N-arachidonoyl glycine

N-Arachidonylglycine

Names
IUPAC name (5Z,8Z,11Z,14Z)-N-Icosa-5,8,11,14-tetraenoylamino-acetic acid
Other names N-Arachidonylglycine Arachidonoyl glycine NA-glycine
Identifiers
CAS Number	179113-91-8 N
3D model (JSmol)	Interactive image Interactive image
Beilstein Reference	7652004
ChEBI	CHEBI:58961 Y
ChemSpider	4446510 Y
MeSH	Anandamide
PubChem CID	5283389
InChI Key: LGEQQWMQCRIYKG-DOFZRALJSA-N Y InChI=1/C22H37NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-22(25)23-20-21-24/h6-7,9-10,12-13,15-16,24H,2-5,8,11,14,17-21H2,1H3,(H,23,25)/b7-6-,10-9-,13-12-,16-15- Key: YLEARPUNMCCKMP-DOFZRALJSA-N InChI=1S/C22H35NO3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-21(24)23-20-22(25)26/h6-7,9-10,12-13,15-16H,2-5,8,11,14,17-20H2,1H3,(H,23,24)(H,25,26)/b7-6-,10-9-,13-12-,16-15-
SMILES O=C(NCC(=O)O)CCC\C=C/C\C=C/C\C=C/C\C=C/CCCCC O=C(NCC(=O)O)CCC\C=C/C\C=C/C\C=C/C\C=C/CCCCC
Properties
Chemical formula	C22H35NO3
Molar mass	361.53 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N  (what is YN ?)
Infobox references

N-Arachidonylglycine (NAGly) is a carboxylic analog of the endocannabinoid anandamide. Since it was first synthesized in 1996, NAGly has been a primary focus of the relatively contemporary field of lipidomics due to its wide range of signaling targets in the brain, the immune system and throughout various other bodily systems. In combination with 2‐arachidonoyl glycerol (2‐AG), NAGly has enabled the identification of a family of lipids often referred to as endocannabinoids. Recently, NAGly has been found to bind to G-protein coupled receptor 18 (GPR18), the putative abnormal cannabidiol receptor. NaGly is found throughout the body and research on its explicit functions is on going.

The exact biosynthesis of NaGly is not completely understood, but there are two proposed pathways found in vitro for its biosynthesis: 1) enzymatically regulated conjugation of arachidonic acid and glycine and 2) the oxidative metabolism of the endogenous cannabinoid anandamide. In the first pathway, Cytochrome c catalyzes the in vitro synthesis of NaGly from arachidonoyl coenzyme A and glycine in the presence of hydrogen peroxide. In the second pathway, alcohol dehydrogenase catalyzes the oxidation of anandamide into N-arachidonoyl glycine.

NAGly has been hypothesized to have a neurophysiological function of pain suppression, supported by evidence that it suppresses formalin-induced pain behavior in rats. In particular, peripherally administered NAGly inhibited phase 2 pain behavior, suggesting either a direct suppression of nociceptive afferents on the nerve or an indirect modulation of the afferents' interstitial environment. In either case, these findings hold promise for NAGly as a means of mitigating postoperative or chronic pain. NAGly is also effective in acute pain models, reducing mechanical allodynia and thermal hyperalgesia induced by intraplantar injection of Fruend's complete adjuvant. Similar mechanical allydonia induced by partial ligation of the sciatic nerve was also reduced by NaGly. Other arachidonic acid-amino acid conjugates did not have the same effects and the actions of NaGly were not affected by cannabinoid receptor agonists in either study, suggesting a novel non-cannabinoid receptor mediated approach to alleviate inflammatory pain.