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Bax channel blocker
Biological Activity for Bax channel blocker
Bax channel blocker is a allosteric inhibitor of Bax channel activation. Binds inactive Bax at allosteric site and inhibits tBID-mediated Bax activation (IC50 = 3.3 μM). Selectively inhibits Bax-dependent apoptosis. Potent inhibitor of Bax-mediated mitochondrial cytochrome c release (IC50 = 0.52 μM).
Compound Libraries for Bax channel blocker
Technical Data for Bax channel blocker
|Storage||Desiccate at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for Bax channel blocker
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for Bax channel blocker
The following data is based on the product molecular weight 540.12. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.85 mL||9.26 mL||18.51 mL|
|5 mM||0.37 mL||1.85 mL||3.7 mL|
|10 mM||0.19 mL||0.93 mL||1.85 mL|
|50 mM||0.04 mL||0.19 mL||0.37 mL|
Product Datasheets for Bax channel blocker
References for Bax channel blocker
References are publications that support the biological activity of the product.
Bombrun et al (2003) 3,6-Dibromocarbazole piperazine derivatives of 2-propanol as first inhibitors of cytochrome c release via Bax channel modulation. J.Med.Chem. 46 21
Garner et al (2019) Small-molecule allosteric inhibitors of BAX. Nat.Chem.Biol. 15 322 PMID: 30718816
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Keywords: Bax channel blocker, Bax channel blocker supplier, inhibitors, inhibits, Bax-mediated, mitochondrial, cytochrome, c, release, Bcl-2, Family, allosteric, activation, BAI1, 2160, Tocris Bioscience
2 Citations for Bax channel blocker
Citations are publications that use Tocris products. Selected citations for Bax channel blocker include:
Sano et al (2016) Vacuolin-1 inhibits autophagy by impairing lysosomal maturation via PIKfyve inhibition. FEBS Lett 590 1576 PMID: 27135648
Ono et al (2017) Feedback activation of AMPK-mediated autophagy acceleration is a key resistance mechanism against SCD1 inhibitor-induced cell growth inhibition. PLoS One 12 e0181243 PMID: 28704514
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Literature in this Area
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Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
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