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Merck

SML1910

Sigma-Aldrich

IC87201

≥98% (HPLC)

别名:

2-[(1H-Benzotriazol-6-ylamino)methyl]-4,6-dichloro-phenol, 2-[(1H-Benzotriazol-6-ylamino)methyl]-4,6-dichlorophenol, IC 87201, IC-87201, Phenol, 2-[(1H-benzotriazol-6-ylamino)methyl]-4,6-dichloro-

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About This Item

经验公式(希尔记法):
C13H10Cl2N4O
分子量:
309.15
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

化驗

≥98% (HPLC)

形狀

powder

顏色

white to brown

溶解度

DMSO: 5 mg/mL, clear

儲存溫度

2-8°C

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 密鑰

QEHVTUCLCBXQIC-UHFFFAOYSA-N

生化/生理作用

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.

象形圖

Exclamation mark

訊號詞

Warning

危險聲明

危險分類

Eye Irrit. 2 - Skin Irrit. 2

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3


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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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