Palmitoylethanolamide
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| Names | |
|---|---|
| Preferred IUPAC name
N-(2-Hydroxyethyl)hexadecanamide[1] | |
Other names
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| Identifiers | |
3D model (JSmol) |
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| Abbreviations | PEA |
| ChEMBL | |
| ChemSpider | |
| ECHA InfoCard | 100.008.062 |
| EC Number |
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| KEGG | |
| MeSH | palmidrol |
PubChem CID |
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| UNII | |
CompTox Dashboard (EPA) |
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| 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 |
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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 (INN), is an endogenous fatty acid amide, and lipid modulator.[2]
PEA is not a classic endocannabinoid because it lacks affinity for the cannabinoid receptors CB1 and CB2.[3][better source needed]
Metabolism
[edit]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.[4]
Safety
[edit]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.[5] Another meta-analysis found that no serious ADRs occurred.[6]
See also
[edit]References
[edit]- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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. PMID 26815246.
Further reading
[edit]- Lambert DM, Vandevoorde S, Jonsson KO, Fowler CJ (March 2002). "The palmitoylethanolamide family: a new class of anti-inflammatory agents?". Current Medicinal Chemistry. 9 (6): 663–74. doi:10.2174/0929867023370707. PMID 11945130.
- Walker JM, Krey JF, Chu CJ, Huang SM (December 2002). "Endocannabinoids and related fatty acid derivatives in pain modulation". Chemistry and Physics of Lipids. 121 (1–2): 159–72. doi:10.1016/S0009-3084(02)00152-4. PMID 12505698.
- Darmani NA, Izzo AA, Degenhardt B, Valenti M, Scaglione G, Capasso R, et al. (June 2005). "Involvement of the cannabimimetic compound, N-palmitoyl-ethanolamine, in inflammatory and neuropathic conditions: review of the available pre-clinical data, and first human studies". Neuropharmacology. 48 (8): 1154–63. doi:10.1016/j.neuropharm.2005.01.001. PMID 15910891. S2CID 14828175.
- O'Sullivan SE (November 2007). "Cannabinoids go nuclear: evidence for activation of peroxisome proliferator-activated receptors". British Journal of Pharmacology. 152 (5): 576–82. doi:10.1038/sj.bjp.0707423. PMC 2190029. PMID 17704824.
- Godlewski G, Offertáler L, Wagner JA, Kunos G (September 2009). "Receptors for acylethanolamides-GPR55 and GPR119". Prostaglandins & Other Lipid Mediators. 89 (3–4): 105–11. doi:10.1016/j.prostaglandins.2009.07.001. PMC 2751869. PMID 19615459.
- Keppel Hesselink JM, de Boer T, Witkamp RF (2013). "Palmitoylethanolamide: A Natural Body-Own Anti-Inflammatory Agent, Effective and Safe against Influenza and Common Cold". International Journal of Inflammation. 2013 151028. doi:10.1155/2013/151028. PMC 3771453. PMID 24066256.
- Keppel Hesselink JM, Costagliola C, Fakhry J, Kopsky DJ (2015). "Palmitoylethanolamide, a Natural Retinoprotectant: Its Putative Relevance for the Treatment of Glaucoma and Diabetic Retinopathy". Journal of Ophthalmology. 2015 430596. doi:10.1155/2015/430596. PMC 4667059. PMID 26664738.
- Davis MP, Behm B, Mehta Z, Fernandez C (December 2019). "The Potential Benefits of Palmitoylethanolamide in Palliation: A Qualitative Systematic Review". The American Journal of Hospice & Palliative Care. 36 (12): 1134–1154. doi:10.1177/1049909119850807. PMID 31113223. S2CID 162169643.