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BH3I-1

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Chemical Structure| 300817-68-9 同义名 : BHI1
CAS号 : 300817-68-9
货号 : A189286
分子式 : C15H14BrNO3S2
纯度 : 98%
分子量 : 400.311
MDL号 : MFCD03453544
存储条件：

粉末 Sealed in dry,2-8°C

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(262.3 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
靶点

  • Bcl-xL

    BH3-Bcl-xL interaction, Ki:2.4 μM
描述 BH3 domain-mediated dimerization plays a key role in the regulation of pro-apoptotic and anti-apoptotic activities of the Bcl-2 family proteins. BH3I-1 is a small-molecule, cell-permeable inhibitor of the BH3-domain-mediated dimerization. The Ki values of BH3I-1 for the inhibition of Bak/Bcl-xL-His6 interaction determined by FP and NMR titration assays are 2.4±0.2 and 7.8±0.9μM, respectively. The addition of BH3I-1 (50 and 200μM) dose-dependently decreased the tBid binding in vitro. Treatment of JK cells with 100μM BH3I-1 induced DNA fragmentation and an increase in caspase-3-like and caspase-9-like activities. BH3I-1 at 100µM also induced cytochrome c release in HeLa cells at 48-h post-treatment. Treatment of JK/Bcl-xL cells with 100 µM BH3I-1 induced the appearance of sub-G1 DNA, indicative of apoptosis.[3] BH3I-1 at a dose of 50μM promoted the apoptosis of murine bone marrow-derived eosinophils and human eosinophils isolated from the peripheral blood of healthy subjects.[4]
作用机制 BH3I-1 inhibited BH3-domain-mediated dimerization by preventing BH3 domain-mediated interaction between Bcl-2 family members.[3]
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.50mL

0.50mL

0.25mL

12.49mL

2.50mL

1.25mL

24.98mL

5.00mL

2.50mL
参考文献

[1]Fullbeck M, Gebhardt N, et al. Computer-assisted identification of small-molecule Bcl-2 modulators. Comput Biol Chem. 2009 Dec;33(6):451-6.

[2]Mitsiades CS, Hayden P, et al. Bcl-2 overexpression in thyroid carcinoma cells increases sensitivity to Bcl-2 homology 3 domain inhibition. J Clin Endocrinol Metab. 2007 Dec;92(12):4845-52.

[3]Degterev A, Lugovskoy A, Cardone M, et al. Identification of small-molecule inhibitors of interaction between the BH3 domain and Bcl-xL. Nat Cell Biol. 2001;3(2):173-182. doi:10.1038/35055085

[4]Schwartz C, Willebrand R, Huber S, et al. Eosinophil-specific deletion of IκBα in mice reveals a critical role of NF-κB-induced Bcl-xL for inhibition of apoptosis. Blood. 2015;125(25):3896-3904. doi:10.1182/blood-2014-10-607788