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Description: Iniparib (SAR-240550; BSI-201; NSC-746045; IND-71677) is a novel, potent, and irreversible inhibitor of PARP1 [poly(ADP-ribose) polymerase-1] with potential anticancer activity. It demonstrated high efficacy and effectiveness in triple-negative breast cancer (TNBC), and was the first putative PARP inhibitor to start phase III clinical trials but discontinued due to disppointing results. Iniparib has a broad-spectrum of antiproliferative activity against various cancer cells, including drug resistant cell lines.
References: Biochem Pharmacol. 1995 Aug 25;50(5):705-14; Biochem Pharmacol. 2002 Feb 1;63(3):455-62; Clin Cancer Res. 2012 Jan 15;18(2):510-23.
NSC-746045, IND-71677; BSI-201; BSI201; BSI 201; NSC746045; NSC-746045; NSC 746045; ND-71677; NIBA; INO-2BA; SAR-240550; SAR 240550; SAR240550; IND-71677; IND 71677; IND71677; Iniparib;
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
In vitro activity: 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
Cell Assay: Cells are exposed to various concentrations of BSI-201 for 5, and 9 days in the presence or absence of buthionine sulfoxamide (BSO). After treatment, cell proliferation is measured by CellTiter-Glo assay
Purity ≥98%
COA
MSDS