Barasertib (AZD1152-HQPA|AZD2811)

Catalog No.S1147 Synonyms: INH 34

Barasertib (AZD1152-HQPA|AZD2811) Chemical Structure

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.

Size Price Stock Quantity  
In DMSO USD 168 In stock
USD 120 In stock
USD 210 In stock
USD 670 In stock
Bulk Discount

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

10 Customer Reviews

  • 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.

    : 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.


    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.

    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.

Purity & Quality Control

Choose Selective Aurora Kinase Inhibitors

Biological Activity

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.
Aurora B [1]
(Cell-free assay)
0.37 nM
In vitro

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 M4TkUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmfmNE02ODBibl2= MWi0POKhcA>? NEDMe4xKSzVyPUK1JI5O NELqPGkzPTJ5N{[1PS=>
LNCaP MnjFRZBweHSxc3nzJGF{e2G7 MVKwMVUxOCCwTR?= NEfNflg1QMLiaB?= NXnZenVYcW6mdXPld{BieG:ydH;0bYMh[2WubDDk[YF1cCC2aILveYdpKGOjc4Dhd4UuOyC3cILl[5Vt[XSrb36= NXzQOXZDOjV{N{e2OVk>
LNCaP M1HxfWZ2dmO2aX;uJGF{e2G7 Ml73OVAhdk1? M3\ET|Q5KGh? NITzWnhqdmS3Y3XzJI1q[3KxboXjcIVqKHerdHigZY5mfWenbnnjJI1m[2ijbnnzcS=> M4LRZ|I2Ojd5NkW5
Ramos M3PwWGZ2dmO2aX;uJGF{e2G7 MnrmOVAxKG6P M1zMfVAuPzJiaB?= NGKwTGVqdmirYnn0d{BCfXKxcnGgRkBscW6jc3W= NXrsZpV2OjF|N{G0OFY>
Daudi  MVvGeY5kfGmxbjDBd5NigQ>? MYS1NFAhdk1? MViwMVczKGh? M{DDSIlvcGmkaYTzJGF2em:{YTDCJItqdmG|ZR?= NH73NIMzOTN5MUS0Oi=>
L540 M3HYXGZ2dmO2aX;uJGF{e2G7 NVO2T2RLPTByIH7N NHfMW|QxNTd{IHi= MWDpcohq[mm2czDBeZJwemFiQjDrbY5ie2V? NXHCZolwOjF|N{G0OFY>
BJAJ MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn23OVAxKG6P M{LoR|AuPzJiaB?= M3;RN4lvcGmkaYTzJINmdGxiZ4Lve5RpKHOrZ37p[olk[W62bIm= Mn7RNlE{PzF2NE[=
Ramos NF7OPFBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2fVUlUxOCCwTR?= NU\nfY41OC15MjDo NH;qc4lqdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 M2HHSVIyOzdzNES2
Raji MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYHBNG1rPTByIH7N NIP6O|ExNTd{IHi= NIT4c4dqdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 MYOyNVM4OTR2Nh?=
Daudi  MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUTzOoh2PTByIH7N M3\VNFAuPzJiaB?= NV\weZF2cW6qaXLpeJMh[2WubDDndo94fGhic3nncolncWOjboTsfS=> MXmyNVM4OTR2Nh?=
L428 M{\NU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmfhOVAxKG6P NFn1fowxNTd{IHi= M122fYlvcGmkaYTzJINmdGxiZ4Lve5Rp NUHuRpJXOjF|N{G0OFY>
KM-H2 MojwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zkSFUxOCCwTR?= NGPDblIxNTd{IHi= NV3zO5d1cW6qaXLpeJMh[2WubDDndo94fGh? M2\RNlIyOzdzNES2
HDLM-2 M4HTOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2DwdVUxOCCwTR?= MorFNE04OiCq NEGxZWRqdmirYnn0d{Bk\WyuIHfyc5d1cA>? NWn5SYpMOjF|N{G0OFY>
L450 NWjWOYlHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEXrTpA2ODBibl2= NF\oN3oxNTd{IHi= Ml2zbY5pcWKrdIOgZ4VtdCCpcn;3eIg> M3HlXlIyOzdzNES2
BJAJ MYfBdI9xfG:|aYOgRZN{[Xl? NFzDRXY2ODBibl2= M2jVZlAuPzJiaB?= M2OzPYlv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy M3LhblIyOzdzNES2
Ramos NGnoc41CeG:ydH;zbZMhSXO|YYm= NWWxOW97PTByIH7N MYewMVczKGh? MULpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NHXoXFUzOTN5MUS0Oi=>
Raji MoT0RZBweHSxc3nzJGF{e2G7 NX33W5NUPTByIH7N M1\6[VAuPzJiaB?= MmDabY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= MXyyNVM4OTR2Nh?=
Daudi  Mn;pRZBweHSxc3nzJGF{e2G7 NWnLUlI1PTByIH7N NHvIPIkxNTd{IHi= MmTibY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= NFnyc5ozOTN5MUS0Oi=>
L428 NYLjS2VRSXCxcITvd4l{KEG|c3H5 NFrBelc2ODBibl2= M13BUlAuPzJiaB?= M4S2bIlv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy NYnn[mp4OjF|N{G0OFY>
KM-H2 NV7USmh7SXCxcITvd4l{KEG|c3H5 MkC1OVAxKG6P MXiwMVczKGh? MVPpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= M4fwclIyOzdzNES2
HDLM-2 M3X4UmFxd3C2b4Ppd{BCe3OjeR?= NWiz[ZhHPTByIH7N NEXZN5oxNTd{IHi= Ml[5bY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= NIXRRlUzOTN5MUS0Oi=>
L450 MonXRZBweHSxc3nzJGF{e2G7 M{\pOVUxOCCwTR?= MmPTNE04OiCq NFz0bHZqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> NXPGRppZOjF|N{G0OFY>
SW620 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIrK[IFGSzVyPUGwxtEzNjFibl2= M4TRNFIyOjR3MEmw
HCT116 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIjPTGlGSzVyPUGxxtE{NjNibl2= M{j2T|IyOjR3MEmw
MDA-MB-435 NW\NR3o5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWrtd49VOC1zMECwNEBvVQ>? MlPINk02KGR? NXnIOVNbTE2VTx?= NWjmS|BDUUN3ME2xNlUhdk1? NYjFVJV[OjBzN{W5NlY>
MDA-MB-468 M{Pzfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF21bGoxNTFyMECwJI5O NYjwVVVuOi13IHS= NVzI[GsxTE2VTx?= MkPjTWM2OD1zNDDuUS=> MXSyNFE4PTl{Nh?=
MDA-MB-231 MoTyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGLEeokxNTFyMECwJI5O NYrpb|E3Oi13IHS= MUDEUXNQ Ml7vTWM2OD1zMEWgcm0> MmDsNlAyPzV7Mk[=
MDA-MB-361 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXWwMVExODByIH7N M3zsbFIuPSCm M{\EZmROW09? NVrB[5FOUUN3ME23NEBvVQ>? Mn[0NlAyPzV7Mk[=
HER18 MmTJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3O4WFAuOTByMECgcm0> Ml33Nk02KGR? Ml\4SG1UVw>? NXKxUodJUUN3ME2yNEBvVQ>? NWrMZpo1OjBzN{W5NlY>
HER18 MVLBdI9xfG:|aYOgRZN{[Xl? MWOxNFAhdk1? NWfVOHM4OC9{ND:0PEBp NUnIepVOTE2VTx?= MYnpcoR2[2W|IHHwc5B1d3OrczDhcoQhemWmdXPld{BkdG:wb3flcolkKHCxdHXueIlidA>? MVWyNFE4PTl{Nh?=
MDA-MB-231 M4DCU2Fxd3C2b4Ppd{BCe3OjeR?= NV3xZmN1OTB3IH7N M{TUUFAwOjRxNEigbC=> MlfkSG1UVw>? MVnpcoR2[2W|IHHwc5B1d3OrczDhcoQhemWmdXPld{BkdG:wb3flcolkKHCxdHXueIlidA>? NUjyO|JLOjBzN{W5NlY>
JHH-1 M4XrVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXnXb5Z5OC5|4pETNVAxOMLibl2= M1fjfFczKGh? NWPXOolETUN3ME2xO{41yrFzLkCgcm0> NVz6NJFiOTl7MUO5N|U>
JHH-2 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn3oNE4{6oDVMUCwNOKhdk1? NYO2PWM5PzJiaB?= Mo\SSWM2OD1{MUiuNOKyOTBwODDuUS=> M3nt[FE6QTF|OUO1
JHH-4 NHKySlJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NI\GUVExNjQkgKOxNFAxyqCwTR?= NGLL[Y44OiCq NFTBUnlGSzVyPUG1OU43yrFzNj64JI5O M2n4RlE6QTF|OUO1
HuH-6 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmO1NE4{6oDVMUCwNOKhdk1? NX3ySW9pPzJiaB?= NIL1WoRGSzVyPUOuO:KyOC54IH7N MWexPVkyOzl|NR?=
HuH-7 Mny5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmLKNE4{6oDVMUCwNOKhdk1? NYX2dnNxPzJiaB?= MlvHSWM2OD14LklCtVAvOyCwTR?= NUi4blByOTl7MUO5N|U>
HLE M3rSOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlG1NE4{6oDVMUCwNOKhdk1? NUf6S2FsPzJiaB?= NFi3eJZGSzVyPUS1MlnDuTZwNDDuUS=> NYnr[YtyOTl7MUO5N|U>
HLF NH\tXXRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVewMlPjiJNzMECwxsBvVQ>? MVu3NkBp M1LTUGVEPTB;MUK2MlHDuTF{LkKgcm0> MUexPVkyOzl|NR?=
PLC/PRF/5 NGj0RYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFGzXpgxNjQkgKOxNFAxyqCwTR?= MYm3NkBp NVfvR4s2TUN3ME23Ok46yrF7Lkmgcm0> MXuxPVkyOzl|NR?=
SK-Hep1 M4DUd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1HXV|AvO+LCk{GwNFDDqG6P NVjzZ|V5PzJiaB?= MXXFR|UxRTJzLkpCtVEvOiCwTR?= MVexPVkyOzl|NR?=
Hep3B MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4XwVVAvO+LCk{GwNFDDqG6P MorwO|IhcA>? NYHnT|Z2TUN3ME23MlbDuTFwMjDuUS=> NWnqWZlmOTl7MUO5N|U>
Daudi  NXrNe3lSSXCxcITvd4l{KEG|c3H5 MVWyOU82OC9zMECgcm0> NFnUZYg1QCCq M17hWolv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> M1[2UVE6QDJ|MU[4
BALM-14 MoDtRZBweHSxc3nzJGF{e2G7 M2nkWFEzNjVxMkWvOVAhdk1? NU\DTZhEPDhiaB?= NH3hc3BqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> MWOxPVgzOzF4OB?=
BALM-27 NWPP[pc5SXCxcITvd4l{KEG|c3H5 NF;xZpEyOi53L{K1M|UxKG6P NXL4T2lxPDhiaB?= NULlcZN[cW6lcnXhd4V{KHSqZTDs[ZZmdHNib3[geIhmKGOuZXH2[YQh\m:{bYOgc4YhWEGUUDDhcoQh[2G|cHHz[UA{ MUKxPVgzOzF4OB?=
NB4 NUPmUIZHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXvOc|NyOC5yMT:wMlEwOSEQvF2= MXm0PEBp MWTpcohq[mm2czDj[YxtKGe{b4f0bEB{cWewaX\pZ4FvfGy7 MofkNVg{Pjd2OES=

... Click to View More Cell Line Experimental Data

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. [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]


Cell Research:[1]
+ Expand
  • Cell lines: HL-60, NB4, MOLM13, PALL-2, MV4-11, EOL-1, and K562 cells
  • Concentrations: Dissolved in DMSO, final concentrations ~100 nM
  • Incubation Time: 24 or 48 hours
  • Method: 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.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Female immune-deficient BALB/c nude mice subcutaneously injected with MOLM13 cells
  • Formulation: Dissolved in 3M Tris, pH 9.0, at a concentration of 2.5 mg/mL
  • Dosages: 5 or 25 mg/kg
  • Administration: Intraperitoneal injection 4 times a week or every another day
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 102 mg/mL (200.96 mM)
Ethanol 3 mg/mL (5.91 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+40% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 507.56


CAS No. 722544-51-6
Storage powder
in solvent
Synonyms INH 34

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

  • Mass
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • 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):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
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
NCT03366675 Recruiting Small Cell Lung Cancer Samsung Medical Center|AstraZeneca December 1 2017 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

Frequently Asked Questions

  • Question 1:

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

  • Answer:

    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 Signaling Pathway Map

Aurora Kinase Inhibitors with Unique Features

Related Aurora Kinase Products5

Tags: buy Barasertib (AZD1152-HQPA|AZD2811) | Barasertib (AZD1152-HQPA|AZD2811) supplier | purchase Barasertib (AZD1152-HQPA|AZD2811) | Barasertib (AZD1152-HQPA|AZD2811) cost | Barasertib (AZD1152-HQPA|AZD2811) manufacturer | order Barasertib (AZD1152-HQPA|AZD2811) | Barasertib (AZD1152-HQPA|AZD2811) distributor
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID