PARP1 inhibitor. Inhibits growth of certain breast cancer cell lines in vitro. Non-selectively modifies cysteine-containing proteins in tumor cells. Inhibits ionizing radiation-induced DNA single-stranded breaks in lymphoid cell lines in vivo.
|Storage||Store at RT|
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 292.03. 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|
|0.5 mM||6.85 mL||34.24 mL||68.49 mL|
|2.5 mM||1.37 mL||6.85 mL||13.7 mL|
|5 mM||0.68 mL||3.42 mL||6.85 mL|
|25 mM||0.14 mL||0.68 mL||1.37 mL|
References are publications that support the biological activity of the product.
Liu et al (2011) Iniparib nonselectively modifies cysteine-containing proteins in tumor cells and is not a bona fide PARP inhibitor. Clin.Cancer Res 18 510 PMID: 22128301
Ma et al (2012) Differential effects of poly(ADP-ribose) polymerase inhibition on DNA break repair in human cells are revealed with Epstein-Barr virus. Proc.Natl.Acad.Sci.U.S.A. 109 6590 PMID: 22493268
If you know of a relevant reference for BSI 201, please let us know.
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Keywords: BSI 201, BSI 201 supplier, BSI201, iniparib, PARP1, inhibitors, inhibits, poly(ADP-ribose), polymerase, cysteine-containing, proteins, modifiers, Iniparib, Poly(ADP-ribose), Polymerase, 5817, Tocris Bioscience
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Literature in this Area
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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.