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Biological Activity for UC 112
UC 112 is an iAP inhibitor (IC50 values from 0.7 - 3.4 μM); inhibits cell growth in multiple cancer cell lines and in a melanoma xenograft model in vivo. Also suppresses X-linked inhibitor of apoptosis protein (XIAP) and survivin levels. Inhibits the growth of P-glycoproteins and activates caspase-3/7 and caspase-9.
Technical Data for UC 112
|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.
Solubility Data for UC 112
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for UC 112
The following data is based on the product molecular weight 348.44. 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||2.87 mL||14.35 mL||28.7 mL|
|5 mM||0.57 mL||2.87 mL||5.74 mL|
|10 mM||0.29 mL||1.43 mL||2.87 mL|
|50 mM||0.06 mL||0.29 mL||0.57 mL|
References for UC 112
References are publications that support the biological activity of the product.
Wang Discovery of novel second mitochondria-derived activator of caspase mimetics as selective inhibitor of apoptosis protein inhibitors. J.Pharmacol.Exp.Ther. 349 319 PMID: 24623800
If you know of a relevant reference for UC 112, please let us know.
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Keywords: UC 112, UC 112 supplier, UC112, inhibitors, inhibits, apoptosis, proteins, antitumor, multidrug, resistant, caspase, Inhibitor, of, Apoptosis, (IAP), 5251, Tocris Bioscience
Citations for UC 112
Citations are publications that use Tocris products.
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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.