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| Names | |
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| IUPAC name 2-O-[(5Z,8Z,11Z,14Z)-Icosa-5,8,11,14-tetrae-1-yl]glycerol | |
| Systematic IUPAC name 2-{[(5Z,8Z,11Z,14Z)-Icosa-5,8,11,14-tetraen-1-yl]oxy}propane-1,3-diol | |
| Other names 2-AGE, 2-arachidonylglyceryl ether, Noladin ether, Noladin, HU-310 | |
| Identifiers | |
3D model (JSmol) | |
| ChEBI | |
| ChEMBL | |
| ChemSpider |
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| UNII | |
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| Properties | |
| C23H40O3 | |
| Molar mass | 364.56 g/mol |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
2-Arachidonyl glyceryl ether (2-AGE,Noladin ether,HU-310) is a putativeendocannabinoid discovered byLumír Hanuš and colleagues at theHebrew University of Jerusalem. It is anether formed from thealcohol analog ofarachidonic acid andglycerol. Its isolation fromporcine brain and its structural elucidation and synthesis were described in 2001.[1]
Lumír Hanuš, Saleh Abu-Lafi, Ester Fride, Aviva Breuer, Zvi Vogel, Deborah E. Shalev, Irina Kustanovich, andRaphael Mechoulam found the endogenousagonist of thecannabinoid receptor type 1 (CB1) in 2000. The discovery was 100 gram of porcine brain, (approximately a single brain) was added to a mixture of 200 mL ofchloroform and 200 mL ofmethanol and mixed in alaboratoryblender for 2 minutes. 100 mL of Water was then added, and the mixing process continued for another minute. After this, the mixture was filtered. Two layers then formed and the layer of water-methanol was separated and evaporated whenpressure was reduced. Synaptosomal membranes were prepared from 250g of the brains of Sabra male rats. AHewlett Packard G 1800B GCD system that has a HP-5971 GC withelectron ionization detector was used.[1]
The production of the endocannabinoid is enhanced in normal, but not inendothelium-denuded rat aorta on reacting withcarbachol, aparasympathomimetic drug. It potently reducesblood pressure inrats and may represent anendothelium-derivedhypotension factor.[1]
2-Arachidonyl glyceryl ether's structure can be determined bymass spectrometry andRutherford backscattering spectrometry. It was confirmed by comparison with asynthetic sample of theendocannabinoid. It binds to theCannabinoid receptor type 1 (Ki = 21.2 ± 0.5 nM), which causessedation,hypothermia, intestinalimmobility, and mild antinociception inmice.[1] The endocannabinoid exhibits Ki values of 21.2 nM and >3 μM at the Cannabinoid receptor type 1 and the peripheral cannabinoid receptors.[2]
The presence of 2-AGE in body tissue is disputed. Although a research group fromTeikyo University,Kanagawa, Japan could not detect it in the brains of mice, hamsters, guinea-pigs or pigs,[3] two other research groups successfully detected it in animal tissues.[4][5]
2-AGE binds with a Ki of 21 nM to theCB1 receptor[1] and 480 nM to theCB2 receptor.[6] It shows agonistic behaviour on both receptors and is a partial agonist for theTRPV1 channel.[7] After binding to CB2 receptors it inhibitsadenylate cyclase and stimulatesERK-MAPK and regulates calcium transients.[8] In comparison to2-arachidonoyl glycerol, noladin is metabolically more stable resulting in a longer half-life.[9] It lowersIntraocular pressure,[9] increases the uptake ofGABA in theglobus pallidus of rats[10] and is neuroprotective by binding to and activation ofPPARα.[11]
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