AZD7762

E, CAL120 cells were either untreated or pretreated with gemcitabine for 24 hours followed by treatment with AZD7762 and /or MK-1775 for an additional 2 hours (top) or 8 hours (bottom), before lysis. Western blot analysis of Cyclin B1, CDK1 (phospho-Y15 and total) expression, and β-tubulin as loading control. F, induction of the intra–S-phase checkpoint was not affected by WEE1 inhibition. CAL120 cells were pulse-labeled with 10 μmol/L BrdU for 30 minutes, washed (W), and then treated with 1 μmol/L camptothecin (CPT) for 30 minutes. After CPT removal (0 hours), BrdU-labeled S-phase cells (BrdU+ , indicated by boxed area) were monitored at the indicated time points in the absence (iii) or presence of MK-1775 (iv) or AZD7762 as a positive control (v). Control cells (ctr) were not exposed to CPT and cultured in the absence (i) or presence of MK-1775 (ii). Arrowheads indicate delayed S-phase progression.

Cancer Discov 2012 2, 524-39. AZD7762 purchased from Selleck.

HNSCC cell lines have in vitro diverse sensitivities to drugs that affect mitotic progression. Fifty-nine HNSCC cell lines were treated with volasertib, AZD1775, or AZD7762 at seven concentrations ranging from 0.018 to 9.613 μM for 72 h, and their viability was estimated using a CellTiter-Glo assay. (A) Representative dose-response curves for cell lines sensitive and resistant to the drugs. (B) Distributions of the IC80 values for the 59 cell lines. The vertical orange line is the Cmax values for each drug.

Cancer Lett, 2017, 392:71-82. AZD7762 purchased from Selleck.

Photomicrographs showing characteristic morphological changes in T24 cells treated with gemcitabine and AZD7762 (24 and 48 h) (c). Scale bar = 100 μm

J Exp Clin Cancer Res, 2017, 36(1):1. AZD7762 purchased from Selleck.

(A) GBM6 and GBM12 cells and (B) GBM5 and GBM14 cells were treated with AZD7762 (300 nM), AZD0530 (100 nM), or AZD7762 + AZD0530 for 48h. Floating and attached cells were isolated after drug exposure, cell viability was measured by trypan blue exclusion based cell staining (±SE M, n= 3) *p < 0.05 greater than CHK1 inhibitor value. (C) GBM5 and GBM14 cells were treated with AZD7762 (300 nM), AZD0530 (100 nM), or AZD7762 +AZD0530 for 24 h and cell lysates were immunoblotted against cleaved caspase 3, PARP 1 and P-ERK1/2. (D) Medulloblastoma cell lines DAOY, VC312 and D283 were treated with AZD7762 (300 nM), AZD0530 (100 nM), or AZD7762 + AZD0530 for 48 h. Floating and attached cells were isolated after drug exposure, cell viability was measured by trypan blue exclusion (±SE M, n = 3) *p < 0.05 greater than CHK1 inhibitor value. The cell lysates were immunoblotted against cleaved caspases-3, cleaved caspases-7 and P-ER K1/2.

Cancer Biol Ther 2012 13. AZD7762 purchased from Selleck.

GBM5, 6, 12 and 14 cells were treated with AZD7762 (300nM), AZD6244 (500nM) or AZD7762 + AZD6244 for 48h. Floating and attached cells were isolated after drug exposure, cell viability was measured by trypan blue exclusion(±SE M, n = 3) *p < 0.05 greater than CHK1 inhibitor value.

Cancer Biol Ther 2012 13. AZD7762 purchased from Selleck.

MCF7 cells were plated in triplicate and treated with vehicle (VEH, DMSO) , AZD0530 (125 nM), AZD7762 (50 nM) or AZD7762 and AZD0530. Cells were isolated 48 h after exposure and subjected to the indicated various cell viability assays. Data for each assay is the mean of all data points from two studies(* p < 0.05 greater than CHK1 inhibitor value).

Cancer Biol Ther 2011 12, 215-28. AZD7762 purchased from Selleck.

SRC family kinases play a key role in the regulation of the ERK1/2 pathway by CHK1 inhibitors. (A) Transformed mouse embryonic fibroblasts, MEF (wild type, WT; deleted for SRC/FYN/Y es , SYF) were treated with vehicle (VE, DMSO) , UCN-01 (100 nM) or AZD7762 (50 nM). Cells were isolated at the indicated time points and subjected to SDS PAGE followed by immunoblotting to determine the phosphorylation of ERK1/2 (p-ERK1/2), the phosphorylation of SRCY461 (p -Y 416 Src ) or the expression of GAPDH . Data are from a representative of three separate studies. (B) MCF7 cells were treated with vehicle (V eh, DMSO) , UCN-01 (100 nM), pp2 (10 μM), AZD7762 (50 nM) or UCN-01+ pp2 or AZD7762+ pp2. Cells were isolated 2 h after drug exposure and subjected to SDS PAGE f ollowed by immunoblotting to determine the phosphorylation of ERK1/2 ( p-ERK1/2) or the expression of e RK2 protein. Data are from a representative of two separate studies.

Cancer Biol Ther 2011 12, 215-28. AZD7762 purchased from Selleck.