User:Þjarkur/Palmitoylethanolamide
Chemical compound / From Wikipedia, the free encyclopedia
Palmitoylethanolamide (PEA, palmitoyl-ethanol-amide) is a saturated fatty acid[2] that is produced by the human body and targets non-classical cannabinoid receptors.[2] It can be found in various sources such as egg yolk and peanut meal.[2] It is a biologically active dietary supplement that has an anti-inflammatory and analgesic effect.[2][3]
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Names | |
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IUPAC name
N-(2-Hydroxyethyl)hexadecanamide[1] | |
Other names
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Identifiers | |
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3D model (JSmol) |
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Abbreviations | PEA |
ChEMBL | |
ChemSpider |
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EC Number |
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KEGG |
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MeSH | palmidrol |
PubChem CID |
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UNII | |
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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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PEA was first isolated in 1957, it was promoted as a biologically active dietary supplement that could treat influenza and the common cold[2][3] along with having an anti-inflammatory effect,[3] but interest in the compound waned around the 1980s.[3]
A main target of PEA is proposed to be the peroxisome proliferator-activated receptor alpha (PPAR-α).[4][5] PEA also has affinity to cannabinoid-like G-coupled receptors GPR55 and GPR119.[6] PEA cannot strictly be considered a classic endocannabinoid because it lacks affinity for the cannabinoid receptors CB1 and CB2.[7] However, primary research supports the conclusion that the presence of PEA (or other structurally related N-acylethanolamines) enhances anandamide activity by an "entourage effect".[8][9][non-primary source needed]
Some primary research reports support the conclusion that PEA levels are altered and that the endocannabinoid system (ECS) is "imbalanced" in acute and chronic inflammation.[10][non-primary source needed]