Name | Palmitoylethanolamide(PEA) |
Synonyms | Palmidrol PEA PALMIDROL PALMITYLETHANOLAMIDE PALMITOYLETHANOLAMIDE N-HEXADECANOYLETHANOLAMINE Palmitoylethanolamide(PEA) N-(2-HYDROXYETHYL)HEXADECANAMIDE n-(2-hydroxyethyl)-hexadecanamid PALMITOYLETHANOLAMIDE N-(2-HYDROXYETHYL)HEXADECANAMIDE |
CAS | 544-31-0 |
EINECS | 208-867-9 |
InChIKey | HXYVTAGFYLMHSO-UHFFFAOYSA-N |
Molecular Formula | C18H37NO2 |
Molar Mass | 299.49 |
Density | 0.910±0.06 g/cm3(Predicted) |
Melting Point | 97-98℃ |
Boling Point | 461.5±28.0 °C(Predicted) |
Water Solubility | 4.01mg/L at 20℃ |
Solubility | Soluble in DMSO (20 mM), ethanol (25 mM), chloroform, THF ( at 30 °C), and DMF (~10 |
Vapor Presure | 0.45Pa at 20℃ |
Appearance | White solid |
Color | White |
pKa | 14.49±0.10(Predicted) |
Storage Condition | -20°C |
Stability | Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 3 months. |
Sensitive | Sensitive to heat |
In vitro study | PEA can effectively prevent rat cerebellar granule cells from glutamate toxicity and enhance the motility of microglia. In the mitochondrial fragments of cells stimulated by PEA, the expression of steroid synthesis rapid regulator protein (StAR) and P450scc, which include some neurosteroid formation proteins, is increased. PEA also has protective effects, such as reducing malondialdehyde formation in cells treated with (S,R)-sulfoximine, the L-buthionine that causes glutathione deficiency. The effect of PEA can be partially inhibited by finasteride (5a-reductase inhibitor). |
In vivo study | PEA attenuated the inflammatory response in wild-type mice, but had no effect in ppar-α-deficient mice. PEA can inhibit peripheral inflammation, mast cell degranulation and exert neuroprotective and analgesic effects in mice and rats. At the same time, NO production, neutrophil influx, and expression of pro-inflammatory proteins such as inducible nitric oxide synthase and cyclooxygenase-2 are altered. In addition, PEA can regulate many physiological processes, including pain perception, seizures and neurotoxicity. |
WGK Germany | 2 |
RTECS | ML8950000 |
TSCA | Yes |
LogP | 3.989 at 20℃ |
EPA chemical substance information | information provided by: ofmpeb.epa.gov (external link) |
Overview | cetylcarboxamide ethanol (PEA) is an endogenous fatty acid amide that belongs to the class of nuclear factor agonists. It has been shown to bind to nuclear receptors (NRS) and exert a large variety of biological functions associated with chronic pain and inflammation. |
action | PEA has been shown to have anti-inflammatory, anti-nociceptive, neuroprotective, and anticonvulsant properties. PEA has been exploring various pain states in people in different clinical trials, on inflammation and pain syndromes. |
Application | hexadecyl amide ethanol is an intermediate in organic synthesis and pharmaceutical intermediates, which can be used in laboratory research and development process and chemical pharmaceutical research and development process. |
biological activity | Palmitoylethanolamide (PEA, Palmidrol, N-palmitoylethanolamine) is an endogenous fatty acid amide, it can selectively activate PPAR-α in vitro with an EC50 of 3.1±0.4 μm. |
Target | Value |
PPARα (In HeLa cells) | 3.1 μM(EC50) |