Barasertib (AZD1152-HQPA|AZD2811)

製品コードS1147 別名:INH 34

Barasertib (AZD1152-HQPA|AZD2811)化学構造


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.

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JPY 27888.00
JPY 19920.00
JPY 34860.00
JPY 111220.00


  • 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|AZD2811) purchased from Selleck.

    Primary MKPs were treated with the Aurora B inhibitor AZD-1152, and then stimulated with 20 ng/ml TPO for 5 d. Cell morphology was analyzed by Giemsa staining (Bar, 20 祄; red arrows denote mature MKs; n = 6).

    J Exp Med 2014 10.1084/jem.20141123. Barasertib (AZD1152-HQPA|AZD2811) 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|AZD2811) 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|AZD2811) 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|AZD2811) 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|AZD2811) 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|AZD2811) 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|AZD2811) purchased from Selleck.

  • Effects of vitamin C and K3 (Vit. C&K3; 300 μM and 1 μM, respectively), barasertib (0.01 μM) and their combination on cell viability, induction of apoptosis, level of reactive oxygen species (ROS) and level of protein-carbonyl products in Jurkat leukemia cells (A) and normal lymphocytes (B), after 24- and 48-h incubation at 37˚C in humidified atmosphere. The data are the mean±SD from three independent experiments.

    Anticancer Res, 2018, 38(3):1407-1414. Barasertib (AZD1152-HQPA|AZD2811) purchased from Selleck.

    1205Lu cells were treated for 48hours with the indicated concentrations of  AZD1152-HQPA. 



    Dr. Gao Zhang of University of Pennsylvania. Barasertib (AZD1152-HQPA|AZD2811) purchased from Selleck.


Aurora Kinase阻害剤の選択性比較


製品説明 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.
Aurora B [1]
(Cell-free assay)
0.37 nM

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. [1]

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
LNCaP MnrPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXvCPGhmOC13MECgcm0> NH\JT3g1QMLiaB?= M{iyTGlEPTB;MkWgcm0> M{H1VFI2Ojd5NkW5
LNCaP NULpeJNwSXCxcITvd4l{KEG|c3H5 NGfYNYMxNTVyMDDuUS=> M1jUfVQ5yqCq MlrMbY5lfWOnczDhdI9xfG:2aXOgZ4VtdCCmZXH0bEB1cHKxdXfoJINie3Cjc3WtN{B2eHKnZ4XsZZRqd25? MXyyOVI4PzZ3OR?=
LNCaP M3PUR2Z2dmO2aX;uJGF{e2G7 NUnmfnU4PTBibl2= NXvhPHgzPDhiaB?= MlH4bY5lfWOnczDtbYNzd263Y3zlbUB4cXSqIHHu[ZVo\W6rYzDt[YNp[W6rc32= MWeyOVI4PzZ3OR?=
Ramos MojYSpVv[3Srb36gRZN{[Xl? MlG3OVAxKG6P M4XIeVAuPzJiaB?= MX;pcohq[mm2czDBeZJwemFiQjDrbY5ie2V? MYSyNVM4OTR2Nh?=
Daudi  NUi4SXRoTnWwY4Tpc44hSXO|YYm= NIXvfZM2ODBibl2= Mm[0NE04OiCq NV7BepFIcW6qaXLpeJMhSXW{b4LhJGIhc2mwYYPl NFzHOmQzOTN5MUS0Oi=>
L540 MX3GeY5kfGmxbjDBd5NigQ>? MWm1NFAhdk1? M13W[|AuPzJiaB?= MVHpcohq[mm2czDBeZJwemFiQjDrbY5ie2V? MXiyNVM4OTR2Nh?=
BJAJ MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYPiO4xjPTByIH7N NGfmSmQxNTd{IHi= NWXM[JN4cW6qaXLpeJMh[2WubDDndo94fGhic3nncolncWOjboTsfS=> MXiyNVM4OTR2Nh?=
Ramos MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXu1NFAhdk1? NWSzZYk2OC15MjDo NHG2WW9qdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 M2C0elIyOzdzNES2
Raji NI\3cIRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXm1NFAhdk1? MU[wMVczKGh? M{PaeYlvcGmkaYTzJINmdGxiZ4Lve5RpKHOrZ37p[olk[W62bIm= M3zRbFIyOzdzNES2
Daudi  NGPKb|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{H5SFUxOCCwTR?= MofMNE04OiCq MUjpcohq[mm2czDj[YxtKGe{b4f0bEB{cWewaX\pZ4FvfGy7 MnrxNlE{PzF2NE[=
L428 NHnzSIxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYj5cHFTPTByIH7N NWm4WnZVOC15MjDo MWfpcohq[mm2czDj[YxtKGe{b4f0bC=> MWGyNVM4OTR2Nh?=
KM-H2 NUjCUldoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF2wWpI2ODBibl2= MmLFNE04OiCq M{HiTolvcGmkaYTzJINmdGxiZ4Lve5Rp NYXKVY9tOjF|N{G0OFY>
HDLM-2 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4K5RVUxOCCwTR?= MoXHNE04OiCq MkPJbY5pcWKrdIOgZ4VtdCCpcn;3eIg> M3;2dFIyOzdzNES2
L450 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWK1NFAhdk1? MXiwMVczKGh? NWDCd5pkcW6qaXLpeJMh[2WubDDndo94fGh? NF3VOWUzOTN5MUS0Oi=>
BJAJ MkC1RZBweHSxc3nzJGF{e2G7 M{\CN|UxOCCwTR?= M3TjeFAuPzJiaB?= MnS3bY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= NWT5[po2OjF|N{G0OFY>
Ramos MkDKRZBweHSxc3nzJGF{e2G7 NH3sWJA2ODBibl2= MmDMNE04OiCq MYDpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NUHmV3Y2OjF|N{G0OFY>
Raji MlXjRZBweHSxc3nzJGF{e2G7 M1G3N|UxOCCwTR?= Mk\5NE04OiCq NYjaeHBScW6mdXPld{BieG:ydH;zbZMhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> NUfRT4cxOjF|N{G0OFY>
Daudi  MWXBdI9xfG:|aYOgRZN{[Xl? MlvDOVAxKG6P NWLrXYF[OC15MjDo M123fIlv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy NWixTYM2OjF|N{G0OFY>
L428 NGrqSFFCeG:ydH;zbZMhSXO|YYm= M3jQXlUxOCCwTR?= Moi1NE04OiCq NXH4NJh6cW6mdXPld{BieG:ydH;zbZMhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> NFmzc|MzOTN5MUS0Oi=>
KM-H2 NUH5dnFYSXCxcITvd4l{KEG|c3H5 NWPk[5NxPTByIH7N NXfFV4IxOC15MjDo NHr0Oo9qdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> NEPYRYszOTN5MUS0Oi=>
HDLM-2 NXuxV3lUSXCxcITvd4l{KEG|c3H5 MUO1NFAhdk1? MYewMVczKGh? MVLpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NXzpXHd6OjF|N{G0OFY>
L450 NGH1UnFCeG:ydH;zbZMhSXO|YYm= NFfQb|A2ODBibl2= MoS5NE04OiCq MVrpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NEj4SJQzOTN5MUS0Oi=>
SW620 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVTFR|UxRTFywsGyMlEhdk1? NV7x[3FUOjF{NEWwPVA>
MDA-MB-435 NVKxXGNnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4LyRVAuOTByMECgcm0> Ml3wNk02KGR? NH\Xb|hFVVOR MlqzTWM2OD1zMkWgcm0> M1rKXlIxOTd3OUK2
MDA-MB-468 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWXTfW9sOC1zMECwNEBvVQ>? MnnuNk02KGR? MW\EUXNQ MmjjTWM2OD1zNDDuUS=> M4[3W|IxOTd3OUK2
BT474 NELsUHBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{e3[FAuOTByMECgcm0> M1HzcFIuPSCm NGnhfopFVVOR MkHqTWM2OD16IH7N MXiyNFE4PTl{Nh?=
MDA-MB-361 M3HEXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVKzeVMzOC1zMECwNEBvVQ>? MnHwNk02KGR? M{TEcmROW09? MmX2TWM2OD15MDDuUS=> NXXiT|BzOjBzN{W5NlY>
HER18 MofqRZBweHSxc3nzJGF{e2G7 MorENVAxKG6P MmfwNE8zPC92ODDo NWHaNmFFTE2VTx?= NFOzZlNqdmS3Y3XzJIFxd3C2b4Ppd{BidmRicnXkeYNmeyClbH;uc4dmdmmlIIDveIVvfGmjbB?= Mk\UNlAyPzV7Mk[=
MDA-MB-231 NVzVPXZISXCxcITvd4l{KEG|c3H5 M1\Mc|ExPSCwTR?= NGXhRlAxNzJ2L{S4JIg> NVvzfo9bTE2VTx?= MlfCbY5lfWOnczDhdI9xfG:|aYOgZY5lKHKnZIXj[ZMh[2yxbn;n[Y5q[yCyb4TlcpRq[Wx? NIHVU|EzODF5NUmyOi=>
JHH-1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXy3ZpNoOC5|4pETNVAxOMLibl2= M{HVfVczKGh? NFe1TFdGSzVyPUG3MlTDuTFwMDDuUS=> NF;ITI8yQTlzM{mzOS=>
JHH-2 Mk\xS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHn3VZMxNjQkgKOxNFAxyqCwTR?= NWTFWnMxPzJiaB?= MnL2SWM2OD1{MUiuNOKyOTBwODDuUS=> NIe2eHYyQTlzM{mzOS=>
HuH-6 MmLmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYD6NI1iOC5|4pETNVAxOMLibl2= M3n2VVczKGh? MnT2SWM2OD1|LkhCtVAvPiCwTR?= NGrSTIMyQTlzM{mzOS=>
HuH-7 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkDNNE4{6oDVMUCwNOKhdk1? MkLjO|IhcA>? NHnuWXJGSzVyPU[uPOKyOC5|IH7N MYKxPVkyOzl|NR?=
HLE M13K[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWKwMlPjiJNzMECwxsBvVQ>? M13TblczKGh? NF7VNHpGSzVyPUS1MlnDuTZwNDDuUS=> MUexPVkyOzl|NR?=
HLF MlHwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mm\pNE4{6oDVMUCwNOKhdk1? M{iwb|czKGh? NVTpVIhYTUN3ME2xNlYvOcLzMUKuNkBvVQ>? M2\YXFE6QTF|OUO1
PLC/PRF/5 MmDMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHT4e5IxNjQkgKOxNFAxyqCwTR?= MUC3NkBp NGrHeoFGSzVyPUe2MlnDuTlwOTDuUS=> MX6xPVkyOzl|NR?=
SK-Hep1 NV\ZR2ZET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVmwTodIOC5|4pETNVAxOMLibl2= NXjY[WF{PzJiaB?= NVfS[o9xTUN3ME2yNU46yrFzLkKgcm0> M{jGV|E6QTF|OUO1
Hep3B M4mwNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2X5T|AvO+LCk{GwNFDDqG6P NYLSc3hjPzJiaB?= MlLWSWM2OD15LkdCtVEvOiCwTR?= NUnKdnBGOTl7MUO5N|U>
HepG2 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFe4dVMxNjQkgKOxNFAxyqCwTR?= Ml\DO|IhcA>? MnK5SWM2OD1zND63xtEyNjdibl2= M2jwbFE6QTF|OUO1
Ramos NXzUfpZ{SXCxcITvd4l{KEG|c3H5 NHnNdYMzPS93MD:xNFAhdk1? NWPyeYtTPDhiaB?= NW[0UVV{cW6lcnXhd4V{KHSqZTDs[ZZmdHNib3[geIhmKGOuZXH2[YQh\m:{bYOgc4YhWEGUUDDhcoQh[2G|cHHz[UA{ NVTFUVBJOTl6MkOxOlg>
Daudi  MnW3RZBweHSxc3nzJGF{e2G7 NEXHZYszPS93MD:xNFAhdk1? MV60PEBp M{[2OIlv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> MmHzNVk5OjNzNki=
BALM-14 M2TPOWFxd3C2b4Ppd{BCe3OjeR?= NIrKbFAyOi53L{K1M|UxKG6P MX:0PEBp M{juZYlv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> MlPwNVk5OjNzNki=
BALM-27 M3\sSmFxd3C2b4Ppd{BCe3OjeR?= NGHkN2wyOi53L{K1M|UxKG6P MXu0PEBp NF32cFJqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> NV;nN2FXOTl6MkOxOlg>
NB4 NVPrXFRRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1;yb|AvODFxMD6xM|Eh|ryP M2noOVQ5KGh? NIrl[WZqdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 NULRbY9xOTh|Nke0PFQ>


体内試験 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. [1] 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. [2]


細胞試験: [1]
+ 展開
  • 細胞株: HL-60, NB4, MOLM13, PALL-2, MV4-11, EOL-1, and K562 cells
  • 濃度: Dissolved in DMSO, final concentrations ~100 nM
  • 反応時間: 24 or 48 hours
  • 実験の流れ: Cells are exposed to various concentrations of AZD1152 for 24 or 48 hours. Cell proliferation is measured by 3H-thymidine uptake (isotope added 6 hours before harvest), and the concentration that induced 50% growth inhibition (IC50) is calculated from dose-response curves. Cell cycle analysis is performed by flow cytometry. Cell apoptosis is measured by annexin V–FITC apoptosis detection kit.
+ 展開
  • 動物モデル: Female immune-deficient BALB/c nude mice subcutaneously injected with MOLM13 cells
  • 製剤: Dissolved in 3M Tris, pH 9.0, at a concentration of 2.5 mg/mL
  • 投薬量: 5 or 25 mg/kg
  • 投与方法: Intraperitoneal injection 4 times a week or every another day

溶解度 (25°C)

体外 DMSO 102 mg/mL (200.96 mM)
Ethanol 3 mg/mL (5.91 mM)
Water Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
2% DMSO+40% PEG 300+2% Tween 80+ddH2O

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。


分子量 507.56


CAS No. 722544-51-6
in solvent
別名 INH 34





質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)


  • 質量





開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1



  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):




チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2


質量 濃度 体積 分子量


NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03366675 Recruiting Small Cell Lung Cancer Samsung Medical Center|AstraZeneca December 1 2017 Phase 2
NCT03217838 Recruiting Acute Myeloid Leukaemia|High-Risk Myelodysplastic Syndrome AstraZeneca July 31 2017 Phase 1|Phase 2
NCT02579226 Recruiting Advanced Solid Tumours AstraZeneca October 28 2015 Phase 1



Handling Instructions


  • * 必須


  • 質問1:

    Can you let me know what solvent I can use for Barasertib, cat # S1147, for in vivo use? (IP injection in mice)

  • 回答:

    S1147 Barasertib (AZD1152-HQPA) can be dissolved in 30% PEG400/0.5% Tween80/5% Propylene glycol at 30mg/ml as a clear solution. Usually, when prepare the solution, we will add organic solvents first, then add Tween 80, then water. But this compound can not dissolve in 30% PEG400/0.5% Tween80/5% Propylene glycol clearly. After water was added, it became a clear solution.

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