产品名称
IC87201, ≥98% (HPLC)
SMILES string
Clc1c(c(cc(c1)Cl)CNc2cc3[nH]nnc3cc2)O
InChI
1S/C13H10Cl2N4O/c14-8-3-7(13(20)10(15)4-8)6-16-9-1-2-11-12(5-9)18-19-17-11/h1-5,16,20H,6H2,(H,17,18,19)
InChI key
QEHVTUCLCBXQIC-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to brown
solubility
DMSO: 5 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
IC87201 is a potent inhibitor of the nNOS/PSD-95 protein-protein interaction that blocks NMDA-induced 3′ ,5′ -cyclic guanosine monophosphate (cGMP) production in hippocampal cultures.
IC87201 is a potent inhibitor of the nNOS/PSD-95 protein-protein interaction that blocks NMDA-induced 3′ ,5′ -cyclic guanosine monophosphate (cGMP) production in hippocampal cultures. IC87201 exhibits analgesic properties in mice pain models. Contrary to NMDA receptor antagonists nNOS/PSD-95 protein-protein interaction inhibitors spared source memory, spatial memory, and motor function in rats.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2
存储类别
11 - Combustible Solids
wgk
WGK 3
法规信息
新产品
此项目有
Alexandra E Smith et al.
Behavioural brain research, 305, 23-29 (2016-02-26)
Limitations of preclinical models of human memory contribute to the pervasive view that rodent models do not adequately predict therapeutic efficacy in producing cognitive impairments or improvements in humans. We used a source-memory model (i.e., a representation of the origin
S K Florio et al.
British journal of pharmacology, 158(2), 494-506 (2009-09-08)
Post-synaptic density protein 95 (PSD95) contains three PSD95/Dosophilia disc large/ZO-1 homology domains and links neuronal nitric oxide synthase (nNOS) with the N-methyl-D-aspartic acid (NMDA) receptor. This report assesses the effects of disruption of the protein-protein interaction between nNOS and PSD95
Anders Bach et al.
Scientific reports, 5, 12157-12157 (2015-07-17)
ZL006 and IC87201 have been presented as efficient inhibitors of the nNOS/PSD-95 protein-protein interaction and shown great promise in cellular experiments and animal models of ischemic stroke and pain. Here, we investigate the proposed mechanism of action of ZL006 and
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