Catalog No.S1087 Synonyms: NSC-746045, IND-71677
Molecular Weight(MW): 292.03
Iniparib (BSI-201) is a PARP1 inhibitor with demonstrated effectiveness in triple-negative breast cancer (TNBC). Phase 3.
Cited by 7 Publications
3 Customer Reviews
Immunoblot analysis of PARylation after treatment with various PARP inhibitors.The asterisk indicates a nonspecific band.
Nat Methods 2013 10(10), 981-4. Iniparib (BSI-201) purchased from Selleck.
Representative Western blot analysis and quantification of the mean intensity of the band of IKB phosphorylation (E) and caspase 3 activation (F) in Wt neurons incubated with TWEAK either alone or in combination with the PARP-1 inhibitor BSI-201.
Neuroscience 2010 171, 1256–1264. Iniparib (BSI-201) purchased from Selleck.
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|Description||Iniparib (BSI-201) is a PARP1 inhibitor with demonstrated effectiveness in triple-negative breast cancer (TNBC). Phase 3.|
BSI-201 is described as a prodrug of 4-iodo-3-nitrosobenzamide, an agent that covalently inhibits PARP1 by binding to its first zinc finger under cell-free conditions. Treatment of 120 μM BSI-201 plus buthionine sulfoximine (BSO) induces a 95% cell death among 855-2 cells, and displays a similar effect in other human cancer cells.  BSI-201 inhibits the growth of E-ras 20 cells, the effect of which can be augmented 4-fold when BOS is added.  Recently BSI-201 shows no ability to inhibit PARP enzymatic or cellular activity, but can non-selectively modify cysteine-containing proteins in tumor cells, suggesting the mechanism of action for BSI-201 is likely not via inhibition of PARP activity.  BSI-201 (100 μM) inhibits ionizing radiation-induced single-strand breaks (SSBs) repair in human lymphoid cell lines based on large endogenous Epstein–Barr virus (EBV) circular episomes assay, resulting in 55% repair by 2 hours, which can be reversed surprisingly by knockdown of PARP1, indicating that the mechanism of inhibition does not involve trapping PARP at SSBs.  BSI-201 is not able to selectively kill homologous recombination (HR)-deficient cells between BRCA2-deficient PEO1 and BRCA2-revertant PEO4, or ATM-deficient GM16666 and ATM-restored GM16667 fibroblasts. BSI-201 is cytotoxic to a variety of cell lines at concentrations above 40 μM reflecting a mechanism independent of PARP. 
-  Mendeleyev J, et al. Biochem Pharmacol, 1995, 50(5), 705-714.
-  Bauer PI, et al. Biochem Pharmacol, 2002, 63(3), 455-462.
-  Liu X, et al. Clin Cancer Res, 2012, 18(2), 510-523.
|In vitro||DMSO||58 mg/mL (198.6 mM)|
|Ethanol||28 mg/mL (95.88 mM)|
* 1 mg/ml means slightly soluble or insoluble.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01551680||Terminated||Brain Metastases||Institut du Cancer de Montpellier - Val dAurelle||September 2012||Phase 1|
|NCT01593228||Completed||Solid Tumors||Sanofi||May 2012||Phase 3|
|NCT01455532||Completed||Neoplasm Malignant||Sanofi||November 2011||Phase 1|
|NCT01213381||Completed||Advance Solid Tumors||Sanofi||September 2010||Phase 1|
|NCT01204125||Active, not recruiting||Breast Cancer Female||Sanofi|SOLTI Breast Cancer Research Group||September 2010||Phase 2|
|NCT01161836||Completed||Advanced Solid Tumors||Sanofi||July 2010||Phase 1|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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