(±)11(12)-<wbr/>EET Ethanolamide

(±)11(12)-EET Ethanolamide

CAT N°: 10008598
Price:

From 134.00 113.90

Arachidonoyl ethanolamide (AEA; anandamide) is an endogenous lipid neurotransmitter with cannibingeric activity, binding to both the central cannabinoid (CB1) and peripheral cannabinoid (CB2) receptors.{2713,14062} Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the hydrolysis and inactivation of AEA.{13132} Metabolism of AEA by cyclooxygenase-2, leading to formation of prostaglandin ethanolamides, and by lipoxygenases has also been documented.{12168} (±)11(12)-EET ethanolamide is a potential cytochrome P450 (CYP450) metabolite of AEA, although specific stereochemistry rather than a racemic mixture would likely ensue from enzymatic metabolism. CYP450 metabolism of AEA may be particularly relevant under conditions of FAAH inhibition. Evidence for the formation of (±)11(12)-EET ethanolamide in vivo has not been documented.

Territorial Availability: Available through Bertin Technologies only in France

  • Synonyms
    • N-(2-hydroxyethyl)-(±)11(12)-epoxy-5Z,8Z,14Z-eicosatrienamide
  • Correlated keywords
    • AEA endocannabinoids Arachidonoyl ethanolamides CYP450 cytochromes metabolism neurochemistry anxiety depression 14,15-EET 14,15-EpETrE 14,15-EET-EA 14,15-EET-ethanolamide 14,15-epetre-ea 14,15-ethanolamide anandamides lipids neurotransmitters cannabinergic cannabinoids CBs FAAH inhibitor fatty acids hydrolases cbs synthetic
  • Product Overview:
    Arachidonoyl ethanolamide (AEA; anandamide) is an endogenous lipid neurotransmitter with cannibingeric activity, binding to both the central cannabinoid (CB1) and peripheral cannabinoid (CB2) receptors.{2713,14062} Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the hydrolysis and inactivation of AEA.{13132} Metabolism of AEA by cyclooxygenase-2, leading to formation of prostaglandin ethanolamides, and by lipoxygenases has also been documented.{12168} (±)11(12)-EET ethanolamide is a potential cytochrome P450 (CYP450) metabolite of AEA, although specific stereochemistry rather than a racemic mixture would likely ensue from enzymatic metabolism. CYP450 metabolism of AEA may be particularly relevant under conditions of FAAH inhibition. Evidence for the formation of (±)11(12)-EET ethanolamide in vivo has not been documented.

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