Palmitoylethanolamide

Palmitoylethanolamide
Skeletal formula of palmitoylethanolamide
Skeletal formula of palmitoylethanolamide
Names
Preferred IUPAC name
N-(2-Hydroxyethyl)hexadecanamide
Other names
  • Hydroxyethylpalmitamide
  • Palmidrol
  • N-Palmitoylethanolamine
  • Palmitylethanolamide
Identifiers
3D model (JSmol)
Abbreviations PEA
ChEMBL
ChemSpider
ECHA InfoCard 100.008.062 Edit this at Wikidata
EC Number
  • 208-867-9
KEGG
MeSH palmidrol
UNII
  • InChI=1S/C18H37NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-18(21)19-16-17-20/h20H,2-17H2,1H3,(H,19,21) X markN
    Key: HXYVTAGFYLMHSO-UHFFFAOYSA-N X markN
  • CCCCCCCCCCCCCCCC(=O)NCCO
Properties
C18H37NO2
Molar mass 299.499 g·mol−1
Appearance White crystals
Density 910 mg mL−1
Melting point 93 to 98 °C (199 to 208 °F; 366 to 371 K)
log P 5.796
Hazards
Flash point 323.9 °C (615.0 °F; 597.0 K)
Related compounds
Related compounds
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Palmitoylethanolamide (PEA), also known as palmidrol (INNTooltip International Nonproprietary Name), is an endogenous fatty acid amide, and lipid modulator.

PEA is not a classic endocannabinoid because it lacks affinity for the cannabinoid receptors CB1 and CB2.[better source needed]

Metabolism

PEA is metabolized by the cellular enzymes fatty acid amide hydrolase (FAAH) and N-acylethanolamine acid amide hydrolase (NAAA), the latter of which has more specificity toward PEA over other fatty acid amides.

Safety

PEA is generally considered safe, and without adverse drug reactions (ADRs) or drug interactions. A 2016 meta‐analysis of PEA as an analgesic concluded that for treatment periods up to 49 days, there were no serious ADRs at an incidence of 1/200 or greater. Another meta-analysis found that no serious ADRs occurred.

See also

References

  1. ↑ NCBI-PubChem Staff (25 March 2005). "Compound Summary: Palmitoylethanolamide" (database entry). PubChem.NCBI.NLM.NIH.gov. Bethesda, MD: US NLM-National Center for Biotechnology Information (NCBI). Retrieved 26 February 2020.
  2. ↑ Petrosino S, Di Marzo V (2017). "The pharmacology of palmitoylethanolamide and first data on the therapeutic efficacy of some of its new formulations". British Journal of Pharmacology. 174 (11): 1349–1365. doi:10.1111/bph.13580. PMC 5429331. PMID 27539936.
  3. ↑ O'Sullivan SE, Kendall DA (August 2010). "Cannabinoid activation of peroxisome proliferator-activated receptors: potential for modulation of inflammatory disease". Immunobiology. 215 (8): 611–6. doi:10.1016/j.imbio.2009.09.007. PMID 19833407.
  4. ↑ Tsuboi K, Takezaki N, Ueda N (August 2007). "The N-acylethanolamine-hydrolyzing acid amidase (NAAA)". Chemistry & Biodiversity. 4 (8): 1914–25. doi:10.1002/cbdv.200790159. PMID 17712833. S2CID 32163665.
  5. ↑ Gabrielsson L, Mattsson S, Fowler CJ (October 2016). "Palmitoylethanolamide for the treatment of pain: pharmacokinetics, safety and efficacy". British Journal of Clinical Pharmacology. 82 (4): 932–42. doi:10.1111/bcp.13020. PMC 5094513. PMID 27220803.
  6. ↑ Paladini A, Fusco M, Cenacchi T, Schievano C, Piroli A, Varrassi G (February 2016). "Palmitoylethanolamide, a Special Food for Medical Purposes, in the Treatment of Chronic Pain: A Pooled Data Meta-analysis". Pain Physician. 19 (2): 11–24. doi:10.36076/ppj/2016.19.11. hdl:11697/104015. PMID 26815246.

Further reading