现货，ABT-888 (Veliparib) ，目录号 S1004，CAS号:912444-00-9，细胞周期(Cell Cycle / Checkpoint) ，PARP YZ剂，美国进口，Selleck_详细资料

分子量(MW):	244.29
化学式:	C₁₃H₁₆N₄O
溶解度:	DMSO ≥49mg/mL Water <1mg/mL Ethanol <1mg/mL
纯度:	>99%
稳定性:	at -20℃ 2 years
CAS号:	912444-00-9

分子量(MW):

244.29

化学式:

C₁₃H₁₆N₄O

溶解度:

DMSO ≥49mg/mL Water <1mg/mL Ethanol <1mg/mL

纯度:

>99%

稳定性:

at -20℃ 2 years

CAS号:

912444-00-9

	T47D breast cancer cells were pretreated with indicated concentrations of ABT-888
	*in vivo* suppression of PAR formation by the PARP inhibitor ABT-888 uponinduction of DNA damage Primary human lung fibroblast cells (MRC-5) were pre-treated with the indicated concentration of the PARP inhibitor ABT-888 for two hours. Oxidative DNA damage was induced by 500 µM H2O2 for 10 min and cellular PARP activity was measured by immuno-staining of poly(ADP)-ribose (PAR) (right panels). The in vivo effect of PARP inhibition was compared to cells without DNA damage induction and inhibitor (control) and H2O2-treated cells without inhibitor. Average nuclear PAR staining intensities of more than 50 cells were statistically analysed by Kruskal-Wallis and the post-hoc Dunn’s Multiple Comparison tests (left panel). Asterisks indicate highly significant (p<1%) differences to H2O2-treated cells without PARP inhibitor. Thick horizontal bars mark medians and error bars the interquartile range.
	Caption: 451 Lu is a melanoma cell line with high PARP expression that is resistant to temozolomide. Treatment with 25 µM ABT-888 greatly increased sensitivity to temozolomide compared to cells without ABT-888 treatment as measured by MTS assay.
	Effect of ABT-888 on the viability of endometrial cancer cell line Hec50 and Ishikawa and ovarian cancer cell line SKOV3,Caov3 and PA-1 was detected by WST-1 method after 3 days treatment.
	PARP inhibitors sensitize OVCAR-8 cells to FdUrd but not 5-FU. A, OVCAR-8 cells were exposed to the indicated concentrations of FdUrd (left) or 5-FU (right) along with vehicle, 3 mmol/L ABT-888 or 300 nmol/L AZD2281 for 24 hours. Following washing, ABT-888 and AZD2281 were readded to the plates initially exposed to these agents, and cells were cultured in the continued presence of ABT-888 or AZD2281 for 8 days until colonies formed. B, OVCAR-8 cells were exposed continuously to the indicated agents for 8 days. C, left, OVCAR-8 cells treated as in (A) except that the indicated concentrations of ABT-888 were used. Data shown are a representative experiment from 3 independent replicates. n =3 +SD. C, right, synergy between FdUrd and ABT-888 was calculated from the data in (C, left) using the median effect method and assuming that the agents are mutually exclusive. Combination index values less than 1 indicate synergy.
	ABT-888 blocks recovery from FdUrd-induced cell-cycle arrest, enhances FdUrd-induced apoptosis, and maximally increases killing when present during and after FdUrd exposure. A, OVCAR-8 cells were incubated with vehicle, 3 mmol/L ABT-888, 25 mmol/L FdUrd, or 3 mmol/L ABT-888 and 25 mmol/L FdUrd for 24 hours. One set of cells was immediately stained with propidium iodide (0 hours). The remaining samples were washed, ABT-888 readded (to the samples initially exposed to ABT-888), and stained 24 and 48 hours later. B, cells were treated as in (A) and stained with Annexin V-FITC 24 and 48 hours after removal of FdUrd (with readdition of ABT-888 to samples initially exposed to ABT-888). Apoptosis was measured as the percentage of Annexin V-positive cells. C and D, OVCAR-8 cells were plated, treated with indicated concentrations of FdUrd and 3 mmol/L ABT-888 using the exposure schemes depicted in (C), and assayed for clonogenicity (D).
	ABT-888 sensitizes multiple ovarian cancer cell lines but not normal cells to FdUrd. A, A2780, SKOV3ip, OVCAR-5, and OVCAR-3 ovarian cancer cells were treated with FdUrd for 24 hours in combination with vehicle or the indicated concentrations of ABT-888 for 24 hours. Following washing, ABT-888 was readded to samples initially exposed to ABT-888, and cells were cultured until colonies formed. Data shown are a representative experiment from 3 independent replicates. n=3+SD. B, OSEtsT/hTERT immortalized ovarian surface epithelial cells and WS1 human fibroblasts were treated with FdUrd with and without 3 mmol/L ABT-888. Cell viability was assessed via MTS assay. Data shown are the averages of 3 independent experiments. N=3+SEM.
	ABT-888 sensitizes to FdUrd and temozolomide more effectively than to other chemotherapy agents. OVCAR-8 cells were treated with indicated concentrations of FdUrd, topotecan, melphalan, cisplatin, doxorubicin, gemcitabine, etoposide, and temozolomide in the presence or absence of 3 mmol/L ABT-888 for 24 hours. Following washing, ABT-888 was readded to samples initially exposed to ABT-888, and cells were cultured until colonies formed. Data shown are a representative experiment from 2 independent replicates. N=3+SD. Experiments with FdUrd, topotecan, melphalan, and temozolomide were independently replicated 3 times

T47D breast cancer cells were pretreated with indicated concentrations of ABT-888

in vivo suppression of PAR formation by the PARP inhibitor ABT-888 uponinduction of DNA damage

Primary human lung fibroblast cells (MRC-5) were pre-treated with the indicated concentration of the PARP inhibitor ABT-888 for two hours. Oxidative DNA damage was induced by 500 µM H2O2 for 10 min and cellular PARP activity was measured by immuno-staining of poly(ADP)-ribose (PAR) (right panels). The in vivo effect of PARP inhibition was compared to cells without DNA damage induction and inhibitor (control) and H2O2-treated cells without inhibitor.
Average nuclear PAR staining intensities of more than 50 cells were statistically analysed by Kruskal-Wallis and the post-hoc Dunn’s Multiple Comparison tests (left panel). Asterisks indicate highly significant (p<1%) differences to H2O2-treated cells without PARP inhibitor. Thick horizontal bars mark medians and error bars the interquartile range.

Caption: 451 Lu is a melanoma cell line with high PARP expression that is resistant to temozolomide. Treatment with 25 µM ABT-888 greatly increased sensitivity to temozolomide compared to cells without ABT-888 treatment as measured by MTS assay.

Effect of ABT-888 on the viability of endometrial cancer cell line Hec50 and Ishikawa and ovarian cancer cell line SKOV3,Caov3 and PA-1 was detected by WST-1 method after 3 days treatment.

PARP inhibitors sensitize OVCAR-8 cells to FdUrd but not 5-FU. A, OVCAR-8 cells were exposed to the indicated concentrations of FdUrd (left) or 5-FU (right) along with vehicle, 3 mmol/L ABT-888 or 300 nmol/L AZD2281 for 24 hours. Following washing, ABT-888 and AZD2281 were readded to the plates initially exposed to these agents, and cells were cultured in the continued presence of ABT-888 or AZD2281 for 8 days until colonies formed. B, OVCAR-8 cells were exposed continuously to the indicated agents for 8 days. C, left, OVCAR-8 cells treated as in (A) except that the indicated concentrations of ABT-888 were used. Data shown are a representative experiment from 3 independent replicates. n =3 +SD. C, right, synergy between FdUrd and ABT-888 was calculated from the data in (C, left) using the median effect method and assuming that the agents are mutually exclusive. Combination index values less than 1 indicate synergy.

ABT-888 blocks recovery from FdUrd-induced cell-cycle arrest, enhances FdUrd-induced apoptosis, and maximally increases killing when present during and after FdUrd exposure. A, OVCAR-8 cells were incubated with vehicle, 3 mmol/L ABT-888, 25 mmol/L FdUrd, or 3 mmol/L ABT-888 and 25 mmol/L FdUrd for 24 hours. One set of cells was immediately stained with propidium iodide (0 hours). The remaining samples were washed, ABT-888 readded (to the samples initially exposed to ABT-888), and stained 24 and 48 hours later. B, cells were treated as in (A) and stained with Annexin V-FITC 24 and 48 hours after removal of FdUrd (with readdition of ABT-888 to samples initially exposed to ABT-888). Apoptosis was measured as the percentage of Annexin V-positive cells. C and D, OVCAR-8 cells were plated, treated with indicated concentrations of FdUrd and 3 mmol/L ABT-888 using the exposure schemes depicted in (C), and assayed for clonogenicity (D).

ABT-888 sensitizes multiple ovarian cancer cell lines but not normal cells to FdUrd. A, A2780, SKOV3ip, OVCAR-5, and OVCAR-3 ovarian cancer cells were treated with FdUrd for 24 hours in combination with vehicle or the indicated concentrations of ABT-888 for 24 hours. Following washing, ABT-888 was readded to samples initially exposed to ABT-888, and cells were cultured until colonies formed. Data shown are a representative experiment from 3 independent replicates. n=3+SD. B, OSEtsT/hTERT immortalized ovarian surface epithelial cells and WS1 human fibroblasts were treated with FdUrd with and without 3 mmol/L ABT-888. Cell viability was assessed via MTS assay. Data shown are the averages of 3 independent experiments. N=3+SEM.

ABT-888 sensitizes to FdUrd and temozolomide more effectively than to other chemotherapy agents. OVCAR-8 cells were treated with indicated concentrations of FdUrd, topotecan, melphalan, cisplatin, doxorubicin, gemcitabine, etoposide, and temozolomide in the presence or absence of 3 mmol/L ABT-888 for 24 hours. Following washing, ABT-888 was readded to samples initially exposed to ABT-888, and cells were cultured until colonies formed. Data shown are a representative experiment from 2 independent replicates. N=3+SD. Experiments with FdUrd, topotecan, melphalan, and temozolomide were independently replicated 3 times

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现货，ABT-888 (Veliparib) ，目录号 S1004，CAS号:912444-00-9， 细胞周期(Cell Cycle / Checkpoint) ，PARP YZ剂 ，美国进口，Selleck

现货，ABT-888 (Veliparib) ，目录号 S1004，CAS号:912444-00-9，细胞周期(Cell Cycle / Checkpoint) ，PARP YZ剂，美国进口，Selleck