Catalog No.S1147 Synonyms: INH 34
Molecular Weight(MW): 507.56
Barasertib (AZD1152-HQPA) is a highly selective Aurora B inhibitor with IC50 of 0.37 nM in a cell-free assay, ~3700 fold more selective for Aurora B over Aurora A. Phase 1.
Cited by 24 Publications
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Targeting PI3K, a common downstream effector of RTKs, with a selective inhibitor (GDC0941) sensitizes SOX10 knockdown cells to vemurafenib. shRNAs targeting SOX10 were introduced into A375 cells by lentiviral transduction. pLKO.1 empty vector served as a control vector (Ctrl). Cells were seeded in 6-well plates at the same density in the presence or absence of drug(s) at the indicated concentration. Cells were cultured for 2 weeks in the absence of vemurafenib or 4 weeks in the presence of vemurafenib before fixing and staining.
Nature 2014 508(7494), 118-22. Barasertib (AZD1152-HQPA) purchased from Selleck.
The alamarBlue assay revealed that AURKB inhibition with AZD1152 was effective in NB TICs at EC50 of 1.5 to 4.6 μmol/L, whereas AURKB inhibition was effective in SKPs at 12.4 μmol/L.
Clin Cancer Res 2010 16, 4572-4582. Barasertib (AZD1152-HQPA) purchased from Selleck.
: Barasertib inhibits AURKB speciﬁcally and triggers mitotic slippage. (a) Barasertib inhibits AURKB without affecting AURKA. Mitotic HeLa cells were obtained by exposure to nocodazole for 16 h followed by mechanical shake off. The cells were incubated with the indicated concentrations of Barasertib for 2 h. Nocodazole and MG132 were included to prevent mitotic exit. Lysates were prepared and analyzed with immunoblotting. Uniform loading was conﬁrmed by immunoblotting for actin. (b) Barasertib induces mitotic slippage. HeLa cells expressing histone H2B-GFP were exposed to buffer or the indicated concentrations of Barasertib. Individual cells were then tracked for 24 h with time- lapse microscopy. Each horizontal bar represents one cell (n ¼ 50). The key is the same as in Figure 1b. (c) Summary of Barasertib-mediated mitotic slippage. Live-cell imaging after Barasertib treatment was described in panel (b). The duration of mitosis (mean±90% conﬁdence interval) and the percentage of cells that underwent mitotic slippage during the imaging period were quantiﬁed. (d) Genome reduplication after Barasertib-mediated mitotic slippage. HeLa cells were treated with the indicated concentrations of Barasertib for 36 h. DNA contents were analyzed with ﬂow cytometry. (e) Barasertib induces mitotic slippage and genome reduplication in HCT116. Cells were treated with the indicated concentrations of Barasertib for 24 h. DNA contents were analyzed with ﬂow cytometry. (f) Cytotoxicity induced by Barasertib. HeLa and HCT116 cells were cultured in the presence of the indicated concentrations of Barasertib for 48 h. Proliferation was assayed with WST-1 assay. (g) Barasertib induces genome reduplication and apoptosis. HeLa cells were incubated with 50 n M of Barasertib either in the presence or absence of the caspase inhibitor Z-VAD(OMe)-FMK. The cells were harvested at the indicated time points and analyzed with ﬂow cytometry.
Oncogene 2014 33, 3550-60. Barasertib (AZD1152-HQPA) purchased from Selleck.
Dual inhibition of Aurora and SRC kinases specifically eliminates hyperploid cells. Experiment shown is same as a, b, but performed following treatment of OVCAR10 cells with MLN8237 (targeting AURKA) or AZD1152 (targeting AURKB);
Oncogene 2012 31, 1217–1227. Barasertib (AZD1152-HQPA) purchased from Selleck.
p53 phosphorylation by Aurora B. A, p53 reporter construct was co-transfected with the indicated plasmids into H1299 cells and reporter activation was determined as described under "Experimental Procedures". B, U2OS cells and H1299 cells were treated with AZD1152 (AZD) for 12 h at the indicated doses. Cell lysates were harvested and immunoblotted with Bax and actin antibodies. C, U2OS cells were treated with 100 ng/ml nocodazole (noc) overnight, and then shake off cells were harvested, washed with PBS, and reseeded. Approximately 2 h later, cells were either lysated or treated with dimethyl sulfoxide (DMSO) or AZD1152 for another 16 h before harvesting. Cell lysates were immunoblotted with Bax, phospho-H3, and actin antibodies. D, GST-p53 or GST control proteins were incubated with Aurora B protein and analyzed for phosphate incorporation (left panel). Coomassie staining of GSTp53 and GST protein is also shown (right panel). E, In vitro phosphorylation sites of GST-p53 identified by mass spectrometry analysis. F, GST-p53 wild-type and 3A mutant proteins were analyzed in a kinase assay as in B. G, plasmids encoding wild-type or 3A mutant (CMV)-FLAG-p53 were transiently transfected into H1299 cells, with or without Myc-Aurora B (AurB) expression vector. 20 h post-transfection, cells were lysed and subjected to immunoprecipitation (IP) with p53 antibody (fl-393). Precipitates were immunoblotted with antibodies to p53 (DO-1), Thr(P) and Ser(P), as indicated. Vec, vector.
J Biol Chem 2011 286, 2236-44. Barasertib (AZD1152-HQPA) purchased from Selleck.
D, induction of aneuploidy was repressed by AKT3. Active AKT3 mutant, either myr-AKT3 or AKT3 (E17K), was transiently expressed either in HCT 116, MCF7, or OVCAR3 cells. The cells were then treated with AZD1152-HQPA for 2 days. Control cells were not treated with the drug, and nocodazole (100 nM for 24 h)-treated HCT 116 cell nuclei were also shown as reference for G2-arrested cells. After fixation, nuclei were stained with DAPI (blue signal) and AKT3-expressing cells were detected with anti-HA staining (red signal). Confocal microscopic analysis was performed, and representative images are shown.
J Biol Chem, 2017, 292(5):1910-1924. Barasertib (AZD1152-HQPA) purchased from Selleck.
Fig. 5.A, inhibition of VEGF-mediated uterine edema. Compounds were administered intravenously at the indicated dose 30 min before estradiol challenge. Uterine edema was assessed 2 h thereafter. Inhibition > 35% of the response was significantly different from vehicle-treated group (P < 0.05). ED50(milligrams per kilogram) is shown within parentheses. Values are expressed as mean S.E.M., n= 6 per group. IV, intravenously. B, induction of plasma PLGF after treatment with ABT-348. Mice-bearing tumors derived from a human NSCLC cell line (HCC827ER) were treated with 25 mg/kg ABT-348 via subcutaneous osmotic minipump. At the indicated time, plasma samples were obtained and assayed for murine PLGF. Values shown are the mean S.E. (n = 5 per group). C, representative longitudinal MRI images showing gadolinium contrast enhancement in a rat glioma model with treatment with vehicle, ABT-348 (6.25 mg/kg i.p. b.i.d., every 7 days; two treatment cycles on days 11 and 18 after inoculation), or AZD1152(25 mg/kg i.v., every 4 days; two treatment cycles commencing on days 11 and 18 after inoculation). b, normal brain; t, tumor, Tx1, first treatment cycl e; Tx2, second treatment cycle. D,K transas a function of treatment cycle. Values represent the mean S.E.M., n =12 per group.**, P < 0.01 vs. vehicle.
J Pharmacol Exp Ther 2012 343(3), 617-27. Barasertib (AZD1152-HQPA) purchased from Selleck.
Purity & Quality Control
Choose Selective Aurora Kinase Inhibitors
|Description||Barasertib (AZD1152-HQPA) is a highly selective Aurora B inhibitor with IC50 of 0.37 nM in a cell-free assay, ~3700 fold more selective for Aurora B over Aurora A. Phase 1.|
AZD1152 displays >3000-fold selectivity for Aurora B as compared with Aurora A which has an IC50 of 1.368 μM. AZD1152 has even less activity against 50 other serine-threonine and tyrosine kinases including FLT3, JAK2, and Abl. AZD1152 inhibits the proliferation of hematopoietic malignant cells such as HL-60, NB4, MOLM13, PALL-1, PALL-2, MV4-11, EOL-1, THP-1, and K562 cells with IC50 of 3-40 nM, displaying ~100-fold potency than another Aurora kinase inhibitor ZM334739 which has IC50 of 3-30 μM. AZD1152 inhibits the clonogenic growth of MOLM13 and MV4-11 cells with IC50 of 1 nM and 2.8 nM, respectively, as well as the freshly isolated imatinib-resistant leukemia cells with IC50 values of 1-3 nM, more significantly compared with bone marrow mononuclear cells with IC50 values of >10 nM. AZD1152 induces accumulation of cells with 4N/8N DNA content, followed by apoptosis in a dose- and time-dependent manner. 
|In vivo||Administration of AZD1152 (25 mg/kg) alone markedly suppresses the growth of MOLM13 xenografts, confirmed by the observation of necrotic tissue with infiltration of phagocytic cells.  In addition, AZD1152 (10-150 mg/kg/day) significantly inhibits the growth of a variety of human solid tumor xenografts, including colon, breast, and lung cancers, in a dose-dependent manner. |
|In vitro||DMSO||102 mg/mL (200.96 mM)|
|Ethanol||3 mg/mL (5.91 mM)|
|Water||slightly soluble or insoluble|
|In vivo||Add solvents individually and in order:
30% PEG 400+0.5% Tween 80+5% Propylene glycol
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