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Palmitoylethanolamide PPAR activator

Cat.No.S4708

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.
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Quality Control

Batch: Purity: 99.93%
99.93

Solubility

In vitro
Batch:

Ethanol : 59 mg/mL

DMSO : 5 mg/mL (16.69 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 299.49 Formula

C18H37NO2

Storage (From the date of receipt)
CAS No. 544-31-0 Download SDF Storage of Stock Solutions

Synonyms Palmidrol|N-palmitoylethanolamine SMILES CCCCCCCCCCCCCCCC(=O)NCCO

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Mechanism of Action

Targets/IC50/Ki
PPARα
(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.
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. 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.
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-07-14)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
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Ulcerative Colitis (UC)
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2026-01-01
NCT07680101 NOT_YET_RECRUITING
Degenerative Joint Disease of Knee; Rheumatoid Arthritis
Universita di Verona
2026-06
NCT07681063 NOT_YET_RECRUITING
Postoperative Cognitive Dysfunction
Fondazione IRCCS San Gerardo dei Tintori
2026-06
NCT06717867 RECRUITING
Healthy; Safety
RDC Clinical Pty Ltd
2025-01-22 PHASE2

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