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Induces cell death and increases the level of reactive oxygen species (ROS) in cancer cells with both wild-type and normal p53. Also inhibits the growth of spontaneous malignant breast tumors in mice. Displays little effect on normal cells. Rapidly depletes androgen receptor expression in human prostate cancer cells via a ROS-dependent, proteasome-mediated mechanism.
|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 317.34. 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||3.15 mL||15.76 mL||31.51 mL|
|5 mM||0.63 mL||3.15 mL||6.3 mL|
|10 mM||0.32 mL||1.58 mL||3.15 mL|
|50 mM||0.06 mL||0.32 mL||0.63 mL|
References are publications that support the biological activity of the product.
Raj et al (2011) Selective killing of cancer cells by a small molecule targeting the stress response to ROS. Nature 475 231 PMID: 21753854
Golovine et al (2012) Piperlongumine induces rapid depletion of the androgen receptor in human prostate cancer cells. Prostate [Epub ahead of print] PMID: 22592999
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1 Citation for Piperlongumine
Citations are publications that use Tocris products. Selected citations for Piperlongumine include:
Farrand et al (2013) An improved quantitative approach for the assessment of mitochondrial fragmentation in chemoresistant ovarian cancer cells. PLoS One 8 e74008 PMID: 24040144
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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.