Catalog No.S4708 Synonyms: Palmidrol|N-palmitoylethanolamine

For research use only.

Palmitoylethanolamide (PEA, Palmidrol, N-palmitoylethanolamine) is an endogenous fatty acid amide and selectively activates PPAR-α in vitro with an EC50 value of 3.1±0.4 μM.

Palmitoylethanolamide Chemical Structure

CAS No. 544-31-0

Selleck's Palmitoylethanolamide has been cited by 2 Publications

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Description Palmitoylethanolamide (PEA, Palmidrol, N-palmitoylethanolamine) is an endogenous fatty acid amide and selectively activates PPAR-α in vitro with an EC50 value of 3.1±0.4 μM.
PPARα [1]
(In HeLa cells)
3.1 μM(EC50)
In vitro

PEA protects cultured mouse cerebellar granule cells from glutamate toxicity and enhances microglial cell motility. In the mitochondrial fraction from cells stimulated with PEA, steroidogenic acute regulatory protein (StAR) and cytochrome P450 enzyme(P450scc) expression increases, both comprising proteins considered to be involved in crucial steps of neurosteroid formation. Moreover, PEA shows a protective effect, reducing malondialdehyde formation in cells treated with L-buthionine-(S,R)-sulfoximine, a glutathione depletor and the effect of PEA is partially inhibited by finasteride, a 5a-reductase inhibitor[2].

In vivo PEA attenuates inflammation in wild-type mice but has no effect in mice deficient in PPAR-α. PEA has been shown to inhibit peripheral inflammation and mast-cell degranulation as well as to exert neuroprotective and antinociceptive effects in rats and mice. These actions are accompanied by changes in nitric oxide production, neutrophil influx, and expression of proinflammatory proteins such as inducible nitric oxide synthase and cyclooxygenase-2[1]. In addition to its known anti-inflammatory activity, PEA regulates many pathophysiological processes, including pain perception, convulsions, and neurotoxicity. In the central nervous system (CNS), where PEA is present at detectable levels, its concentrations significantly increase under pathological conditions, such as excitotoxicity, brain ischaemia and neuroinflammation[2].

Protocol (from reference)

Cell Research:[2]
  • Cell lines: Rat C6 glioma cells
  • Concentrations: 10 μM
  • Incubation Time: 24 h
  • Method: C6 glioma cells (300 000⁄P60 dish) or astrocyte primary culture are incubated in serum-free DMEM at 37℃ for at least 24 h before each experiment. Then, cells are treated with PEA (10 μM) for 24 h in serum-free medium, in the presence and absence of GW6471 (10 μM) added 30 min before ethanolamide treatment. The concentration of PEA is chosen on the basis of preliminary experiments, assessing drug efficacy without modifi-cation of cell viability. PEA and GW6471 are first dissolved in absolute ethanol and then diluted with DMEM. The final ethanol concentration was< 0.5%. Mitochondrial protein extracts from C6 or astrocytes are obtained. Alternatively after 24 h of starvation in serum-free DMEM, C6 cells are treated with FIN (100 nM). After 30 min, PEA (10 μM) and⁄or ALLO (3 μM) is added and, 30 min later, are stimulated with BSO (10 mM). After 18 h, MDA is evaluated. In this set of experiments, FIN and⁄or PEA are dissolved in dimethylsulphoxide (DMSO) and then diluted with DMEM (0.1% final DMSO concentration).
Animal Research:[1]
  • Animal Models: C57BL6 mice, male C57BL6 PPAR-α-/- mice
  • Dosages: 10 mg/kg
  • Administration: i.p

Solubility (25°C)

In vitro

Chemical Information

Molecular Weight 299.49


CAS No. 544-31-0
Storage 3 years -20°C powder
2 years -80°C in solvent

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Clinical Trial Information

NCT Number Recruitment Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03564379 Completed Drug: JNJ-42165279|Drug: Placebo Healthy Janssen Research & Development LLC June 12 2018 Phase 1
NCT01092845 Completed Drug: PF-04457845 / matched placebo Healthy|Sleep Pfizer April 2010 Phase 1
NCT01370720 Unknown status Dietary Supplement: Recoclix|Other: Placebo Irritable Bowel Syndrome MARIA CRISTINA COMELLI|CM&D Pharma Limited February 2010 Phase 2

(data from, updated on 2022-01-17)

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