroside accumulation, but markedly decreased accumulation of glucocerebrosides originating from glucosylation of a long-chain ceramide (Lc-Cer) produced upon C6-Cer treatment. NOE also inhibits fatty acid hydrolase (or FAAH), an integral membrane hydrolase possessing an unusual catalytic triad Ser-Ser-Lys. FAAH catalysis is based on the formation of a tetrahedral intermediate, which is a product of the nucleophilic attack of Ser241 on the carbonyl group of the substrate. In the presence of NOE, TNFa leads to a sustained accumulation of ceramide and induces DNA fragmentation in renal mesangial cells. Membrane & Receptor Interactions: NOE forms stable complexes with phospholipid vesicles, lowering diphenylhexatriene polarization ratios in dimyristoylphosphatidylcholine and dipalmitoylphosphatidylcholine uni- and multilamellar bilayer vesicles. Once incorporated into the lipid bilayer of phospholipid vesicles, N-oleoylethanolamine partitions preferentially into more fluid areas, producing a concentration-dependent decrease in their phase transitions. N-Oleoylethanolamine is also an effective inhibitor of mitochondrial swelling, but does not inhibit phospholipase A2 or ruthenium red-induced Ca2+ release. Moreover, among naturally occurring Nacylethanolamines, only NOE (at 10 μM) inhibits the accumulation of Narachidonoylethanolamine (or Anandamide, AEA), a putative endogenous ligand of the cannabinoid receptor, into cerebellar granule cells occurs by means of facilitated diffusion. Ethanolamides of palmitic acid and linolenic acid are inactive at 10 μM. Role as an Anorexic Lipid Mediator: NOleoylethanolamine is a structural analogue of the endogenous cannabinoid anandamide, but does not activate cannabinoid receptors. NOE biosynthesis in rat small intestine is increased by feeding and reduced by fasting. NOE decreases food intake in food-deprived rats via a mechanism that requires intact sensory fibers. Such results suggest that OEA may contribute to the peripheral regulation of feeding. NOE may contribute to regulation of satiety, providing a chemical scaffold for the design of novel appetitesuppressing medications. Despite its designation as endocannabinoidlike compound, NOE is unable to bind with significant affinity to either CB1 or CB2 cannabinoid receptors. SIRT6 Activation: N-Oleoylethanolamine binds to and activates Sirtuin 6 (EC50 = 3.1 μM), an NAD+-dependent histone deacetylase that selectively deacylates H3K9Ac and H3K56Ac, but acts preferentially on long-chain fatty acyl groups over acetyl groups in vitro. (See also Oleamide; N-Oleoyl-2-amino-1,3-propanediol; Oleoyl-Nhydroxylamide) | [storage]
Store at -20°C | [References]
1) Lo Verme?et al.?(2005),?Regulation of food intake by oleoylethanolamide; Cell Mol. Life Sci.?62?708
2) Magotti?et al.?(2015),?Structure of human N-acylphosphatidylethanolamine-hydrolyzing phospholipase D: regulation of fatty acid ethanolamide biosynthesis by bile acids; Structure?23?598
3) Overton?et al.?(2006),?Deorphanization of a G protein-coupled receptor for oleoylethanolamide and its use in the discovery of small-molecules hypophagic agents; Cell Metab.?3?167
4) Brown (2007),?Novel cannabinoid receptors; Br. J. Pharmacol.?152?567
5) Nielson?et al.?(2004),?Food intake is inhibited by oral oleoylethanolamide; J. Lipid Res.?45?1027
6) Folick?et al.?(2015),?Aging. Lysosomal signaling molecules regulate longevity in Caenorhabditis elegans; Science?347?83 |
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