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    Iniparib (SAR240550; BSI201; NSC746045; IND71677)
    Iniparib (SAR240550; BSI201; NSC746045; IND71677)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0303
    CAS #: 160003-66-7Purity ≥98%

    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.

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    Molecular Weight (MW)292.03
    FormulaC7H5IN2O3
    CAS No.160003-66-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 58 mg/mL (198.6 mM)
    Water: <1 mg/mL
    Ethanol: 28 mg/mL (95.9 mM)
    Other info
    Chemical Name: 4-iodo-3-nitrobenzamide
    InChi Key: MDOJTZQKHMAPBK-UHFFFAOYSA-N
    InChi Code: InChI=1S/C7H5IN2O3/c8-5-2-1-4(7(9)11)3-6(5)10(12)13/h1-3H,(H2,9,11)
    SMILES Code: O=C(N)C1=CC=C(I)C([N+]([O-])=O)=C1 
    Synonyms

    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; 


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    In Vitro

    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

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    Animal modelN/A
    Formulation & DosageN/A
    ReferencesBiochem 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.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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