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Bax activator (EC50 = 3.3 μM); binds at the BH3-binding site. Selective for Bax over other antiapoptotic and proapoptotic proteins. Triggers Bax oligomerization in vitro; induces Bax-mediated apoptosis in mouse embryonic fibroblasts.
|Storage||Store at +4°C|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 405.47. 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|
|0.1 mM||24.66 mL||123.31 mL||246.63 mL|
|0.5 mM||4.93 mL||24.66 mL||49.33 mL|
|1 mM||2.47 mL||12.33 mL||24.66 mL|
|5 mM||0.49 mL||2.47 mL||4.93 mL|
References are publications that support the biological activity of the product.
Gavathiotis et al (2012) Direct and selective small-molecule activation of proapoptotic BAX. Nat.Chem.Biol. 8 639 PMID: 22634637
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.
Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.