High affinity and selective activator of Bax (Ki = 43.3 nM). Binds to the S184 binding pocket to block Bax phosphorylation. Does not bind to other Bcl-2 family members, including Bcl-2, Bak and Bid. Facilitates Bax insertion into the mitochondrial membrane and promotes Bax-dependent cytochrome c release. Induces apoptosis in lung cancer cell lines expressing high levels of Bax selectively over normal cells expressing low levels of Bax. Represses tumor growth of A549 lung cancer xenografts in mice.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|ethanol||3.15||10mM with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 315.32. Batch specific molecular weights may vary from batch to batch due to solvent 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||3.17 mL||15.86 mL||31.71 mL|
|5 mM||0.63 mL||3.17 mL||6.34 mL|
|10 mM||0.32 mL||1.59 mL||3.17 mL|
|50 mM||0.06 mL||0.32 mL||0.63 mL|
References are publications that support the products' biological activity.
Xin et al (2014) Small-molecule Bax agonists for cancer therapy. Nat.Commun. 5 4935 PMID: 25230299
If you know of a relevant reference for SMBA 1, please let us know.
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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.
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.