536697-79-7

Basic information

• Product Name: O-1918
• Synonyms: 1,3-DIMETHOXY-5-METHYL-2-[(1R,6R)-3-METHYL-6-(1-METHYLETHENYL)-2-CYCLOHEXEN-1-YL]-BENZENE;O-1918
• CAS NO: 536697-79-7
• Molecular Formula: C19H26O2
• Molecular Weight: 286.41
• Mol File: 536697-79-7.mol
• Article Data: 2

Chemical Properties

• Boiling Point: 383.9 °C at 760 mmHg
• Flash Point: 134.6 °C
• Appearance: /
• Density: 0.981 g/cm³
• Vapor Pressure: 9.38E-06mmHg at 25°C
• Refractive Index: 1.515
• Storage Temp.: Store at -20°C
• CAS DataBase Reference: O-1918(CAS DataBase Reference)
• NIST Chemistry Reference: O-1918(536697-79-7)
• EPA Substance Registry System: O-1918(536697-79-7)

Safety Data

• Hazardous Substances Data: 536697-79-7(Hazardous Substances Data)

Usage

Uses

O-1918 is a cannabidiol analog and a selective antagonist at the endothelial cannabidiol receptor. It is an inhibitor of GPR18. O-1918 can also induce endothelium-dependent vasodilation.

Biological Activity

Selective, silent antagonist of a putative endothelial anandamide receptor distinct from CB 1 or CB 2 receptors. Inhibits vasodilation and cell migration induced by abnormal-cannabidiol (abn-CBD; 4-[(1R,6R)-3-Methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl]-5-pentyl-1,3-benzenediol).

Enzyme inhibitor

This endocannabinoid antagonist (FW = 286.42 g/mol; CAS 536697-79-7), systematically named 1,3-dimethoxy-5-methyl-2-[(1R,6R)-3-methyl-6-(1- methylethenyl)-2-cyclohexen-1-yl]benzene, is a cannabidinodiol analogue that selectively targets a putative G-coupled endothelial anandamide receptor that is distinct from CB1 or CB2 endocannabinoid receptors. O- 1918 does not bind to CB1 or CB2 receptors and does not cause vasorelaxation at concentrations up to 30 μM, but inhibits the vasorelaxant effects of abn-cbd and anandamide in a concentration-dependent manner (1- 30 μM). (See abn-cbd; Anandamide; Oleamide). While the atypical cannabinoids O-1602 and abn-cbd (or abnormal cannabidiol) stimulate GPR55-dependent GTPgS activity (EC50 ~ 2 nM), O-1918 antagonizes such effects. O-1918 is involved in the delayed hypotension induced by anandamide in anaesthetized rats.

InChI:InChI=1/C19H26O2/c1-12(2)15-8-7-13(3)9-16(15)19-17(20-5)10-14(4)11-18(19)21-6/h9-11,15-16H,1,7-8H2,2-6H3/t15-,16+/m0/s1

Upstream product

• 22771-44-4 (+)-p-mentha-2,8-dien-1-ol 
• 500-66-3 Olivetol 
• 35482-50-9 O 1821 
• 74-88-4 methyl iodide 

Relevant articles and documents

Selective ligands and cellular effectors of a G protein-coupled endothelial cannabinoid receptor

The cannabinoid analog abnormal cannabidiol [abn-cbd; (-)-4-(3-3,4-trans-p-menthadien-[1,8]-yl)-olivetol] does not bind to CB1 or CB2 receptors, yet it acts as a full agonist in relaxing rat isolated mesenteric artery segments. Vasorelaxation by abn-cbd is endothelium-dependent, pertussis toxin-sensitive, and is inhibited by the BKca channel inhibitor charybdotoxin, but not by the nitric-oxide synthase inhibitor Nω-nitro-L-arginine methyl ester or by the vanilloid VR1 receptor antagonist capsazepine. The cannabidiol analog O-1918 does not bind to CB1 or CB2 receptors and does not cause vasorelaxation at concentrations up to 30 μM, but it does cause concentration-dependent (1-30 μM) inhibition of the vasorelaxant effects of abn-cbd and anandamide. In anesthetized mice, O-1918 dose-dependently inhibits the hypotensive effect of abn-cbd but not the hypotensive effect of the CB1 receptor agonist (-)-11-Δ9-tetrahydro-cannabinol dimethylheptyl. In human umbilical vein endothelial cells, abn-cbd induces phosphorylation of p42/44 mitogen-activated protein kinase and protein kinase B/Akt, which is inhibited by O-1918, by pertussis toxin or by phosphatidylinositol 3 (PI3) kinase inhibitors. These findings indicate that abn-cbd is a selective agonist and that O-1918 is a selective, silent antagonist of an endothelial anandamide receptor , which is distinct from CB1 or CB2 receptors and is coupled through Gi/Go to the PI3 kinase/Akt signaling pathway.