Barasertib (AZD1152-HQPA)

製品コードS1147 別名:INH 34

Barasertib (AZD1152-HQPA)化学構造


Barasertib (AZD1152-HQPA)は一種の高度選択性のオーロラ B阻害剤で、無細胞試験でIC50値が0.37 nMです。Barasertib (AZD1152-HQPA)はオーロラ Bに作用する選択性はオーロラAに作用する選択性より3700左右倍が高くなります。臨床1期。

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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.

    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) 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.


    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.

  • : 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.

    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.

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



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


Aurora Kinase阻害剤の選択性比較


製品説明 Barasertib (AZD1152-HQPA)は一種の高度選択性のオーロラ B阻害剤で、無細胞試験でIC50値が0.37 nMです。Barasertib (AZD1152-HQPA)はオーロラ Bに作用する選択性はオーロラAに作用する選択性より3700左右倍が高くなります。臨床1期。
Aurora B [1]
(Cell-free assay)
Aurora A [1]
(Cell-free assay)
0.37 nM 1368 nM
In vitro試験

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 Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
LNCaP NEnxeZNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MojTNE02ODBibl2= MnLYOFjDqGh? NHfsS5NKSzVyPUK1JI5O NGmwTXUzPTJ5N{[1PS=>
LNCaP MnTnRZBweHSxc3nzJGF{e2G7 NHzPT3UxNTVyMDDuUS=> NWHpOJcxPDkEoHi= MoPtbY5lfWOnczDhdI9xfG:2aXOgZ4VtdCCmZXH0bEB1cHKxdXfoJINie3Cjc3WtN{B2eHKnZ4XsZZRqd25? MU[yOVI4PzZ3OR?=
LNCaP NXPCZmNxTnWwY4Tpc44hSXO|YYm= M4HPTlUxKG6P MV[0PEBp Ml:5bY5lfWOnczDtbYNzd263Y3zlbUB4cXSqIHHu[ZVo\W6rYzDt[YNp[W6rc32= NVHscHBROjV{N{e2OVk>
Daudi  NX\nOYNyTnWwY4Tpc44hSXO|YYm= NYrkS3R7PTByIH7N NUHNfnlROC15MjDo NH\PT45qdmirYnn0d{BCfXKxcnGgRkBscW6jc3W= NYTuV2NSOjF|N{G0OFY>
L540 M3vTbGZ2dmO2aX;uJGF{e2G7 NYPUVoU4PTByIH7N NV7kWoNiOC15MjDo MmjabY5pcWKrdIOgRZVzd3KjIFKgb4lv[XOn M{SxT|IyOzdzNES2
BJAJ NH;EWo9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXfFSGVqPTByIH7N M3LkbFAuPzJiaB?= MXrpcohq[mm2czDj[YxtKGe{b4f0bEB{cWewaX\pZ4FvfGy7 MnLXNlE{PzF2NE[=
Ramos NE\JTmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXz3bHU5PTByIH7N MUOwMVczKGh? MmHTbY5pcWKrdIOgZ4VtdCCpcn;3eIghe2mpbnnmbYNidnSueR?= MYSyNVM4OTR2Nh?=
Raji M2j4RWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYH2RoRzPTByIH7N M3fHbFAuPzJiaB?= MkH5bY5pcWKrdIOgZ4VtdCCpcn;3eIghe2mpbnnmbYNidnSueR?= NFfzOGszOTN5MUS0Oi=>
Daudi  M3G0UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mmr4OVAxKG6P MnT2NE04OiCq NXTBWox{cW6qaXLpeJMh[2WubDDndo94fGhic3nncolncWOjboTsfS=> NGnGZVQzOTN5MUS0Oi=>
L428 M1S3c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1rMclUxOCCwTR?= MVywMVczKGh? Mn6zbY5pcWKrdIOgZ4VtdCCpcn;3eIg> NWrrZoZFOjF|N{G0OFY>
KM-H2 M2jMe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4DPR|UxOCCwTR?= MknYNE04OiCq NEP3ZmZqdmirYnn0d{Bk\WyuIHfyc5d1cA>? NH7ablczOTN5MUS0Oi=>
HDLM-2 NGrBN2RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnTwOVAxKG6P Ml3DNE04OiCq MYLpcohq[mm2czDj[YxtKGe{b4f0bC=> NGDWZ5YzOTN5MUS0Oi=>
L450 M3X2WWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTvVHg2ODBibl2= MUOwMVczKGh? NXPZcFYycW6qaXLpeJMh[2WubDDndo94fGh? NVnue3JLOjF|N{G0OFY>
BJAJ NVzkd4lWSXCxcITvd4l{KEG|c3H5 NHLOS5c2ODBibl2= MV:wMVczKGh? M4LRXYlv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy NUnsZmJjOjF|N{G0OFY>
Ramos MoHJRZBweHSxc3nzJGF{e2G7 MV21NFAhdk1? M1LyN|AuPzJiaB?= MWDpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NFX5fWozOTN5MUS0Oi=>
Raji M4nXSGFxd3C2b4Ppd{BCe3OjeR?= MWq1NFAhdk1? M1vRblAuPzJiaB?= Mkf2bY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= MVKyNVM4OTR2Nh?=
Daudi  Ml3xRZBweHSxc3nzJGF{e2G7 M2O3O|UxOCCwTR?= M1rrUFAuPzJiaB?= MofhbY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= M2H6dlIyOzdzNES2
L428 NW\jWG5LSXCxcITvd4l{KEG|c3H5 NH;O[|Q2ODBibl2= NH;Ib48xNTd{IHi= NIm2VJNqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> MYOyNVM4OTR2Nh?=
KM-H2 Mnr4RZBweHSxc3nzJGF{e2G7 MkX1OVAxKG6P NITYSnYxNTd{IHi= NUHtTVNLcW6mdXPld{BieG:ydH;zbZMhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> MornNlE{PzF2NE[=
HDLM-2 MmPYRZBweHSxc3nzJGF{e2G7 M2n3TFUxOCCwTR?= NFrOT5AxNTd{IHi= MlvWbY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= MljXNlE{PzF2NE[=
L450 MoT1RZBweHSxc3nzJGF{e2G7 M2O5fFUxOCCwTR?= M{e0blAuPzJiaB?= MYXpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NFrkWoczOTN5MUS0Oi=>
SW620 M2LhUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn\XSWM2OD1zMNMxNk4yKG6P Mkn2NlEzPDVyOUC=
MDA-MB-435 NEKwRo5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkjkNE0yODByMDDuUS=> NYnWUZUxOi13IHS= NGXEd2lFVVOR MnvoTWM2OD1zMkWgcm0> NYnMO2FWOjBzN{W5NlY>
MDA-MB-468 MnnWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3niZVAuOTByMECgcm0> NHnPTXIzNTViZB?= NHLBepRFVVOR M1ex[2lEPTB;MUSgcm0> MXWyNFE4PTl{Nh?=
MDA-MB-231 NWPmZ4c2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV6wMVExODByIH7N M1TKc|IuPSCm MkmzSG1UVw>? MmjTTWM2OD1zMEWgcm0> MV6yNFE4PTl{Nh?=
BT474 M3jhS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1rYUlAuOTByMECgcm0> M4X5Z|IuPSCm M1vhOGROW09? NHfaV4hKSzVyPUigcm0> MmraNlAyPzV7Mk[=
MDA-MB-361 M2jte2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3iwc|AuOTByMECgcm0> MUSyMVUh\A>? Mk[0SG1UVw>? MnX0TWM2OD15MDDuUS=> M1G0NlIxOTd3OUK2
HER18 MkXRRZBweHSxc3nzJGF{e2G7 NV3ncndSOTByIH7N M1rCXFAwOjRxNEigbC=> NF;veINFVVOR NInTUIVqdmS3Y3XzJIFxd3C2b4Ppd{BidmRicnXkeYNmeyClbH;uc4dmdmmlIIDveIVvfGmjbB?= MmjmNlAyPzV7Mk[=
MDA-MB-231 MX\BdI9xfG:|aYOgRZN{[Xl? MmXGNVA2KG6P M2f6WlAwOjRxNEigbC=> NXTEVGRGTE2VTx?= MoTZbY5lfWOnczDhdI9xfG:|aYOgZY5lKHKnZIXj[ZMh[2yxbn;n[Y5q[yCyb4TlcpRq[Wx? NWHYS5ZKOjBzN{W5NlY>
JHH-1 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYiwMlPjiJNzMECwxsBvVQ>? NGD0ZpQ4OiCq M{izdGVEPTB;MUeuOOKyOS5yIH7N NGPZXIgyQTlzM{mzOS=>
JHH-4 NYrvdmJOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFPte4YxNjQkgKOxNFAxyqCwTR?= M3vBbVczKGh? NXvTfFhbTUN3ME2xOVUvPsLzMU[uPEBvVQ>? MnTINVk6OTN7M{W=
HuH-1 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mo[2NE4{6oDVMUCwNOKhdk1? NFr6S|k4OiCq MYjFR|UxRTJ5LkRCtVUvOCCwTR?= NFrrO4wyQTlzM{mzOS=>
HuH-6 NEKyd|RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4nRWVAvO+LCk{GwNFDDqG6P MmDBO|IhcA>? MkewSWM2OD1|LkhCtVAvPiCwTR?= NIDYc2QyQTlzM{mzOS=>
HuH-7 M3\a[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NE[1WFkxNjQkgKOxNFAxyqCwTR?= MnXaO|IhcA>? M4XDPWVEPTB;Nj64xtExNjNibl2= MX6xPVkyOzl|NR?=
HLF MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYSwMlPjiJNzMECwxsBvVQ>? NEXWZmI4OiCq MUHFR|UxRTF{Nj6xxtEyOi5{IH7N NIXFe3kyQTlzM{mzOS=>
PLC/PRF/5 NXGxd|hDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkLkNE4{6oDVMUCwNOKhdk1? MXq3NkBp M33QNGVEPTB;N{[uPeKyQS57IH7N MYmxPVkyOzl|NR?=
SK-Hep1 M2PzTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYLheI9IOC5|4pETNVAxOMLibl2= MX[3NkBp NYfnOIZRTUN3ME2yNU46yrFzLkKgcm0> NUC4b4N5OTl7MUO5N|U>
Hep3B MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV\URpZrOC5|4pETNVAxOMLibl2= MlLsO|IhcA>? M{O2XWVEPTB;Nz62xtEyNjJibl2= M{PVWlE6QTF|OUO1
HepG2 Mn74S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIL3cmkxNjQkgKOxNFAxyqCwTR?= NHPMVJM4OiCq MWrFR|UxRTF2LkhCtVEvPyCwTR?= NIH0cWwyQTlzM{mzOS=>
Ramos MXzBdI9xfG:|aYOgRZN{[Xl? M4LPdFI2NzVyL{GwNEBvVQ>? NHfDdHg1QCCq NWnwSXk3cW6lcnXhd4V{KHSqZTDs[ZZmdHNib3[geIhmKGOuZXH2[YQh\m:{bYOgc4YhWEGUUDDhcoQh[2G|cHHz[UA{ NHLPU3EyQTh{M{G2PC=>
Daudi  MkHvRZBweHSxc3nzJGF{e2G7 NHSxZ48zPS93MD:xNFAhdk1? NG\nZ5Q1QCCq M2TaOolv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> MUixPVgzOzF4OB?=
BALM-27 NETLVWtCeG:ydH;zbZMhSXO|YYm= NFS0d5MyOi53L{K1M|UxKG6P NXHFR243PDhiaB?= M2rMVIlv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> M1ThZ|E6QDJ|MU[4
NB4 NYfYd4lnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGnHZZkxNjBzL{CuNU8yKM7:TR?= NYW5bVRzPDhiaB?= M376eIlvcGmkaYTzJINmdGxiZ4Lve5RpKHOrZ37p[olk[W62bIm= MUCxPFM3PzR6NB?=

... Click to View More Cell Line Experimental Data

In vivo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]


細胞アッセイ: [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 <1 mg/mL
体内 30% PEG 400+0.5% Tween 80+5% Propylene glycol 30mg/mL

* <1 mg/mlは製品が微弱に溶解する或いは溶解しないことを示します。
* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)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





マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)


  • マス




貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

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 ( 輸入 輸出 )

  • 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


マス 濃度 ボリューム 分子量



Handling Instructions


  • * 必須


  • 問題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.

Aurora Kinase信号経路図

Aurora Kinase Inhibitors with Unique Features

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Tags: Barasertib (AZD1152-HQPA)を買う | Barasertib (AZD1152-HQPA) ic50 | Barasertib (AZD1152-HQPA)供給者 | Barasertib (AZD1152-HQPA)を購入する | Barasertib (AZD1152-HQPA)費用 | Barasertib (AZD1152-HQPA)生産者 | オーダーBarasertib (AZD1152-HQPA) | Barasertib (AZD1152-HQPA)化学構造 | Barasertib (AZD1152-HQPA)分子量 | Barasertib (AZD1152-HQPA)代理店
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID