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150493-34-8

中文名称 150493-34-8
英文名称 2-amino-1-(4-chlorobenzyl)-5-trifluoromethylbenzimidazole
CAS 150493-34-8
分子式 C15H11ClF3N3
分子量 325.72
MOL 文件 150493-34-8.mol
150493-34-8 结构式 150493-34-8 结构式

基本信息

中文别名
化合物NS 638
1-[(4-氯苯基)甲基]-5-(三氟甲基)苯并咪唑-2-胺
1-[(4-氯苯基)甲基]-5-(三氟甲基)苯并咪唑-2-胺, >98%
英文别名
NS 638
NS638, >98%
NS-638
NS 638
2-amino-1-(4-chlorobenzyl)-5-trifluoromethylbenzimidazole
1-[(4-Chlorophenyl)Methyl]-5-(Trifluoromethyl)Benzimidazol-2-Amine
1H-Benzimidazol-2-amine,1-[(4-chlorophenyl)methyl]-5-(trifluoromethyl)-
所属类别
生物化工:激动剂抑制剂

物理化学性质

沸点476.3±55.0 °C(Predicted)
密度1.45±0.1 g/cm3(Predicted)
储存条件-20°C储存
溶解度DMF: 5 mg/ml; DMSO: 5 mg/ml; Ethanol: 2 mg/ml; PBS (pH 7.2): insol
酸度系数(pKa)5.15±0.10(Predicted)
形态固体

安全数据

危险性符号(GHS)
GHS07
警示词警告
危险性描述H302-H315-H319-H335
150493-34-8价格(试剂级)
报价日期产品编号产品名称CAS号包装价格
2024/04/30HY-101428150493-34-8
NS-638
150493-34-82mg500元
2024/04/30HY-101428150493-34-8
NS-638
150493-34-810mM * 1mLin DMSO896元
2024/04/30HY-101428150493-34-8
NS-638
150493-34-85mg940元

常见问题列表

生物活性
NS-638是具有阻断Ca2+-离子通道性质的非肽类小分子。细胞内阻断由K+激活的Ca2+浓度升高的IC50值为3.4 μM。
靶点

IC50: 3.4 μM (K + -stimulated intracellular Ca 2+ -elevation)

体外研究

NS-638 dose dependently inhibits K + -stimulated [45 Ca 2+ ]-uptake in chick cortical synaptosomes and 2-amino-3-(3-hydroxy-5-methylisoxazol-4-yl)propionic acid (AMPA)- stimulated [ 3 H]GABA-release from cultured cortical neurons with IC 50 values of 2.3 and 4.3 μM, respectively. K + -stimulated intracellular Ca 2+ -elevation in cultured cerebellar granule cells is equipotently blocked with an IC 50 value of 3.4 μM. At this concentration no effect on Ca 2+ -induced contractions in K + -depolarized guinea pig taenia coli is observed. NS-638 reversibly blocks N- and L-type Ca 2+ -channels in cultured chick dorsal root ganglion cells in the concentration range of 1-30 μM.

体内研究

In the mouse middle cerebral artery occlusion model, NS-638 administered i.p. (50 mg kg-1) at 1 h and 6 h post-ischemia, and once a day for the next two days, results in a 48% reduction in total infarct volume. It does not show protection against ischemic neuronal damage in the gerbil model of bilateral carotid artery occlusion.

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