N-Arachidonoyl dopamine
Names | |
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IUPAC name
(5Z,8Z,11Z,14Z)-N-[2-(3,4-dihydroxyphenyl)-ethyl]icosa-5,8,11,14-tetraenamide
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Other names
NADA
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Identifiers | |
199875-69-9 | |
ChEMBL | ChEMBL138921 |
ChemSpider | 4445314 |
4261 | |
Jmol 3D model | Interactive image |
PubChem | 5282105 |
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Properties | |
C28H41NO3 | |
Molar mass | 439.63 g/mol |
Vapor pressure | {{{value}}} |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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verify (what is ?) | |
Infobox references | |
N-Arachidonoyl dopamine (NADA) is an endocannabinoid that acts as an agonist of the CB1 receptor and the transient receptor potential V1 (TRPV1) ion channel. NADA was first described as a putative endocannabinoid (agonist for the CB1 receptor) in 2000[1] and was subsequently identified as an endovanilloid (agonist for TRPV1) in 2002.[2] NADA is an endogenous arachidonic acid based lipid found in the brain of rats, with especially high concentrations in the hippocampus, cerebellum, and striatum.[2] It activates the TRPV1 channel with an EC50 of approximately of 50nM which makes it the putative endogenous TRPV1 agonist.[3]
In mice, NADA was shown to induce the tetrad of physiological paradigms associated with cannabinoids: hypothermia, hypo-locomotion, catalepsy, and analgesia.[1][4][5] NADA has been found to play a regulatory role in both the peripheral and central nervous systems, and displays antioxidant and neuroprotectant properties.[2][6][6][7][8] NADA has also been implicated in smooth muscle contraction and vasorelaxation in blood vessels.[9][10][11][12] Additionally, NADA has been observed to suppress inflammatory activation of human Jurkat T cells and to inhibit the release of prostaglandin E2 (PGE2) from lipopolysaccharide (LPS)-activated astrocytes, microglia and mouse brain ECs (MEC-Brain).[13][14][15] NADA also promotes the inflammatory resolution of human endothelial cells activated by both endogenous (i.e. TNF) and exogenous (i.e. bacterial derived LPS (TLR4 agonist) and FSL-1 (TLR2/6 agonist)) inflammatory mediators.[16] Furthermore, NADA also displays inhibitory activity in HIV-1 replication assays.[17] Finally, NADA can prevent the degranulation and release of TNF from RBL- 2H3 mast cells treated with an IgE-antigen complex.[18] Together, theses studies show that physiological functions attributed to NADA are multifaceted, and include the ability to modulate the immune response.
See also
References
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External links
- General information about NADA.