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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8 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.

    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

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Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

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.
Targets
Aurora B [1]
(Cell-free assay)
Aurora A [1]
(Cell-free assay)
0.37 nM 1368 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 MoLjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mo[2NE02ODBibl2= NYDUW2tvPDkEoHi= M4nRfmlEPTB;MkWgcm0> MXiyOVI4PzZ3OR?=
LNCaP MknVRZBweHSxc3nzJGF{e2G7 MUSwMVUxOCCwTR?= MnrGOFjDqGh? NXLFO4ptcW6mdXPld{BieG:ydH;0bYMh[2WubDDk[YF1cCC2aILveYdpKGOjc4Dhd4UuOyC3cILl[5Vt[XSrb36= NF;oTowzPTJ5N{[1PS=>
LNCaP NUn3cJNRTnWwY4Tpc44hSXO|YYm= M3zyOlUxKG6P NFXVd4E1QCCq NX24d2dVcW6mdXPld{BucWO{b371Z4xmcSC5aYToJIFv\XWpZX7pZ{Bu\WOqYX7pd40> MV6yOVI4PzZ3OR?=
Ramos NWH4dGM{TnWwY4Tpc44hSXO|YYm= MVG1NFAhdk1? MVqwMVczKGh? NFnqUnNqdmirYnn0d{BCfXKxcnGgRkBscW6jc3W= NHjvR4UzOTN5MUS0Oi=>
Daudi  Mn[wSpVv[3Srb36gRZN{[Xl? MoXtOVAxKG6P NVTWR4d5OC15MjDo MWLpcohq[mm2czDBeZJwemFiQjDrbY5ie2V? NXLFTnpxOjF|N{G0OFY>
L540 MlztSpVv[3Srb36gRZN{[Xl? MWC1NFAhdk1? NVHYbJUyOC15MjDo Mlr5bY5pcWKrdIOgRZVzd3KjIFKgb4lv[XOn MlSyNlE{PzF2NE[=
BJAJ M4jFVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1PwTlUxOCCwTR?= MXWwMVczKGh? MoTmbY5pcWKrdIOgZ4VtdCCpcn;3eIghe2mpbnnmbYNidnSueR?= M4rE[lIyOzdzNES2
Ramos MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVi1NFAhdk1? NGf1eZQxNTd{IHi= NXX4dZkzcW6qaXLpeJMh[2WubDDndo94fGhic3nncolncWOjboTsfS=> M2XOOVIyOzdzNES2
Raji M4Dpd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUW1NFAhdk1? MUiwMVczKGh? MVfpcohq[mm2czDj[YxtKGe{b4f0bEB{cWewaX\pZ4FvfGy7 NHjQTpUzOTN5MUS0Oi=>
Daudi  MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkC5OVAxKG6P NUTFOpBTOC15MjDo NFXpOXNqdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 MkG3NlE{PzF2NE[=
L428 NVq1bFdnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoK1OVAxKG6P NWLmUoFoOC15MjDo NWLPO3JXcW6qaXLpeJMh[2WubDDndo94fGh? M3nsb|IyOzdzNES2
KM-H2 NYLpdodOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX7j[5k5PTByIH7N NWXCOZVROC15MjDo NFvoSGVqdmirYnn0d{Bk\WyuIHfyc5d1cA>? NXHGXldoOjF|N{G0OFY>
HDLM-2 M1O1XWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4jKV|UxOCCwTR?= M1rzPFAuPzJiaB?= NIPQVItqdmirYnn0d{Bk\WyuIHfyc5d1cA>? MonqNlE{PzF2NE[=
L450 M13QZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NI\zZmE2ODBibl2= Mn7xNE04OiCq MkXobY5pcWKrdIOgZ4VtdCCpcn;3eIg> Ml74NlE{PzF2NE[=
BJAJ M2rUWWFxd3C2b4Ppd{BCe3OjeR?= MlPPOVAxKG6P NHfQO5gxNTd{IHi= M2rEe4lv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy NUjkR4luOjF|N{G0OFY>
Ramos MoTTRZBweHSxc3nzJGF{e2G7 M2HBbVUxOCCwTR?= NVjTWpJ1OC15MjDo NXizeWRQcW6mdXPld{BieG:ydH;zbZMhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> NFfsZXYzOTN5MUS0Oi=>
Raji Mo\iRZBweHSxc3nzJGF{e2G7 M37seFUxOCCwTR?= M16yO|AuPzJiaB?= NGHtXo9qdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> M1H5[VIyOzdzNES2
Daudi  MUnBdI9xfG:|aYOgRZN{[Xl? M3jicVUxOCCwTR?= MXiwMVczKGh? NEDwPYVqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> NVPpUHp7OjF|N{G0OFY>
L428 MVLBdI9xfG:|aYOgRZN{[Xl? NGHHTYQ2ODBibl2= MnjUNE04OiCq NGrP[mZqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> MlnKNlE{PzF2NE[=
KM-H2 M1HKVGFxd3C2b4Ppd{BCe3OjeR?= MYG1NFAhdk1? MYGwMVczKGh? Mn\VbY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= MVGyNVM4OTR2Nh?=
HDLM-2 MXrBdI9xfG:|aYOgRZN{[Xl? M3rzd|UxOCCwTR?= M{K0V|AuPzJiaB?= NGe4ZlNqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> MmfqNlE{PzF2NE[=
L450 MmPhRZBweHSxc3nzJGF{e2G7 NFy5Zm42ODBibl2= M1X3W|AuPzJiaB?= NWW0UYRWcW6mdXPld{BieG:ydH;zbZMhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> NH23VIEzOTN5MUS0Oi=>
SW620 M3LWRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH;4ZWNGSzVyPUGwxtEzNjFibl2= NFnqcWIzOTJ2NUC5NC=>
HCT116 NWnqeotZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlH2SWM2OD1zMdMxN{4{KG6P Mn:zNlEzPDVyOUC=
MDA-MB-435 M3KwTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1r2eFAuOTByMECgcm0> NHm2d40zNTViZB?= NWO0OoZNTE2VTx?= NW\ETFZiUUN3ME2xNlUhdk1? M{\LTlIxOTd3OUK2
MDA-MB-468 NH;MUJZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWC0[mpxOC1zMECwNEBvVQ>? Mn;3Nk02KGR? M{\hSWROW09? NWHIc3BmUUN3ME2xOEBvVQ>? MlT4NlAyPzV7Mk[=
MDA-MB-231 NHjoUWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHH3WZkxNTFyMECwJI5O NH;5SpczNTViZB?= MVXEUXNQ MYTJR|UxRTFyNTDuUS=> NWrGV4MzOjBzN{W5NlY>
BT474 NWrmN4ZyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWKwMVExODByIH7N NHP2PJEzNTViZB?= NHrqeZVFVVOR M2LtVmlEPTB;ODDuUS=> MUmyNFE4PTl{Nh?=
MDA-MB-361 NWS5SmV[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4LicFAuOTByMECgcm0> MnHaNk02KGR? MYrEUXNQ M2\DR2lEPTB;N{Cgcm0> M{nHNVIxOTd3OUK2
HER18 MmXNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MojUNE0yODByMDDuUS=> MUWyMVUh\A>? NH7pfoZFVVOR M1PIRmlEPTB;MkCgcm0> NHzjcFAzODF5NUmyOi=>
HER18 NIHiR|FCeG:ydH;zbZMhSXO|YYm= NGjaPZMyODBibl2= NYLQeXNpOC9{ND:0PEBp NGD5fZdFVVOR NWXrbYF5cW6mdXPld{BieG:ydH;zbZMh[W6mIILl[JVk\XNiY3zvco9o\W6rYzDwc5RmdnSrYXy= NUnLUWw{OjBzN{W5NlY>
MDA-MB-231 M4rHWGFxd3C2b4Ppd{BCe3OjeR?= NWLuZZJ6OTB3IH7N M4KxflAwOjRxNEigbC=> MV7EUXNQ M3;QR4lv\HWlZYOgZZBweHSxc3nzJIFv\CC{ZXT1Z4V{KGOub37v[4VvcWNicH;0[Y51cWGu NFT0eWIzODF5NUmyOi=>
JHH-1 M4P6Umdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1q4VFAvO+LCk{GwNFDDqG6P MnTzO|IhcA>? NWXLfnRbTUN3ME2xO{41yrFzLkCgcm0> MnLBNVk6OTN7M{W=
JHH-2 NWT4fVBiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MknnNE4{6oDVMUCwNOKhdk1? NX33Z5c1PzJiaB?= NGjmWmhGSzVyPUKxPE4xyrFzMD64JI5O NX3ZVYF2OTl7MUO5N|U>
JHH-4 NED3S|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1raPVAvO+LCk{GwNFDDqG6P MlXFO|IhcA>? MkLDSWM2OD1zNUWuOuKyOTZwODDuUS=> MYqxPVkyOzl|NR?=
HuH-1 MonZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mnj1NE4{6oDVMUCwNOKhdk1? MnG0O|IhcA>? NVKxVnQ{TUN3ME2yO{4{yrF3LkCgcm0> NYnPXGRmOTl7MUO5N|U>
HuH-6 NXj1OpdCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV[wMlPjiJNzMECwxsBvVQ>? M{\TfFczKGh? M3X4UmVEPTB;Mz63xtExNjZibl2= Mn;YNVk6OTN7M{W=
HuH-7 NHjwXmFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnLiNE4{6oDVMUCwNOKhdk1? NYrUWIRXPzJiaB?= MWjFR|UxRTZwONMxNE4{KG6P MYexPVkyOzl|NR?=
HLE MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIjwNmgxNjQkgKOxNFAxyqCwTR?= NV;BPY4yPzJiaB?= NILEWnlGSzVyPUS1MlnDuTZwNDDuUS=> M3nh[VE6QTF|OUO1
HLF MljxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MW[wMlPjiJNzMECwxsBvVQ>? MlHVO|IhcA>? MoexSWM2OD1zMk[uNeKyOTJwMjDuUS=> MnzqNVk6OTN7M{W=
PLC/PRF/5 NH74cXFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXuwMlPjiJNzMECwxsBvVQ>? NX7HNnFSPzJiaB?= NIDxbWRGSzVyPUe2MlnDuTlwOTDuUS=> NV25W5Z4OTl7MUO5N|U>
SK-Hep1 NUXDTHU{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXSwMlPjiJNzMECwxsBvVQ>? M1nNOlczKGh? M2qxNGVEPTB;MkGuPeKyOS5{IH7N MX6xPVkyOzl|NR?=
Hep3B MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUCwMlPjiJNzMECwxsBvVQ>? NWHEbYViPzJiaB?= MXrFR|UxRTdwNtMxNU4zKG6P NVHxbGhvOTl7MUO5N|U>
HepG2 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoizNE4{6oDVMUCwNOKhdk1? MVm3NkBp MUDFR|UxRTF2LkhCtVEvPyCwTR?= M1H1NFE6QTF|OUO1
Ramos NIjLTmNCeG:ydH;zbZMhSXO|YYm= MmHUNlUwPTBxMUCwJI5O NHr5cJU1QCCq NXfGSFlOcW6lcnXhd4V{KHSqZTDs[ZZmdHNib3[geIhmKGOuZXH2[YQh\m:{bYOgc4YhWEGUUDDhcoQh[2G|cHHz[UA{ NYXtUVZwOTl6MkOxOlg>
Daudi  MV;BdI9xfG:|aYOgRZN{[Xl? Mlv3NlUwPTBxMUCwJI5O MmPZOFghcA>? NF3h[5dqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> MXexPVgzOzF4OB?=
BALM-14 NVGweIw2SXCxcITvd4l{KEG|c3H5 NXPNR2RKOTJwNT:yOU82OCCwTR?= MlXVOFghcA>? NH7YdG5qdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> MUexPVgzOzF4OB?=
BALM-27 MUXBdI9xfG:|aYOgRZN{[Xl? NI\jUXcyOi53L{K1M|UxKG6P MlXhOFghcA>? MoLpbY5kemWjc3XzJJRp\SCuZY\lcJMhd2ZidHjlJINt\WG4ZXSg[o9zdXNib3[gVGFTWCCjbnSgZ4F{eGG|ZTCz NGPO[ZAyQTh{M{G2PC=>
NB4 M1jYN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX3PdVVbOC5yMT:wMlEwOSEQvF2= NFnGc4I1QCCq MnzRbY5pcWKrdIOgZ4VtdCCpcn;3eIghe2mpbnnmbYNidnSueR?= MXOxPFM3PzR6NB?=

... 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]

Protocol

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 <1 mg/mL
In vivo 30% PEG 400+0.5% Tween 80+5% Propylene glycol 30mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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
Formula

C26H30FN7O3

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

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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
    Concentration
    Volume
    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
    V1
    C2
    V2

* 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

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.

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