Barasertib (AZD1152-HQPA)

Catalog No.S1147 Synonyms: INH 34

Barasertib (AZD1152-HQPA) 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.

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9 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) 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.

    : 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.

    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.

  • 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.

    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.

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 M1Szdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPxNE02ODBibl2= M4n1VlQ5yqCq MYTJR|UxRTJ3IH7N NV7zOIdEOjV{N{e2OVk>
LNCaP NEnmbJBCeG:ydH;zbZMhSXO|YYm= MYmwMVUxOCCwTR?= MV60POKhcA>? NVHrTllscW6mdXPld{BieG:ydH;0bYMh[2WubDDk[YF1cCC2aILveYdpKGOjc4Dhd4UuOyC3cILl[5Vt[XSrb36= M4G3NFI2Ojd5NkW5
LNCaP NHrVbXRHfW6ldHnvckBCe3OjeR?= M{j1e|UxKG6P MVK0PEBp NEXhNFBqdmS3Y3XzJI1q[3KxboXjcIVqKHerdHigZY5mfWenbnnjJI1m[2ijbnnzcS=> MVqyOVI4PzZ3OR?=
Ramos M3;EUGZ2dmO2aX;uJGF{e2G7 Mnz2OVAxKG6P NFHmSYUxNTd{IHi= M{H2b4lvcGmkaYTzJGF2em:{YTDCJItqdmG|ZR?= MX[yNVM4OTR2Nh?=
Daudi  MmrTSpVv[3Srb36gRZN{[Xl? MVW1NFAhdk1? NE\SN5QxNTd{IHi= MljRbY5pcWKrdIOgRZVzd3KjIFKgb4lv[XOn MUWyNVM4OTR2Nh?=
L540 M1ziO2Z2dmO2aX;uJGF{e2G7 NYTyV45xPTByIH7N MnjsNE04OiCq MULpcohq[mm2czDBeZJwemFiQjDrbY5ie2V? NEfa[YwzOTN5MUS0Oi=>
BJAJ NUTESIVkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEjlTYw2ODBibl2= NXvpOph6OC15MjDo MYfpcohq[mm2czDj[YxtKGe{b4f0bEB{cWewaX\pZ4FvfGy7 NYfUT4Z1OjF|N{G0OFY>
Ramos MnS4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{S0SFUxOCCwTR?= M{PsdlAuPzJiaB?= M1npVYlvcGmkaYTzJINmdGxiZ4Lve5RpKHOrZ37p[olk[W62bIm= M1y2blIyOzdzNES2
Raji MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXq1NFAhdk1? M17pdFAuPzJiaB?= NGHhW2FqdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 NFzubJAzOTN5MUS0Oi=>
Daudi  NF2xZ2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmH4OVAxKG6P MlL6NE04OiCq MmnrbY5pcWKrdIOgZ4VtdCCpcn;3eIghe2mpbnnmbYNidnSueR?= NIiyd5gzOTN5MUS0Oi=>
L428 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYrtfIpEPTByIH7N MmXENE04OiCq M2rxd4lvcGmkaYTzJINmdGxiZ4Lve5Rp NV\MR|BoOjF|N{G0OFY>
KM-H2 NEnBOmZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGCzcFI2ODBibl2= NYrHO2h7OC15MjDo NELwO21qdmirYnn0d{Bk\WyuIHfyc5d1cA>? NGD5cpAzOTN5MUS0Oi=>
HDLM-2 MkLjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWW1NFAhdk1? MofUNE04OiCq MmrObY5pcWKrdIOgZ4VtdCCpcn;3eIg> MUGyNVM4OTR2Nh?=
L450 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2\idVUxOCCwTR?= MXKwMVczKGh? MnLjbY5pcWKrdIOgZ4VtdCCpcn;3eIg> MkXmNlE{PzF2NE[=
BJAJ MWHBdI9xfG:|aYOgRZN{[Xl? NX[4[FhDPTByIH7N M2mwPFAuPzJiaB?= M4PnW4lv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy MUOyNVM4OTR2Nh?=
Ramos NHPTN25CeG:ydH;zbZMhSXO|YYm= NXrkN5Q4PTByIH7N M1e5N|AuPzJiaB?= MYfpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NELrOXYzOTN5MUS0Oi=>
Raji NUfYPZh1SXCxcITvd4l{KEG|c3H5 MorWOVAxKG6P NWTsZ|VCOC15MjDo MnvlbY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= Mli1NlE{PzF2NE[=
Daudi  NGn5emJCeG:ydH;zbZMhSXO|YYm= M{G5bVUxOCCwTR?= M37mPVAuPzJiaB?= NVjDOoNIcW6mdXPld{BieG:ydH;zbZMhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> MX6yNVM4OTR2Nh?=
L428 Mom0RZBweHSxc3nzJGF{e2G7 NH7aWWY2ODBibl2= NInSOXAxNTd{IHi= NIHmbFZqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> NVX2OIF7OjF|N{G0OFY>
HDLM-2 NGXGOJlCeG:ydH;zbZMhSXO|YYm= M1e4T|UxOCCwTR?= NEPxNJcxNTd{IHi= MnjxbY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= M3PQW|IyOzdzNES2
L450 MXzBdI9xfG:|aYOgRZN{[Xl? MXe1NFAhdk1? M3nibVAuPzJiaB?= MmPEbY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= Mn;1NlE{PzF2NE[=
HCT116 MmPZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MojBSWM2OD1zMdMxN{4{KG6P MXWyNVI1PTB7MB?=
MDA-MB-361 M1;LUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXKwMVExODByIH7N NVjuNHhVOi13IHS= MlPmSG1UVw>? MnjmTWM2OD15MDDuUS=> MX:yNFE4PTl{Nh?=
HER18 MVTBdI9xfG:|aYOgRZN{[Xl? M1n1UVExOCCwTR?= NGHabWkxNzJ2L{S4JIg> NHfsVnpFVVOR NHXVV5ZqdmS3Y3XzJIFxd3C2b4Ppd{BidmRicnXkeYNmeyClbH;uc4dmdmmlIIDveIVvfGmjbB?= NIH6cYQzODF5NUmyOi=>
MDA-MB-231 NV\WfGszSXCxcITvd4l{KEG|c3H5 NFv1c2MyODVibl2= M3zLN|AwOjRxNEigbC=> M{LDcGROW09? MkHVbY5lfWOnczDhdI9xfG:|aYOgZY5lKHKnZIXj[ZMh[2yxbn;n[Y5q[yCyb4TlcpRq[Wx? MVGyNFE4PTl{Nh?=
JHH-1 M3XYTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUOwMlPjiJNzMECwxsBvVQ>? NGfFOYw4OiCq NU\UfYQ6TUN3ME2xO{41yrFzLkCgcm0> Mn\XNVk6OTN7M{W=
JHH-2 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYmwMlPjiJNzMECwxsBvVQ>? M1TScFczKGh? NXnzZol[TUN3ME2yNVgvOMLzMUCuPEBvVQ>? MX:xPVkyOzl|NR?=
JHH-4 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlfnNE4{6oDVMUCwNOKhdk1? Mn3XO|IhcA>? NHPSbI9GSzVyPUG1OU43yrFzNj64JI5O NVfy[nVLOTl7MUO5N|U>
HuH-1 NF7R[XNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{PQe|AvO+LCk{GwNFDDqG6P NYX4VotUPzJiaB?= MYPFR|UxRTJ5LkRCtVUvOCCwTR?= NIj2bmQyQTlzM{mzOS=>
HuH-6 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF;xWpAxNjQkgKOxNFAxyqCwTR?= NFiyTpI4OiCq NUnHXosyTUN3ME2zMlfDuTBwNjDuUS=> NIfWXHIyQTlzM{mzOS=>
HuH-7 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn\ZNE4{6oDVMUCwNOKhdk1? NVTrOGx1PzJiaB?= NYO0RZJxTUN3ME22MljDuTBwMzDuUS=> M3vYNlE6QTF|OUO1
HLF MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4XNSVAvO+LCk{GwNFDDqG6P NH33Xms4OiCq MVPFR|UxRTF{Nj6xxtEyOi5{IH7N MVqxPVkyOzl|NR?=
PLC/PRF/5 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIXzXoMxNjQkgKOxNFAxyqCwTR?= MXO3NkBp MWnFR|UxRTd4LkpCtVkvQSCwTR?= NIfxclgyQTlzM{mzOS=>
SK-Hep1 NUXCcpp3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4fk[|AvO+LCk{GwNFDDqG6P MVS3NkBp NHHGNlBGSzVyPUKxMlnDuTFwMjDuUS=> NHXrR3cyQTlzM{mzOS=>
Hep3B M{O3SWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVrSOXBCOC5|4pETNVAxOMLibl2= M3HOSFczKGh? NIHJcoJGSzVyPUeuOuKyOS5{IH7N MVuxPVkyOzl|NR?=
HepG2 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmX2NE4{6oDVMUCwNOKhdk1? Mm\5O|IhcA>? NWnBOmZRTUN3ME2xOE44yrFzLkegcm0> MnrXNVk6OTN7M{W=
Ramos Mn\ORZBweHSxc3nzJGF{e2G7 NGjJNlEzPS93MD:xNFAhdk1? NUSxO4d[PDhiaB?= M3vtZYlv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> Mn21NVk5OjNzNki=
Daudi  M2CwUGFxd3C2b4Ppd{BCe3OjeR?= NV\oWFZrOjVxNUCvNVAxKG6P M2nidFQ5KGh? NHnTZolqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> NIHjNFAyQTh{M{G2PC=>
BALM-14 MXzBdI9xfG:|aYOgRZN{[Xl? MVyxNk42NzJ3L{WwJI5O MUi0PEBp NFHhNIZqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> NETUT2syQTh{M{G2PC=>
BALM-27 MoP2RZBweHSxc3nzJGF{e2G7 MoO5NVIvPS9{NT:1NEBvVQ>? MWS0PEBp M{izdolv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> MlPiNVk5OjNzNki=
NB4 NULlNVVqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlTZNE4xOS9yLkGvNUDPxE1? MYC0PEBp NUHNeoNwcW6qaXLpeJMh[2WubDDndo94fGhic3nncolncWOjboTsfS=> NEHx[40yQDN4N{S4OC=>

... 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

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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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID