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NS-638 Sale

目录号 : GC30997

An N- and L-type calcium channel inhibitor

NS-638 Chemical Structure

Cas No.:150493-34-8

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥806.00
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5mg
¥846.00
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10mg
¥1,260.00
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50mg
¥4,230.00
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100mg
¥5,760.00
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Sample solution is provided at 25 µL, 10mM.

产品文档

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实验参考方法

Cell experiment:

The effect of NS-638 on neuronal Ca2+-channels is evaluated using whole cell patch clamp techniques[1].

Animal experiment:

Mice: In the mouse middle cerebral artery occlusion model, NS-638 is administered i.p. (50 mg kg-1) at 1 h and 6 h post-ischemia, and once a day for the next two days[1].

References:

[1]. Møller A, et al. Pharmacological profile and anti-ischemic properties of the Ca(2+)-channel blocker NS-638. Neurol Res. 1995 Oct;17(5):353-60.

产品描述

NS 638 is an inhibitor of the N-type voltage-gated calcium channel Cav2.2 and CNS L-type calcium channels.1 It inhibits potassium-induced calcium uptake in chick cortical synaptosomes (IC50 = 3.4 ?M) and AMPA-induced GABA release from primary chick cortical neurons (IC50 = 4.3 ?M), effects that can be blocked by the N-type calcium channel inhibitor ω-conotoxin GVIA but not the L-type calcium channel inhibitor nifedipine . It also inhibits potassium-induced calcium level increases in primary chick cerebellar granule cells (IC50 = 3.4 ?M), an effect that can be blocked by nifedipine but not ω-conotoxin GVIA. NS 638 (50 mg/kg) reduces infarct volume in a mouse model of focal ischemia induced by middle cerebral artery occlusion (MCAO) but not in a gerbil model of global ischemia induced by bilateral carotid artery occlusion (BCAO).

1.M?ller, A., Christophersen, P., Drejer, J., et al.Pharmacological profile and anti-ischemic properties of the Ca2+-channel blocker NS-638Neurol. Res.17(5)353-360(1995)

Chemical Properties

Cas No. 150493-34-8 SDF
Canonical SMILES NC1=NC2=CC(C(F)(F)F)=CC=C2N1CC3=CC=C(Cl)C=C3
分子式 C15H11ClF3N3 分子量 325.72
溶解度 DMSO : ≥ 34 mg/mL (104.38 mM) 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 3.0701 mL 15.3506 mL 30.7012 mL
5 mM 0.614 mL 3.0701 mL 6.1402 mL
10 mM 0.307 mL 1.5351 mL 3.0701 mL
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Research Update

Pharmacological profile and anti-ischemic properties of the Ca(2+)-channel blocker NS-638

Included in the sequence of events leading to neuronal death in ischemic tissue following stroke is an excessive and toxic rise in the intracellular Ca(2+)-concentration, predominantly due to an influx of Ca2+ through nonselective cation-channels as well as Ca(2+)-channels. In the present study we have characterized the pharmacological profile and anti-ischemic effects of 2-amino-1-(4-chlorobenzyl)-5-trifluoromethylbenzimidazole (NS-638), a small nonpeptide molecule with Ca(2+)-channel blocking properties. NS-638 dose dependently inhibited K(+)-stimulated [45Ca2+]-uptake in chick cortical synaptosomes and 2-amino-3-(3-hydroxy-5-methylisoxazol-4-yl)propionic acid (AMPA)-stimulated [3H]GABA-release from cultured cortical neurons with IC50 values of 2.3 and 4.3 microM, respectively. K(+)-stimulated intracellular Ca(2+)-elevation in cultured cerebellar granule cells was equipotently blocked with an IC50 value of 3.4 microM. At this concentration no effect on Ca(2+)-induced contractions in K(+)-depolarized guinea pig taenia coli was observed. The effect of NS-638 on neuronal Ca(2+)-channels was evaluated using whole cell patch clamp techniques. The compound reversibly blocked N- and L-type Ca(2+)-channels in cultured chick dorsal root ganglion cells in the concentration range of 1-30 microM. In the mouse middle cerebral artery occlusion (MCAO) 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, resulted in a 48% reduction in total infarct volume. The compound did not show protection against ischemic neuronal damage in the gerbil model of bilateral carotid artery occlusion (BCAO). This data suggests, that neuronal Ca(2+)-channel blockers may have potential in ameliorating the pathological damage after focal ischemia.

Regional measurements of NO formed in vivo during brain ischemia

Nitric oxide formed in vivo in the rat brain regions of hippocampus, striatum, neocortex and cerebellum was spin trapped and measured ex vivo by cryogenic electron paramagnetic resonance spectroscopy. In non-ischemic control animals the rate of nitric oxide (NO) formation in the individual brain regions ranged from 15 to 42 pmol.g-1.min-1. During exposure to global ischemia for 7 min the generation of NO increased in all parts of the brain. In the hippocampus the rate of NO formation during ischemia increased by 6-fold from a control rate of 19 pmol.g-1.min-1. This increase was attenuated 47% by pretreatment with the NO synthase antagonist 7-nitroindazole, whereas pretreatment with the non-NMDA receptor anatogonist NBQX and the Ca2+ channel blocker NS638 did not influence the NO formation. The data show that short-duration ischemia elicits a significant, NO-synthase-dependent formation of NO in all brain regions.