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WR 1065 dihydrochloride
Cell-permeable reactive oxygen species scavenger that activates p53 through a JNK-dependent signaling pathway. Activates p21waf-1 and MDM2, represses transcription of Myc and thymidine kinase, and inhibits DNA topoisomerase IIα. Induces cell cycle arrest and exhibits cytoprotective activity towards normal cells but not cancer cells in vivo. Also exhibits broad spectrum antiviral activity in vitro.
|Storage||Desiccate 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 207.16. 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||4.83 mL||24.14 mL||48.27 mL|
|5 mM||0.97 mL||4.83 mL||9.65 mL|
|10 mM||0.48 mL||2.41 mL||4.83 mL|
|50 mM||0.1 mL||0.48 mL||0.97 mL|
References are publications that support the biological activity of the product.
North et al (2000) The cytoprotective aminothiol WR1065 activates p21waf-1 and down regulates cell cycle progression through a p53-dependent pathway. Oncogene 19 1206 PMID: 10713709
Pluquet et al (2003) The cytoprotective aminothiol WR1065 activates p53 through a non-genotoxic signaling pathway involving c-Jun N-terminal kinase. J.Biol.Chem. 278 11879 PMID: 12531896
Walker et al (2009) WR1065 mitigates AZT-ddl-induced mutagenesis and inhibits viral replication. Enviorn.Mol.Mutagen. 50 460
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.