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YM 155 is a survivin suppressor. Down-regulates survivin expression and sensitizes human NSCLC cell lines to radiation. Enhances radiation-induced tumor regression in nude mice bearing NSCLC xenografts. Also induces apoptosis in TRAIL-resistant glioma cells in vitro.
YM 155 is also offered as part of the Tocriscreen 2.0 Max. Find out more about compound libraries available from Tocris.
|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|
The following data is based on the product molecular weight 443.29. 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||2.26 mL||11.28 mL||22.56 mL|
|5 mM||0.45 mL||2.26 mL||4.51 mL|
|10 mM||0.23 mL||1.13 mL||2.26 mL|
|50 mM||0.05 mL||0.23 mL||0.45 mL|
References are publications that support the biological activity of the product.
Iwasa et al (2008) Radiosensitizing effect of YM155, a novel small-molecule survivin suppressant, in non-small cell lung cancer cell lines. Clin.Cancer Res. 14 6496 PMID: 18927289
Premkumar et al (2013) Survivin inhibitor YM-155 sensitizes tumor necrosis factor- related apoptosis-inducing ligand-resistant glioma cells to apoptosis through Mcl-1 downregulation and by engaging the mitochondrial death pathway. J.Pharmacol.Exp.Ther. 346 201 PMID: 23740602
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Keywords: YM 155, YM 155 supplier, YM155, survivin, suppressor, inhibits, inhibitors, induces, apoptosis, sepantronium, bromide, Inhibitor, of, Apoptosis, (IAP), 6491, Tocris Bioscience
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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.