Oleoyl ethanolamide
111-58-0
Oleoyl ethanolamide
Oleoylethanolamide (OEA) is an endogenous lipid mediator that acts as a high-affinity agonist for peroxisome proliferator-activated receptor-alpha (PPAR-α), primarily investigated for its role in regulating food intake and energy metabolism . It is also studied for its anti-inflammatory, neuroprotective, and cardioprotective properties, with potential applications in metabolic disorders, atherosclerosis, and liver fibrosis.
Overview
Oleoylethanolamide is an endogenous N-acylethanolamine structurally related to the endocannabinoid anandamide but functionally distinct, as it does not bind cannabinoid receptors. It appears as a white to off-white crystalline powder with a melting point of 50-60°C, soluble in organic solvents such as ethanol, DMSO, and DMF, but practically insoluble in water. OEA is biosynthesized in the small intestine following feeding through a two-step process: first, an N-acyltransferase joins oleic acid to phosphatidylethanolamine, followed by hydrolysis via N-acyl phosphatidylethanolamine-specific phospholipase D (NAPE-PLD) . The compound functions primarily as a potent endogenous agonist of PPAR-α, exhibiting an EC₅₀ value of 120 nM in transactivation assays . Activation of PPAR-α by OEA regulates multiple physiological processes including satiety, lipid metabolism, and inflammation . Systemically administered OEA suppresses food intake and reduces weight gain in rodents through a PPAR-α-mediated mechanism, with effects absent in PPAR-α knockout mice . Beyond appetite regulation, OEA promotes lipolysis and fatty acid oxidation in the liver, increases expression of fatty acid translocase CD36, and enhances energy expenditure . In cardiovascular research, OEA inhibits TNF-α-induced expression of adhesion molecules in endothelial cells, suggesting anti-atherosclerotic effects . Preclinical studies demonstrate that OEA attenuates liver fibrosis by suppressing TGF-β1-induced activation of hepatic stellate cells through inhibition of Smad2/3 phosphorylation and α-SMA expression. The compound also exhibits anti-inflammatory properties in models of acute ischemic stroke, reducing oxidative stress markers and improving functional outcomes. OEA is metabolized primarily by fatty acid amide hydrolase (FAAH) and N-acylethanolamine-hydrolyzing acid amidase (NAAA), with a half-life suitable for research applications.
EINECS: 203-884-8
Product Categories: Intracellular receptor;Fluorobenzene
Characteristics
Melting point: 63-64 °C
Boiling point: 496.4±38.0 °C
Density: 0.915±0.06 g/cm3
Storage temp.: -20°C
Solubility: Soluble in DMSO (up to 25 mg/ml) or in Ethanol (up to 35 mg/ml)
Pka: 14.49±0.10
Form: White solid
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.
Applications
1.Metabolic and Appetite Regulation Research: OEA is extensively studied for its role in controlling food intake and body weight through PPAR-α activation. It suppresses appetite, increases feeding latency, and promotes fat oxidation in the liver, with implications for obesity research and metabolic disorder interventions . Studies show that OEA signaling may be disrupted in diet-induced obesity, making it a target for understanding hyperphagia .
2.Cardiovascular and Atherosclerosis Research: OEA demonstrates anti-atherosclerotic potential by activating PPAR-α, which inhibits inflammatory marker expression and reduces monocyte adhesion to vascular endothelium . It suppresses TNF-α-induced adhesion molecules in human umbilical vein endothelial cells, suggesting therapeutic applications in preventing atherosclerosis and cardiovascular disease .
3.Anti-inflammatory and Neuroprotection Research: OEA exhibits neuroprotective effects in acute ischemic stroke models, reducing oxidative stress, inflammation, and apoptosis via inhibition of TLR4/NF-κB and ERK1/2 signaling pathways. Clinical studies in stroke patients suggest that OEA supplementation (300 mg/day) improves inflammatory status and biochemical parameters.
4.Hepatic Fibrosis and Liver Research: OEA attenuates liver fibrosis by blocking hepatic stellate cell activation through PPAR-α-dependent inhibition of TGF-β1 signaling, reducing expression of fibrotic markers including α-SMA, collagen 1a, and collagen 3a in animal models . This positions OEA as a potential therapeutic agent for fibrotic liver diseases.
5.Industrial and Cosmetic Applications: OEA is used as a natural surfactant in cosmetic formulations, biopesticides, detergents, and enhanced oil recovery applications due to its amide bond structure and surface-active properties . Sustainable synthesis methods from palm oil-derived oleic acid enable large-scale production for industrial use .
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