Short answer. Palmitoylethanolamide (PEA, CAS 544-31-0) is an endogenous N-acylethanolamine — mammals synthesise it, and it also occurs in egg yolk, soy and peanut. Published research has investigated PEA in relation to anti-inflammatory and analgesic pathways, principally through PPAR-α and through mast-cell and glial signalling. This page is written for formulators and sourcing teams. It covers what the literature has examined, which identity and particle-size fields belong on a specification, and where the claim boundary sits for a US dietary supplement. It does not tell you what a finished product will do for a consumer, and it is not written to be lifted onto a label.
Identity: specify the molecule, not the acronym
"PEA" is ambiguous on a purchase order — the same three letters are used for polyethylene adipate and for phenylethylamine. If you are buying palmitoylethanolamide, put identifiers on the specification. Every value in the table below was read from PubChem while this page was written, not quoted from memory.
| Field | Value |
|---|---|
| Common name | Palmitoylethanolamide (PEA) |
| Alternative name / INN | Palmidrol |
| IUPAC name | N-(2-hydroxyethyl)hexadecanamide |
| CAS | 544-31-0 |
| PubChem CID | 4671 |
| Molecular formula | C18H37NO2 |
| Molecular weight | 299.5 |
| InChIKey | HXYVTAGFYLMHSO-UHFFFAOYSA-N |
| Chemical class | N-acylethanolamine; fatty acid amide of palmitic acid and ethanolamine |
The InChIKey is the field worth insisting on. It survives translation, transcription and a supplier’s own naming conventions in a way that "PEA 98%" does not.
What published research has investigated: anti-inflammatory pathways
Two lines of work are cited most often, and it is worth being precise about what each one actually established, because the distinction matters when your regulatory team reads the file.
PPAR-α as a molecular target
Lo Verme and colleagues identified the nuclear receptor PPAR-α as the molecular target responsible for the anti-inflammatory actions of palmitoylethanolamide described in that paper, reporting selective activation in vitro with an EC50 of roughly 3.1 µM, alongside rodent models (Lo Verme et al., Mol Pharmacol 2005;67(1):15–19; PMID 15465922). This is in vitro and rodent work. It establishes a receptor mechanism; it does not establish an outcome in people, and we do not present it as one.
Mast cells and glia
A review by Skaper, Facci and Giusti describes PEA as being produced and hydrolysed by microglia and as down-modulating mast cell activation, framing mast cell–glia communication as the surface of interest for neuroinflammation (Mol Neurobiol 2013;48(2):340–352; PMID 23813098). This is a review, not primary data — useful for orientation and for finding the primary sources underneath it, not as evidence in its own right.
What published research has investigated: analgesic and nociceptive pathways
Human trial literature exists here, which is unusual for an ingredient at this price point and is the main reason PEA gets specified at all. A 2023 systematic review and meta-analysis in Nutrients pooled double-blind randomised controlled trials of PEA in chronic pain (Lang-Illievich et al., 2023;15(6):1350; PMID 36986081). A broader 2021 review in International Journal of Molecular Sciences surveys the compound across health-management contexts (Clayton et al., 2021;22(10):5305; PMID 34069940).
We deliberately do not reproduce the pooled effect sizes from that meta-analysis on this page. Describing a study design and the endpoint it examined is literature description. Printing an effect size directly beside an ingredient we sell reads as a finished-product efficacy claim, and that is a line we hold on the sell side regardless of how the sentence is worded. The PMIDs are above; your regulatory and medical affairs people should read the papers and reach their own conclusion, which is what they are for.
Particle size: the specification field most buyers forget
PEA is poorly water-soluble, and the literature on it is not written about one single material. Petrosino and Di Marzo review formulations with reduced particle size — micronised and ultra-micronised — as a distinct category, including combinations with flavonoids such as luteolin and stilbenes such as polydatin (Br J Pharmacol 2017;174(11):1349–1365; PMID 27539936).
The practical consequence for sourcing: a specification reading only "palmitoylethanolamide, 98%" does not tell you which material you are buying. Two lots can both be compliant with that spec and behave differently in a tablet, a stick pack or a softgel. Ask for a particle size distribution with a stated method — laser diffraction, with D10, D50 and D90 reported — and treat "micronised" as a marketing word until a number and a method sit behind it.
If you are evaluating flavonoid or stilbene co-formulation, our apigenin vs luteolin and polydatin vs resveratrol comparisons cover the form questions on those two.
Where the claim boundary sits
This is the part buyers most often get wrong, and it is worth stating plainly rather than leaving it to a footer disclaimer. Everything above describes what researchers have investigated about a molecule. None of it is a claim about what a finished product does for a person, and a citation does not create claim room.
Under US rules a dietary supplement may carry structure/function statements; it may not be marketed to treat, prevent, cure or mitigate a disease, and adding "studies suggest" in front of a disease claim does not convert it into a permitted one. Pain conditions in particular sit close to that line. If you are drafting label or marketing copy from an ingredient dossier, our structure/function vs disease claims reference walks through the distinction with a worked example.
What we supply is the raw material and its documentation. Claim substantiation for a finished product is the brand’s responsibility and depends on the formula, the dose and the population — none of which we control.
Documentation to request before you sample
- Certificate of analysis for the specific lot, with assay method stated
- Full specification sheet, including identity by CAS and InChIKey
- Particle size distribution with method (D10 / D50 / D90)
- Residual solvent and heavy metals data
- Microbiological specification
- Allergen and GMO status statements — relevant here, since PEA occurs naturally in soy, peanut and egg
- Stability data in a format resembling yours, not a generic powder study
Our certification position is set out on the quality and certifications page; documents are provided under buyer review.
Frequently asked questions
Is palmitoylethanolamide a dietary ingredient in the US?
Regulatory status is the buyer’s determination to make and document, and it depends on the intended use and the marketing claims. We supply the material and its documentation; we do not issue regulatory opinions, and you should not accept one from any ingredient supplier in place of your own counsel.
What does "micronised" mean on a PEA specification?
On its own, nothing enforceable. It becomes meaningful when it is expressed as a particle size distribution with a stated measurement method. Ask for the numbers.
Which formats does PEA suit?
It is a poorly water-soluble waxy solid, which makes capsules, tablets, softgels and oil-phase systems the straightforward routes. Clear beverages are the hard case. Tell us the format at the sample stage so the right material is sent.
Why does the literature use the name Palmidrol?
Palmidrol is an alternative name for the same molecule. When searching literature or registries, CAS 544-31-0 and InChIKey HXYVTAGFYLMHSO-UHFFFAOYSA-N will find material that a name search misses.
Can you supply a sample and a COA?
Yes. Tell us the format, target use level and market, and we will send the specification and lot COA alongside the sample.
Request a sample, specification or COA
Nutrition BioTech supplies palmitoylethanolamide to US formulators. Contact our team with your format and use level, or browse the ingredient selection guides for related comparisons.
References
- Lo Verme J, Fu J, Astarita G, La Rana G, Russo R, Calignano A, Piomelli D. The nuclear receptor peroxisome proliferator-activated receptor-alpha mediates the anti-inflammatory actions of palmitoylethanolamide. Mol Pharmacol. 2005;67(1):15–19. doi:10.1124/mol.104.006353. PMID 15465922.
- Skaper SD, Facci L, Giusti P. Glia and mast cells as targets for palmitoylethanolamide, an anti-inflammatory and neuroprotective lipid mediator. Mol Neurobiol. 2013;48(2):340–352. doi:10.1007/s12035-013-8487-6. PMID 23813098.
- Petrosino S, Di Marzo V. The pharmacology of palmitoylethanolamide and first data on the therapeutic efficacy of some of its new formulations. Br J Pharmacol. 2017;174(11):1349–1365. doi:10.1111/bph.13580. PMID 27539936.
- Clayton P, Hill M, Bogoda N, Subah S, Venkatesh R. Palmitoylethanolamide: a natural compound for health management. Int J Mol Sci. 2021;22(10):5305. doi:10.3390/ijms22105305. PMID 34069940.
- Lang-Illievich K, Klivinyi C, Lasser C, Brenna CTA, Szilagyi IS, Bornemann-Cimenti H. Palmitoylethanolamide in the treatment of chronic pain: a systematic review and meta-analysis of double-blind randomized controlled trials. Nutrients. 2023;15(6):1350. doi:10.3390/nu15061350. PMID 36986081.
Scope note: this page is written for business-to-business ingredient buyers and describes published research and specification practice. It is not consumer-directed marketing, not medical advice, and not a claim that any finished product diagnoses, treats, cures or prevents any disease. Citations are provided so readers can check the primary sources rather than take our summary of them on trust.