1. Metabolic Enzyme/Protease
    Cell Cycle/DNA Damage
  2. Endogenous Metabolite

Oleoylethanolamide (Synonyms: N-(2-Hydroxyethyl)oleamide; N-Oleoyl-2-aminoethanol; N-Oleoylethanolamide; Oleamide MEA; Oleic acid monoethanolamide)

Cat. No.: HY-107542
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Oleoylethanolamide is a high affinity endogenous PPAR-α agonist, which plays an important role in the treatment of obesity and arteriosclerosis.

For research use only. We do not sell to patients.

Oleoylethanolamide Chemical Structure

Oleoylethanolamide Chemical Structure

CAS No. : 111-58-0

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Oleoylethanolamide is a high affinity endogenous PPAR-α agonist, which plays an important role in the treatment of obesity and arteriosclerosis.

IC50 & Target[1]

Human Endogenous Metabolite




In Vitro

Oleoylethanolamide (OEA), an endogenous PPAR-α ligand, attenuates liver fibrosis targeting hepatic stellate cells. Oleoylethanolamide suppresses TGF-β1 induced hepatic stellate cells (HSCs) activation in vitro via PPAR-α. To assess the impact of Oleoylethanolamide on HSCs activation, the expression levels of α-SMA and Col1a in TGF-β1-stimulated HSCs are examined by qPCR. The mRNA levels of α-SMA and Col1a are markedly induced in the group of CFSC cells with TGF-β1 (5 ng/mL) stimulation for 48h, while the mRNA levels are suppressed when treated with Oleoylethanolamide in a dose-dependent manner. Immunofluorescence and western blot results show that Oleoylethanolamide treatment dose-dependently inhibits the protein expression of α-SMA, the marker of HSC activation. The inhibitory effects of Oleoylethanolamide on HSCs activation are completely blocked by PPAR-α antagonist MK886 (10 μM). Moreover, the mRNA and protein expression levels of PPAR-α are down-regulated with TGF-β1 stimulation, while Oleoylethanolamide treatment restores these changes in dose-dependent manner. In addition, the phosphorylation of Smad 2/3 is upregulated in the presence of TGF-β1 stimulation, consistent with the observed effects on HSC activation, while Oleoylethanolamide (10 μM) reduces the phosphorylation of Smad2/3 in CFSC simulated with TGF-β1[1].

In Vivo

Oleoylethanolamide (OEA) can significantly suppress the pro-fibrotic cytokine TGF-β1 negatively regulate genes in the TGF-β1 signaling pathway (α-SMA, collagen 1a, and collagen 3a) in mice models of hepatic fibrosis. Treatment with Oleoylethanolamide (5 mg/kg/day, intraperitoneal injection, i.p.) significantly attenuates the progress of liver fibrosis in both two experimental animal models by blocking the activation of hepatic stellate cells (HSCs)[1].

Cell Assay

CFSC, HSC cell lines are first obtained from cirrhotic rat liver, and have a similar phenotype to that of early passage primary HSCs. CFSC cells are cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin. All cells are cultured in 6-well culture plates under 37°C and 5% CO2 in an incubator. The medium is replaced every two days, and the cells are harvested and diluted at a ratio of 1:3 twice a week. In experiments, HSCs are pretreated with the experimental concentration of Oleoylethanolamide (30 μM, 10 μM, 3 μM) before stimulation with 5 ng/mL TGF-β1. mRNA expression levels of α-SMA (A) and Col1a (B) are analyzed by real-time PCR[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration

The Sv/129 mice and PPAR-α knockout mice are maintained in a room with controlled temperature (21-23°C), humidity (55-60%) and lighting (12 h light/dark cycles) and given water ad libitum. Mice are randomly divided for methionine choline-deficient (MCD) and thioacetamide (TAA) experiments. In the MCD-diet feeding experiment, wild-type Sv/129 mice and PPAR-α knockout mice are each divided into three groups (n=8 /group): (i) control group receive normal diet; (ii) fed with MCD diet and injected with the vehicle (5% Tween-80+5% PEG400+90% saline, 5 mL/kg/day, 8 weeks, intraperitoneal injection, i.p.); (iii) fed with MCD diet along with Oleoylethanolamide administration (5 mg/kg/day; 8 weeks, i.p.). In another set of experiment, all the wild-type mice and PPAR-α knockout mice are given standard chow diet, and are randomly separated into three groups: the control group is not administrated TAA or Oleoylethanolamide but is injected with the saline; the TAA group is injected with TAA (160 mg/kg, three times per week, 6 weeks, dissolved in saline, i.p.) plus the corresponding vehicle; the Oleoylethanolamide group is both injected with TAA and Oleoylethanolamide (5 mg/kg/day; 6 weeks, i.p.)[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Molecular Weight









Please store the product under the recommended conditions in the Certificate of Analysis.


Room temperature in continental US; may vary elsewhere

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Cat. No.: HY-107542