Stereochemistry | ACHIRAL |
Molecular Formula | C18H37NO2 |
Molecular Weight | 299.4919 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCCCCCCCCCCCCCC(=O)NCCO
InChI
InChIKey=HXYVTAGFYLMHSO-UHFFFAOYSA-N
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)
Molecular Formula | C18H37NO2 |
Molecular Weight | 299.4919 |
Charge | 0 |
Count |
MOL RATIO
1 MOL RATIO (average) |
Stereochemistry | ACHIRAL |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Optical Activity | NONE |
Palmidrol (palmitoylethanolamide, PEA) is a natural fatty acid amide found in a variety of foods, which was initially identified in egg yolk. It is an endogenous compound, locally synthesized in animal and human tissues and body fluids, to protect against perturbing inflammation. In addition to its anti-inflammatory activity, palmidrol (palmitoylethanolamide, PEA) also produces analgesia, neuroprotection, and possesses anti-epileptic properties. It also reduces gastrointestinal motility and cancer cell proliferation, as well as protecting the vascular endothelium in the ischemic heart. The physiological stimuli that regulate palmidrol (palmitoylethanolamide, PEA) levels in mammalian tissues are largely unknown, however, multiple studies indicate that this lipid accumulates during cellular stress, particularly following tissue injury. Palmidrol (palmitoylethanolamide, PEA) is a potent and selective agonist of orphan receptor GPR55.
CNS Activity
Originator
Approval Year
PubMed
Patents
Sample Use Guides
Ultra-micronized palmitoylethanolamide 600 mg twice daily.
Route of Administration:
Oral
Palmitoylethanolamide (PEA) potently enhances the anti-proliferative effects of arachidonoylethanolamide (AEA) on human breast cancer cells (HBCCs), in part by inhibiting the expression of fatty acid amide hydrolase (FAAH), the major enzyme catalyzing AEA degradation. PEA (1-10 microM) enhanced in a dose-related manner the inhibitory effect of AEA on both basal and nerve growth factor (NGF)-induced HBCC proliferation, without inducing any cytostatic effect by itself. PEA (5 microM) decreased the IC50 values for AEA inhibitory effects by 3-6-fold. The effect of PEA was due in part to inhibition of AEA degradation, since treatment of MCF-7 breast cancer cells with 5 microM PEA caused an approximately 30-40% down-regulation of FAAH expression and activity.