N-Arachidonoyl dopamine

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N-Arachidonoyl dopamine
N-Arachidonoyl dopamine.svg
IUPAC name
Other names
199875-69-9 N
ChEMBL ChEMBL138921 YesY
ChemSpider 4445314 YesY
Jmol interactive 3D Image
PubChem 5282105
Molar mass 439.63 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Infobox references

N-Arachidonoyl dopamine (NADA) is an endocannabinoid that acts as an agonist of the CB1 receptor[1] and the transient receptor potential V1 (TRPV1) ion channel. Its discovery was described in 2002 by an academic research group from Italy and the USA. It was found in the brain of rats, with especially high concentrations in the hippocampus, cerebellum, and striatum. It activates the TRPV1 channel with an EC50 of approximately of 50nM. The high potency makes it the putative endogenous TRPV1 agonist.[2]

Several cytochrome P450 endoplasmic reticulum-bound enzymes, i.e. CYP4A11, CYP4F2, CYP4F3, CYP4Z1, and CYP2U1 in humans,[3][4][5][6][7][8] Cyp4a12a and Cyp4a12b ins mice,[9] and Cyp4a1, Cyp4a2, Cyp4a3, and Cyp4a8 in rats[3] ω-hydroxylate arachidonic acid to form 20-hydroxyeicosatetraenoic acid (20-HETE) and lesser amounts of 19-hydroxyeicosatetraenoate (19-HETE) (see 20-Hydroxyeicosatetraenoic acid). Rat liver endoplasmic reticulum (i.e. microsome) preparations hydroxylated MADA to 20-hydroxy and lesser amounts of 19-hydroxy arachidonoyl dopamine products; both metabolites as well as 18-hydroxy arachidonoyl dopamine stimulated recombinant human TRPV(1) receptors, being about 10-fold less potent than NADA in doing so.[10] These results identify a variety of metabolically modified NADA's as potential TRPV1 agonists and suggest that one or more of the cited cytochrome P450 enzymes may be involved in inactivating NADA.

See also[edit]


  1. ^ Ralevic V (July 2003). "Cannabinoid modulation of peripheral autonomic and sensory neurotransmission". European Journal of Pharmacology 472 (1–2): 1–21. doi:10.1016/S0014-2999(03)01813-2. PMID 12860468. 
  2. ^ Huang SM, Bisogno T, Trevisani M, Al-Hayani A, De Petrocellis L, Fezza F, Tognetto M, Petros TJ, Krey JF, Chu CJ, Miller JD, Davies SN, Geppetti P, Walker JM, Di Marzo V (June 2002). "An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors". Proceedings of the National Academy of Sciences of the United States of America 99 (12): 8400–5. doi:10.1073/pnas.122196999. PMC 123079. PMID 12060783. 
  3. ^ a b Hoopes SL, Garcia V, Edin ML, Schwartzman ML, Zeldin DC (Jul 2015). "Vascular actions of 20-HETE". Prostaglandins & Other Lipid Mediators 120: 9–16. doi:10.1016/j.prostaglandins.2015.03.002. PMID 25813407. 
  4. ^ Curr Top Med Chem. 2013;13(12):1429-40.
  5. ^ Cardiol Rev. 2014 Jan-Feb;22(1):1-12. doi: 10.1097/CRD.0b013e3182961659. Review
  6. ^ Toxicol Appl Pharmacol. 2012 Oct 1;264(1):73-83. doi: 10.1016/j.taap.2012.07.019
  7. ^ Prostaglandins Leukot Essent Fatty Acids. 2010 Aug;83(2):105-10. doi: 10.1016/j.plefa.2010.06.005
  8. ^ Alcohol Clin Exp Res. 2015 May;39(5):790-7. doi: 10.1111/acer.12697
  9. ^ Prostaglandins Other Lipid Mediat. 2015 Jul;120:40-9. doi:10.1016/j.prostaglandins.2015.05.004
  10. ^ Prostaglandins Other Lipid Mediat. 2009 Jan;88(1-2):10-7. doi: 10.1016/j.prostaglandins.2008.08.004

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