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Details

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
Structure of PALMIDROL

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)

HIDE SMILES / InChI

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

Description

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

Targets

Primary TargetPharmacologyConditionPotency
3.1 µM [EC50]
4.0 nM [EC50]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Palliative
Unknown

PubMed

Sample Use Guides

In Vivo Use Guide
Ultra-micronized palmitoylethanolamide 600 mg twice daily.
Route of Administration: Oral
In Vitro Use Guide
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.
Substance Class Chemical
Record UNII
6R8T1UDM3V
Record Status Validated (UNII)
Record Version