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From the body

PEAPalmitoylethanolamide

An endogenous N-acylethanolamine with no notable direct affinity for CB1/CB2; a PPAR-α agonist (Lo Verme et al. 2005).

Unscheduled
Level of detail

C₁₈H₃₇NO₂

CAS 544-31-0

Family
Endocannabinoid or related mediatorEndocannabinoidome
First described
1957
Molar mass
299.49 g/mol

Updated on

In plain terms

PEA is a lipid the body makes naturally, from the same family as anandamide, and it is also found in foods. It barely binds the cannabinoid receptors CB1 and CB2. It acts mainly on a receptor in the cell nucleus called PPAR-α.

Receptors and activity

Target network

GPR55Agonistno measured value
  • Activates
  • Binds or modulates

The lower the cited value, the closer the target sits to PEA: one ring per factor of 100. A target with no measured value stays on the edge.

Where these targets live

Where each target has been found in humans, according to the cited studies. The map shows the target, not an effect of PEA.

Brain, side view
Body, front view
Blood

GPR55GPR55 found in 4 regions of the body

  1. Basal gangliapresentmRNA found in the caudate nucleus and putamen1
  2. BonepresentOsteoclasts and osteoblasts2
  3. Adipose tissuepresentExpressed in visceral adipose tissue3
  4. LiverpresentExpressed in the liver3

Map sources

  1. Sawzdargo M et al. Identification and cloning of three novel human G protein-coupled receptor genes GPR52, PsiGPR53 and GPR55: GPR55 is extensively expressed in human brain. Brain Res Mol Brain Res, 1999 (new tab)
  2. Whyte LS et al. The putative cannabinoid receptor GPR55 affects osteoclast function in vitro and bone mass in vivo. Proc Natl Acad Sci U S A, 2009 (new tab)
  3. Moreno-Navarrete JM et al. The L-α-lysophosphatidylinositol/GPR55 system and its potential role in human obesity. Diabetes, 2012 (new tab)

Cited values

  1. PPARαAgonistEC50 = 3.1 µM · not specified25 out of 100

    Lo Verme et al. 2005, Mol Pharmacol 67:15 (PPAR-α, EC50 3.1 µM) (new tab) · selective transactivation of PPAR-α in vitro

  2. GPR55Agonistno measured value cited
  3. TRPV1Modulatorno measured value cited
Bar length follows the measured value (Ki, Kd, EC50 or IC50), on one scale shared by every entry, from 100 µM to 0.1 nM. A target with no cited value has no bar.

Pharmacology

Palmitoylethanolamide (palmidrol) was identified in 1957 as a naturally occurring anti-inflammatory factor in animal models (Kuehl et al., J Am Chem Soc 79:5577), from lipid fractions of egg yolk, soybean and peanut (Petrosino & Di Marzo 2017). Like the other N-acylethanolamines, it is formed from a membrane phospholipid, N-palmitoyl-phosphatidylethanolamine, notably by NAPE-PLD (Okamoto et al. 2004), and then hydrolysed into palmitic acid and ethanolamine by FAAH or NAAA. It is not an endocannabinoid in the IUPHAR sense: first taken for a CB2 ligand, it has only very weak affinity for that receptor (Petrosino & Di Marzo 2017) and was inactive at the CB2 receptor of HL-60 cells (Sugiura et al. 2000). It selectively activates PPAR-α in vitro (EC50 3.1 µM), and its effect in two mouse oedema models disappears in animals lacking PPAR-α (Lo Verme et al. 2005). Its activation of GPR55 was reported in a [35S]GTPγS assay (Pertwee et al. 2010) but remains debated. In cells expressing human TRPV1, it enhanced the effect of anandamide, a form of “entourage effect” (De Petrocellis et al. 2001). A meta-analysis of double-blind randomised trials in chronic pain (774 patients in total) reported lower pain scores with PEA than with comparators (Lang-Illievich et al. 2023).

Key sources.

History

Source
Endogenous (endocannabinoidome mediator); also present in plant and animal foods

Biosynthetic pathway

In vivo

Formed from membrane N-palmitoyl-phosphatidylethanolamine, notably by NAPE-PLD (Okamoto et al. 2004); hydrolysed into palmitic acid and ethanolamine by FAAH or NAAA (Petrosino & Di Marzo 2017)

Classification

Family, origin and source verification

Family

Endocannabinoid or related mediator › Endocannabinoidome

Chemistry

Saturated N-acylethanolamine (NAE 16:0)

Verification

Every fact on this entry was checked against its primary sources on 20 October 2026.

Wikipedia (English)

Palmitoylethanolamide (new tab)

Article paired by the molecule's structure (InChIKey), revision read on 19 October 2026. Read as a second opinion, never cited as a source.

References

  1. Kuehl et al. 1957, J Am Chem Soc 79:5577 (identification as a natural anti-inflammatory factor) (new tab)DOI 10.1021/ja01577a066
  2. Petrosino & Di Marzo 2017, Br J Pharmacol 174:1349 (pharmacology review) (new tab)PMID 27539936
  3. Lo Verme et al. 2005, Mol Pharmacol 67:15 (PPAR-α, EC50 3.1 µM) (new tab)PMID 15465922
  4. Sugiura et al. 2000, J Biol Chem 275:605 (inactive at CB2, HL-60 cells) (new tab)PMID 10617657
  5. De Petrocellis, Davis & Di Marzo 2001, FEBS Lett (potentiation of anandamide at human TRPV1) (new tab)PMID 11602256
  6. Lang-Illievich et al. 2023, Nutrients 15:1350 (meta-analysis of double-blind trials, chronic pain) (new tab)PMID 36986081

Identifiers

Names

Common name
Palmitoylethanolamide
Other names
Palmidrol

Identifiers

Formula
C₁₈H₃₇NO₂
CAS
544-31-0
PubChem CID
4671(new tab)
ChEBI
CHEBI:71464(new tab)
InChIKey
HXYVTAGFYLMHSO-UHFFFAOYSA-N
SMILES
CCCCCCCCCCCCCCCC(=O)NCCO

Machine-readable entry (JSON)

LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.