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Signal Inhibitors and Activators
Iniparib (BSI-201)
$376.5/ sIncubation Time
5
QuantityTotal: $377
Ship worldwide. Contact order@enogene.com for ordering and bulk pricing or contact your local distributor.
Product Information
Kinase Inhibitor Name Iniparib (BSI-201)
M.W.292.03
FormulaC7H5IN2O3
SolubilityDMSO 58mg/mL, Water <1mg/mL, Ethanol 28mg/mL
Purity99.80%
Biological ActivityIniparib (BSI-201) is a potent PARP1 inhibitor with strong anti-neoplastic effect. BSI-201 covalently binds and inhibits PARP-1. When given as a single agent and in combination with other cytotoxic agents, Iniparib (BSI-201) is active against a broad range of cancer cells in culture.Iniparib (BSI-201) has first-in-class and best-in-class potential as targeted therapy for several types of cancer. Iniparib (BSI-201) has demonstrated activity in multiple types of solid tumors, with prolonged inhibition of its target. Iniparib (BSI-201) has shown a strong safety profile. Iniparib (BSI-201) is a leading candidate in the field of PARP inhibitors and is the furthest along in clinical development of this novel therapeutic approach.
Storage/Stabilityat -20℃ 2 years
BackgroundBSI-201 (Iniparib, SAR240550) is a PARP1 inhibitor.
In vitro
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.
Protocol(Only for Reference)
Cell Assay:
Cell lines
MDA-MB-231, and MDA-MB-436
In vitro
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.
Protocol(Only for Reference)
Cell Assay:
Cell lines
MDA-MB-231, and MDA-MB-436
References[1] Cancer Biology & Therapy 1 January 2009;8:1, 2-3
[2] Acta Pharmacologica Sinica 2010;31: 1172–1180；
[3] Neuroscience 2010;171:1256–1264
[4] Mendeleyev J, et al. Biochem Pharmacol, 1995, 50(5), 705-714.
[5] Bauer PI, et al. Biochem Pharmacol, 2002, 63(3), 455-462.
[6] Liu X, et al. Clin Cancer Res, 2012, 18(2), 510-523.
[7] Ma W, et al. Proc Natl Acad Sci U S A, 2012, 109(17), 6590-6595.
[8] Patel AG, et al. Clin Cancer Res, 2012, 18(6), 1655-1662.
The pharmacological and toxicological properties of this product have not been fully investigated. Exercise caution in use and handling. This product must not be used in humans.
[2] Acta Pharmacologica Sinica 2010;31: 1172–1180；
[3] Neuroscience 2010;171:1256–1264
[4] Mendeleyev J, et al. Biochem Pharmacol, 1995, 50(5), 705-714.
[5] Bauer PI, et al. Biochem Pharmacol, 2002, 63(3), 455-462.
[6] Liu X, et al. Clin Cancer Res, 2012, 18(2), 510-523.
[7] Ma W, et al. Proc Natl Acad Sci U S A, 2012, 109(17), 6590-6595.
[8] Patel AG, et al. Clin Cancer Res, 2012, 18(6), 1655-1662.
The pharmacological and toxicological properties of this product have not been fully investigated. Exercise caution in use and handling. This product must not be used in humans.
Price376.5$
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