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Inhibitor of Bcl-2 family members (IC50 values are 1.11 - 7 μM). Inhibits the interaction of a BH3 domain peptide with 6 members of the Bcl-2 family (Bcl-2, Bcl-XL, Mcl-1, Bcl-W, A1, and Bcl-B) in vitro. Has antiapoptotic and antitumor effects in several tumor bearing mouse models.
|Storage||Store at -20°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 413.49. 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|
|0.5 mM||4.84 mL||24.18 mL||48.37 mL|
|2.5 mM||0.97 mL||4.84 mL||9.67 mL|
|5 mM||0.48 mL||2.42 mL||4.84 mL|
|25 mM||0.1 mL||0.48 mL||0.97 mL|
References are publications that support the biological activity of the product.
Nguyen et al (2007) Small molecule obatoclax (GX15-070) antagonizes MCL-1 and overcomes MCL-1-mediated resistance to apoptosis. Proc.Natl.Acad.Sci.U.S.A. 104 19512 PMID: 18040043
Zhai et al (2006) Comparison of chemical inhibitors of antiapoptotic Bcl-2-family proteins. Cell Death Differ. 13 1419 PMID: 16645636
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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!
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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.