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VU0483605
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
VU0483605图片
CAS NO:1623101-11-0
包装与价格:
包装价格(元)
1mg电议
5mg电议
10mg电议

产品介绍
VU0483605 是一种有效且可穿透大脑的 mGlu1 受体正变构调节剂 (PAM)。
Cas No.1623101-11-0
化学名3-chloro-N-[3-chloro-4-(4-chloro-1,3-dihydro-1,3-dioxo-2H-isoindol-2-yl)phenyl]-2-pyridinecarboxamide
Canonical SMILESO=C1N(C2=CC=C(NC(C3=C(Cl)C=CC=N3)=O)C=C2Cl)C(C4=CC=CC(Cl)=C41)=O
分子式C20H10Cl3N3O3
分子量446.7
溶解度≤20mg/ml in DMSO;20mg/ml in dimethyl formamide
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

VU0483605 is a selective positive allosteric modulator (PAM) of mGluR1 [1].

The metabotropic glutamate receptors (mGluRs), members of G-protein-coupled receptors, have been involved in a variety of functions in the central and peripheral nervous systems, such as learning, memory, anxiety, and the perception of pain. The mGluRs exist in pre- and postsynaptic neurons in synapses of the hippocampus, cerebellum, the cerebral cortex, as well as other parts of the brain and in peripheral tissues. Mice deficient in mGluR1 showed severe motor coordination and spatial learning deficient [2].

VU0483605 is a selective positive allosteric modulator (PAM) of mGluR1. VU0483605 displayed EC50 values of 0.39 and 0.36 μM at human and rat mGluR1 receptors, respectively. VU0483605 showed no activity against mGlu4 PAM with the EC50 of >10 μM. VU0483605 potentiated the response to glutamate in cells stably expressing mGlu1 and partially restored the reduction in glutamate-mediated calcium signaling in a mutant cell model of schizophrenia [1].

References:
[1] Cho H P, Garcia-Barrantes P M, Brogan J T, et al.  Chemical modulation of mutant mGlu1 receptors derived from deleterious GRM1 mutations found in schizophrenics[J]. ACS chemical biology, 2014, 9(10): 2334-2346.
[2] Conquet F, Bashir Z I, Davies C H, et al.  Motor deficit and impairment of synaptic plasticity in mice lacking mGluR1[J]. Nature, 1994, 372(6503): 237.