893736-89-5

Basic information

• Product Name: 3'-(BENZYLOXY)[1,1'-BIPHENYL]-3-CARBONITRILE
• Synonyms: AKOS BAR-1033;3'-(BENZYLOXY)[1,1'-BIPHENYL]-3-CARBONITRILE;3-[3-(Benzyloxy)phenyl]benzonitrile
• CAS NO: 893736-89-5
• Molecular Formula: C₂₀H₁₅NO
• Molecular Weight: 285.34
• Mol File: 893736-89-5.mol
• Article Data: 3

Chemical Properties

• Boiling Point: 461.2±33.0 °C(Predicted)
• Appearance: /
• Density: 1.17±0.1 g/cm3(Predicted)
• CAS DataBase Reference: 3'-(BENZYLOXY)[1,1'-BIPHENYL]-3-CARBONITRILE(CAS DataBase Reference)
• NIST Chemistry Reference: 3'-(BENZYLOXY)[1,1'-BIPHENYL]-3-CARBONITRILE(893736-89-5)
• EPA Substance Registry System: 3'-(BENZYLOXY)[1,1'-BIPHENYL]-3-CARBONITRILE(893736-89-5)

Safety Data

• Hazardous Substances Data: 893736-89-5(Hazardous Substances Data)

Upstream product

• 53087-13-1 3-(benzyloxy)phenyl bromide 
• 150255-96-2 (3‐cyanophenyl)boronic acid 

Downstream Products

• 893736-16-8 3-(3-benzyloxy-phenyl)-benzaldehyde 

Relevant articles and documents

DUAL MODULATION OF ENDOCANNABINOID TRANSPORT AND FATTY-ACID AMIDE HYDROLASE FOR TREATMENT OF EXCITOTOXICITY

The endocannabinoid transporter and FAAH are sites of modulation that allow pharmacological enhancement of protective endocannabinergic signals. Selective inhibitors of the transporter and inhibitors of FAAH caused additive augmentation of endogenous signaling events mediated by the cannabinoid CB1 receptor.Disruption of such signals has been shown to prevent neuronal maintenance processes and increase vulnerability to brain damage. Here, blocking endocannabinoid inactivation enhanced cannabinergic activity and ameliorated cellular disturbances associated with excitotoxicity. Modulating the endocannabinoid system in this way also prevented excitotoxic behavioral abnormalities including memory impairment. Collectively, these results indicate that increasing endocannabinoid responses by inhibiting the endocannabinoid transported and/or the inhibiting FAAH leads to molecular, cellular, and functional protection against excitotoxic insults like stroke and traumatic brain injury.

FATTY ACID AMIDE HYDROLASE INHIBITORS

Disclosed are compounds of formula R-X-Y that may be used to inhibit the action of fatty acid amide hydrolase (FAAH). Inhibition of fatty acid amide hydrolase (FAAH) will slow the normal degradation and inactivation of endogenous cannabinoid ligands by FAAH hydrolysis and allow higher levels of those endogenous cannabinergic ligands to remain present. These higher levels of endocannabinoid ligands provide increased stimulation of the cannabinoid CBl and CB2 receptors and produce physiological effects related to the activation of the cannabinoid receptors. They will also enhance the effects of other exogenous cannabinergic ligands and allow them to produce their effects at lower concentrations as compared to systems in which fatty acid amide hydrolase (FAAH) action is hot inhibited. Thus, a compound that inhibits the inactivation of endogenous cannabinoid ligands by fatty acid amide hydrolase (FAAH) may increase the levels of endocannabinoids and, thus, enhance the activation of cannabinoid receptors. Thus, the compound may not directly modulate the cannabinoid receptors but has the effect of indirectly stimulating the cannabinoid receptors by increasing the levels of endocannabinoid ligands. It may also enhance the effects and duration of action of other exogenous cannabinergic ligands that are administered in order to elicit a cannabinergic response.