AEG 40730 dihydrochloride
IAP antagonist; binds to the BIR3 domain of cIAP1, cIAP2 and XIAP with nanomolar affinity. Reduces cIAP1, cIAP2 and XIAP protein levels in human breast cancer MDA-MB-231 cells. Induces apoptosis in combination with TNF, and potentiates TRAIL-mediated apoptosis in human colorectal carcinoma HCT 116 cells. Cell permeable.
|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|
Preparing Stock Solutions
The following data is based on the product molecular weight 1120.06. 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||0.89 mL||4.46 mL||8.93 mL|
|5 mM||0.18 mL||0.89 mL||1.79 mL|
|10 mM||0.09 mL||0.45 mL||0.89 mL|
|50 mM||0.02 mL||0.09 mL||0.18 mL|
References are publications that support the products' biological activity.
Beug et al (2014) Smac mimetics and innate immune stimuli synergize to promote tumor death. Nat.Biotechnol. 32 182 PMID: 24463573
Galbán et al (2009) Cytoprotective effects of IAPs revealed by a small molecule antagonist. Biochem.J. 417 765 PMID: 18851715
Bertrand et al (2008) cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination. Mol. Cell 30 689 PMID: 18570872
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Keywords: AEG 40730 dihydrochloride, supplier, AEG40730, dihydrochloride, 934963583, 934963, 58, 3, IAP, inhibitors, inhibits, apoptosis, antagonists, cIAP1, cIAP2, XIAP, cellular, BIR3, Apoptosis, Inducers, Apoptosis, Inducers, Tocris Bioscience
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Literature in this Area
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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.