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BTB06584
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。
BTB06584图片
CAS NO:219793-45-0
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
10mg电议
25mg电议

产品介绍
BTB06584 是一种选择性和 IF1 依赖性线粒体 F1Fo-ATPase 抑制剂,不会影响 ATP 合成。 BTB06584 可以延迟缺血性细胞死亡。
Cas No.219793-45-0
化学名[5-(benzenesulfonyl)-2-nitrophenyl] 4-chlorobenzoate
Canonical SMILESC1=CC=C(C=C1)S(=O)(=O)C2=CC(=C(C=C2)[N+](=O)[O-])OC(=O)C3=CC=C(C=C3)Cl
分子式C19H12ClNO6S
分子量417.82
溶解度≥ 17.05mg/mL in DMSO
储存条件Store at -20° C
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

Ischaemia compromises mitochondrial respiration. Consequently, the mitochondrial 1Fo-ATP synthase reverses and plays as a proton-pumping ATPase, so maintaining the mitochondrial membrane potential (ΔΨm), while accelerating ATP depletion and cell death. BTB06584 is an IF1-dependent selective inhibitor of the mitochondrial F1Fo-ATPase.

In vitro: BTB inhibited F1Fo-ATPase activity with no effect on the mitochondrial membrane potential (ΔΨm) or O2 consumption. ATP consumption decreased via inhibition of respiration, and ischaemic cell death was reduced. BTB efficiency increased by IF1 overexpression and reduced by silencing this protein. In addition, BTB rescued defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants in which expression of the Atpif1a gene is lost [1].

In vivo: The BTB-mediated protection was further tested in neurons. Primary cultured cortical neurons of mice were exposed to OGD, treated or not with BTB, followed by RX. The resulting cell death was significantly reduced by BTB, as scored by PI staining, compared with cells left untreated during OGD [1].

Clinical trials: Currenlty no clinical data are available.

Reference:
[1] Ivanes F, Faccenda D, Gatliff J, Ahmed AA, Cocco S, Cheng CH, Allan E, Russell C, Duchen MR, Campanella M.   The compound BTB06584 is an IF1-dependent selective inhibitor of the mitochondrial F1 Fo-ATPase. Br J Pharmacol. 2014;171(18):4193-206.