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High affinity PARP-2 and PARP-1 inhibitor (Ki values are 2.9 and 5.2 nM, respectively). Inhibits repair of radiation-induced DNA damage and sensitizes lung cancer cells to radiation. Also increases autophagy and apoptosis in lung cancer cells. Enhances radiation-induced tumor growth delay in mice bearing lung tumor xenografts. Also chemosensitizer. Potentiates effects of temozolomide (Cat. No. 2706) in a mouse melanoma model. Orally bioavailable and brain penetrant.
|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 317.21. 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||31.52 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.
Albert et al (2007) Inhibition of poly(ADP-ribose) polymerase enhances cell death and improves tumor growth delay in irradiated lung cancer models. Clin.Cancer Res. 13 3033 PMID: 17505006
Donawho et al (2007) ABT-888, an orally active poly(ADP-ribose) polymerase inhibitor that potentiates DNA-damaging agents in preclinical tumor models. Clin.Cancer Res. 13 2728 PMID: 17473206
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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.