160754-76-7

160754-76-7 structure

Name: CNS-5161,N'-(2-CHLORO-5-METHYLSULFANYL-PHENYL)-N-METHYL-N-(3-METHYLSULFANYL-PHENYL)-GUANIDINE
Chemical Name: 2-(2-chloro-5-methylsulfanylphenyl)-1-methyl-1-(3-methylsulfanylphenyl)guanidine
CAS Number: 160754-76-7
Molecular Formula: C₁₆H₁₈ClN₃S₂
Molecular Weight: 351.92
Catalog: Signaling Pathways Membrane Transporter/Ion Channel iGluR
Create Date: 2016-04-29 13:14:55
Modify Date: 2024-01-15 15:04:08
CNS-5161 is a novel NMDA ion-channel antagonist that interacts with the NMDA receptor/ion channel site to produce a noncompetitive blockade of the actions of glutamate.

Name	2-(2-chloro-5-methylsulfanylphenyl)-1-methyl-1-(3-methylsulfanylphenyl)guanidine
Synonyms	CNS-5161 2-[2-chloro-5-(methylsulfanyl)phenyl]-1-methyl-1-[3-(methylsulfanyl)phenyl]guanidine

Description	CNS-5161 is a novel NMDA ion-channel antagonist that interacts with the NMDA receptor/ion channel site to produce a noncompetitive blockade of the actions of glutamate.
Related Catalog	Signaling Pathways >> Neuronal Signaling >> iGluR Research Areas >> Cardiovascular Disease Signaling Pathways >> Membrane Transporter/Ion Channel >> iGluR
Target	NMDA receptor/ion channel[1]
In Vitro	CNS-5161 (CNS 5161) is a novel and selective noncompetitive antagonist of the NMDA subset of glutamate receptors in the mammalian brain. CNS-5161 has potent inhibitory activity in vitro at the NMDA ion channel and is able to displace [3H] MK-801 binding with a Ki of 1.8 nM in synaptosomal membrane preparations from rat brain[1].
In Vivo	In the neonatal rat NMDA excitotoxicity model in vivo, CNS-5161 (CNS 5161) protects against the necrotic effects of exogenous N-methyl-D-aspartate with an ED80 of 4 mg/kg by the intraperitoneal (i.p.) route. CNS-5161 also shows a 91% inhibition of audiogenic seizures in DBA/2 mice at 4 mg/kg i.p., and has a neuroprotective effect following hypoxix/ischaemic brain injury in neonatal rats[1].
References	[1]. Walters MR, et al. Early clinical experience with the novel NMDA receptor antagonist CNS 5161. Br J Clin Pharmacol. 2002 Mar;53(3):305-11.