{"id":550,"date":"2022-10-13T11:20:42","date_gmt":"2022-10-13T09:20:42","guid":{"rendered":"https:\/\/modafinil.pl\/sklep\/palmitoylethanolamide-pea-%e2%89%a5-99-1000mg\/"},"modified":"2026-10-06T13:20:39","modified_gmt":"2026-10-06T11:20:39","slug":"palmitoylethanolamide-2","status":"publish","type":"product","link":"https:\/\/modafinil.pl\/en\/sklep\/palmitoylethanolamide-2\/","title":{"rendered":"Palmitoylethanolamide \/ PEA (CAS 544-31-0) \u2014 laboratory reagent 1000 mg, purity \u2265 99%"},"content":{"rendered":"

N-(2-hydroxyethyl)hexadecanamide<\/strong> (palmitoylethanolamide, PEA), crystalline powder, 1000 mg pack. Material intended exclusively for laboratory and analytical in vitro research<\/strong>. This product is not intended for human or animal consumption<\/strong>; it is not a medicinal product, food supplement, foodstuff or cosmetic.<\/p>\n

Three different entities that must not be confused<\/h2>\n

For this molecule, separating the layers calls for a different approach than for substances registered as medicines. Palmitoylethanolamide has never obtained registration as a medicinal product in any country<\/strong> \u2014 it is, however, marketed under a different regulatory regime, as a food for special medical purposes or a food supplement. This difference is a source of misunderstanding as often as with medicinal substances, which is why we separate the layers just as carefully:<\/p>\n\n\n\n\n\n\n\n
Separating the layers: substance \u2014 commercial product \u2014 reagent<\/caption>\n
Entity<\/th>\nWhat it is<\/th>\nStatus<\/th>\n<\/tr>\n<\/thead>\n
Chemical substance
palmitoylethanolamide (PEA), CAS 544-31-0<\/th>\n		A chemical concept \u2014 an N-acylethanolamine of defined structure, originally identified as a natural constituent of dietary fats. In itself it is neither a food product nor a reagent \u2014 its status is conferred only by the form in which it has been manufactured.<\/td>\n\u2014<\/td>\n<\/tr>\n
Commercial product
food for special medical purposes \/ food supplement<\/th>\n		Micronised or ultramicronised PEA preparations with a defined particle size, manufactured under the producer\u2019s supervision, with product documentation. In Italy classified explicitly as a \u201cfood for special medical purposes\u201d [14<\/a>], in other countries offered as a food supplement or functional ingredient under trade names (including Levagen). PEA has never obtained the status of a medicinal product<\/strong>.<\/td>\nthis entity was the subject of the clinical studies and human safety studies<\/strong> cited below<\/td>\n<\/tr>\n
Chemical reagent
material offered here<\/th>\n		Material for laboratory and analytical work \u2014 raw crystalline powder, not micronised, without food-product or supplement documentation. It does not have, and cannot have, authorisation for use in humans or animals.<\/strong><\/td>\nanalytics, chemistry, reference standards<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

The consequence is unambiguous.<\/strong> The study results cited further on this page were obtained either using finished commercial preparations<\/strong> (micronised or ultramicronised PEA, in clinical and observational studies involving humans) or using the substance administered to laboratory animals or cell cultures under controlled experimental conditions<\/strong> (preclinical studies). None of these studies was conducted using the analytical reagent<\/strong>, and none of their results transfers to the material offered. The reagent is not a form in which the substance has ever been studied in humans, and it cannot be used in such a way.<\/p>\n

Reagent identification sheet<\/h2>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
Registry data and identifiers \u2014 palmitoylethanolamide<\/caption>\n
Systematic name (IUPAC)<\/th>\nN-(2-hydroxyethyl)hexadecanamide<\/td>\n<\/tr>\n
Common name<\/th>\npalmitoylethanolamide (PEA, Palmidrol)<\/td>\n<\/tr>\n
CAS number<\/th>\n544-31-0<\/td>\n<\/tr>\n
Molecular formula<\/th>\nC18<\/sub>H37<\/sub>NO2<\/sub><\/td>\n<\/tr>\n
Molar mass<\/th>\n299.5 g\u00b7mol\u22121<\/sup><\/td>\n<\/tr>\n
Monoisotopic mass<\/th>\n299.2824 Da<\/td>\n<\/tr>\n
Melting point<\/th>\n98.5 \u00b0C<\/td>\n<\/tr>\n
InChIKey<\/th>\nHXYVTAGFYLMHSO-UHFFFAOYSA-N<\/td>\n<\/tr>\n
SMILES<\/th>\nCCCCCCCCCCCCCCCC(=O)NCCO<\/td>\n<\/tr>\n
PubChem CID<\/th>\n4671<\/a><\/td>\n<\/tr>\n
ChEMBL<\/th>\nCHEMBL3986110<\/a><\/td>\n<\/tr>\n
Form<\/th>\ncrystalline powder, white to off-white<\/td>\n<\/tr>\n
Packaging<\/th>\nsealed aluminium zip-lock bag<\/td>\n<\/tr>\n
Purity<\/th>\n\u2265 99%<\/td>\n<\/tr>\n
Intended use<\/th>\nresearch reagent \u2014 not for human or animal consumption<\/strong><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Lineage of the molecule: from egg-yolk fat to a nuclear receptor ligand<\/h2>\n

Palmitoylethanolamide has an unusual lineage for a molecule with such an extensive modern literature \u2014 it did not originate in a medicinal chemistry laboratory, but was isolated from natural dietary fats long before any model of its action existed.<\/p>\n

Discovery in dietary fats<\/h3>\n

The compound was identified in the mid-1950s as a naturally occurring factor with anti-inflammatory activity, present among other sources in hen\u2019s egg yolk. For the following decades it remained a biochemical curiosity: an effect was observed, but there was no method allowing it to be linked to a specific molecular target \u2014 mass spectrometry and molecular receptor pharmacology, which make this possible today, did not yet exist in laboratory practice.<\/p>\n

From an \u201canti-inflammatory factor\u201d to a nuclear receptor ligand<\/h3>\n

The breakthrough came in the 1990s, when it was shown that the compound limits oedema and inflammatory hypersensitivity after oral administration in laboratory animals, by inhibiting mast cell activation [1<\/a>]. The natural question was whether the mechanism had anything in common with the cannabinoid system being discovered in the same period and its endogenous ligand, anandamide. The answer proved complex: PEA does not bind directly<\/strong> to CB1 or CB2 receptors [2<\/a>], but enhances the action of anandamide by a separate mechanism, described as the \u201centourage effect\u201d [3<\/a>][4<\/a>]. Only in 2005 was the nuclear receptor PPAR-\u03b1 identified as the actual molecular target mediating the compound\u2019s anti-inflammatory action [5<\/a>][6<\/a>], which shifted the whole line of research from cannabinoid pharmacology to nuclear receptor pharmacology.<\/p>\n

Timeline<\/h2>\n\n\n\n\n\n\n\n\n\n\n\n\n\n
Timeline: from isolation from egg yolk to contemporary clinical studies<\/caption>\n
1950s<\/th>\nidentification of N-(2-hydroxyethyl)hexadecanamide as a naturally occurring anti-inflammatory factor, isolated among other sources from hen\u2019s egg yolk<\/td>\n<\/tr>\n
1960s\u20131980s<\/th>\na period of limited interest \u2014 no identified mechanism of action<\/td>\n<\/tr>\n
1993\u20131996<\/th>\ndemonstration of the compound\u2019s inhibitory effect on mast cell activation and of its anti-inflammatory activity after oral administration in laboratory animals [1<\/a>]<\/td>\n<\/tr>\n
1999<\/th>\nthe question of a cannabimimetic mechanism of PEA raised in view of the absence of CB1\/CB2 receptor binding [2<\/a>]<\/td>\n<\/tr>\n
2001\u20132002<\/th>\ndescription of the \u201centourage effect\u201d \u2014 enhancement of anandamide\u2019s action by PEA without direct cannabinoid receptor binding [3<\/a>][4<\/a>]<\/td>\n<\/tr>\n
2005<\/th>\nidentification of the nuclear receptor PPAR-\u03b1 as the molecular target mediating the anti-inflammatory action [5<\/a>][6<\/a>]<\/td>\n<\/tr>\n
2006<\/th>\ndescription of two distinct polymorphic crystal forms of PEA [8<\/a>]<\/td>\n<\/tr>\n
2014<\/th>\ndemonstration of the higher oral efficacy of the micronised form over the non-micronised form in an animal model of inflammatory pain [13<\/a>]<\/td>\n<\/tr>\n
2016<\/th>\nfirst pooled meta-analysis of clinical data classifying micronised PEA as a food for special medical purposes [14<\/a>]<\/td>\n<\/tr>\n
2017<\/th>\ntoxicological study of micronised PEA \u2014 mutagenicity, cytotoxicity, acute and subchronic toxicity in animals [15<\/a>]<\/td>\n<\/tr>\n
2023<\/th>\nmeta-analysis of double-blind randomised trials of PEA in chronic pain [18<\/a>] and a review comparing the mechanism of PEA with cannabidiol [17<\/a>]<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Research centres and context<\/h2>\n

The literature on PEA is more geographically dispersed than for substances with a single originating centre, but three recurring clusters can be identified in it:<\/p>\n