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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  • 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

Choose Selective Aurora Kinase Inhibitors

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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 Mmi4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1LLPVAuPTByIH7N Mlm3OFjDqGh? M2WxWmlEPTB;MkWgcm0> MmjGNlUzPzd4NUm=
LNCaP MkjkRZBweHSxc3nzJGF{e2G7 M2j2cVAuPTByIH7N M{TkO|Q5yqCq NFXl[4hqdmS3Y3XzJIFxd3C2b4TpZ{Bk\WyuIHTlZZRpKHSqcn;1[4gh[2G|cHHz[U0{KHWycnXneYxifGmxbh?= MnzhNlUzPzd4NUm=
LNCaP NGHkO3FHfW6ldHnvckBCe3OjeR?= MkLJOVAhdk1? M3zXPVQ5KGh? NGLybVhqdmS3Y3XzJI1q[3KxboXjcIVqKHerdHigZY5mfWenbnnjJI1m[2ijbnnzcS=> M{PqfFI2Ojd5NkW5
Ramos MlvNSpVv[3Srb36gRZN{[Xl? MmDEOVAxKG6P MWmwMVczKGh? NFnPeGpqdmirYnn0d{BCfXKxcnGgRkBscW6jc3W= MUmyNVM4OTR2Nh?=
Daudi  NX;4Z3NFTnWwY4Tpc44hSXO|YYm= NGHsOYI2ODBibl2= NVfLRohbOC15MjDo MXnpcohq[mm2czDBeZJwemFiQjDrbY5ie2V? NUjvTIFqOjF|N{G0OFY>
L540 NETrW5BHfW6ldHnvckBCe3OjeR?= NH75Roc2ODBibl2= MUiwMVczKGh? NFfqbWdqdmirYnn0d{BCfXKxcnGgRkBscW6jc3W= M4P3bVIyOzdzNES2
BJAJ MkPiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmW1OVAxKG6P MnfqNE04OiCq MkjkbY5pcWKrdIOgZ4VtdCCpcn;3eIghe2mpbnnmbYNidnSueR?= NXu2[FRtOjF|N{G0OFY>
Ramos MknhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXzZNIxxPTByIH7N NEfNRWwxNTd{IHi= MWjpcohq[mm2czDj[YxtKGe{b4f0bEB{cWewaX\pZ4FvfGy7 M1fUW|IyOzdzNES2
Raji NWC3O2VVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHn1fWY2ODBibl2= MmDqNE04OiCq NWf6RnhQcW6qaXLpeJMh[2WubDDndo94fGhic3nncolncWOjboTsfS=> MoTyNlE{PzF2NE[=
Daudi  NYjPWXdNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFXl[GI2ODBibl2= NHHDO|QxNTd{IHi= MkXpbY5pcWKrdIOgZ4VtdCCpcn;3eIghe2mpbnnmbYNidnSueR?= NEPwcI4zOTN5MUS0Oi=>
L428 M{K3RWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1jnSFUxOCCwTR?= NIfG[GsxNTd{IHi= MnXUbY5pcWKrdIOgZ4VtdCCpcn;3eIg> NE\GU4UzOTN5MUS0Oi=>
KM-H2 MknCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn[xOVAxKG6P NWO0bYlGOC15MjDo MXfpcohq[mm2czDj[YxtKGe{b4f0bC=> M4X4RVIyOzdzNES2
HDLM-2 Ml\rS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGrkPGY2ODBibl2= MkHnNE04OiCq NIDGT2NqdmirYnn0d{Bk\WyuIHfyc5d1cA>? NHnsc2czOTN5MUS0Oi=>
L450 M4P1NGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX:1NFAhdk1? M33scVAuPzJiaB?= M3XjSolvcGmkaYTzJINmdGxiZ4Lve5Rp NYrvenBnOjF|N{G0OFY>
BJAJ NF7RTVVCeG:ydH;zbZMhSXO|YYm= NGjnboY2ODBibl2= NEH1bW8xNTd{IHi= MVHpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= M1LUbFIyOzdzNES2
Ramos NYjuV|doSXCxcITvd4l{KEG|c3H5 NG\6OGs2ODBibl2= M2G2WFAuPzJiaB?= MWTpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= M4Xqb|IyOzdzNES2
Raji NE\OOWtCeG:ydH;zbZMhSXO|YYm= MUS1NFAhdk1? NEDSUooxNTd{IHi= M3PldIlv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy MoX4NlE{PzF2NE[=
Daudi  M3W4[mFxd3C2b4Ppd{BCe3OjeR?= NV:1SJQyPTByIH7N NX25NpFKOC15MjDo NF7mOldqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> MnjNNlE{PzF2NE[=
L428 MY\BdI9xfG:|aYOgRZN{[Xl? Mo[zOVAxKG6P MnvRNE04OiCq MULpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= MYKyNVM4OTR2Nh?=
KM-H2 MnvhRZBweHSxc3nzJGF{e2G7 MX21NFAhdk1? NHfhNYoxNTd{IHi= NFK4PJhqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> NXfCUmZmOjF|N{G0OFY>
HDLM-2 NFu2VndCeG:ydH;zbZMhSXO|YYm= M{jQVVUxOCCwTR?= MVewMVczKGh? MnT1bY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= NF\3WIozOTN5MUS0Oi=>
L450 MnzJRZBweHSxc3nzJGF{e2G7 NFfKR4Y2ODBibl2= NHuwNVQxNTd{IHi= Ml7ubY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= MmPsNlE{PzF2NE[=
SW620 MmDtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3jpd2VEPTB;MUFCtVIvOSCwTR?= NVK4blh[OjF{NEWwPVA>
HCT116 NGG4VIZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYfFR|UxRTFzwsGzMlMhdk1? MXuyNVI1PTB7MB?=
MDA-MB-435 NXPxcI9VT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn3ONE0yODByMDDuUS=> NXv1R4VFOi13IHS= NWDsTGx1TE2VTx?= MkjnTWM2OD1zMkWgcm0> NXvRSVRZOjBzN{W5NlY>
MDA-MB-468 M4j4cWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1jWeVAuOTByMECgcm0> NVLlPXJVOi13IHS= MkPaSG1UVw>? NV60cpZRUUN3ME2xOEBvVQ>? Ml;HNlAyPzV7Mk[=
MDA-MB-231 M1HKemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWqwMVExODByIH7N NETMWHozNTViZB?= NX;xZ3hjTE2VTx?= MmDCTWM2OD1zMEWgcm0> Ml;yNlAyPzV7Mk[=
BT474 NXLkcWNKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWCwMVExODByIH7N M2T3d|IuPSCm NVHGZldjTE2VTx?= MXzJR|UxRThibl2= MV[yNFE4PTl{Nh?=
MDA-MB-361 NYWyc4t4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVOwMVExODByIH7N M1X5clIuPSCm NHn5[I5FVVOR MVHJR|UxRTdyIH7N M4n2flIxOTd3OUK2
HER18 NGD2T5hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFjo[lkxNTFyMECwJI5O MWiyMVUh\A>? MoD6SG1UVw>? NVWzT5hKUUN3ME2yNEBvVQ>? M4HoTlIxOTd3OUK2
HER18 Mo\DRZBweHSxc3nzJGF{e2G7 NEXUSoUyODBibl2= NFzydZgxNzJ2L{S4JIg> M2T4eWROW09? MlXGbY5lfWOnczDhdI9xfG:|aYOgZY5lKHKnZIXj[ZMh[2yxbn;n[Y5q[yCyb4TlcpRq[Wx? NWGwdIxrOjBzN{W5NlY>
MDA-MB-231 M2DxXGFxd3C2b4Ppd{BCe3OjeR?= NELmUFQyODVibl2= NHrmc4QxNzJ2L{S4JIg> MWXEUXNQ M{S4[Ilv\HWlZYOgZZBweHSxc3nzJIFv\CC{ZXT1Z4V{KGOub37v[4VvcWNicH;0[Y51cWGu MmHxNlAyPzV7Mk[=
JHH-1 MlTDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXWwMlPjiJNzMECwxsBvVQ>? M13MW|czKGh? NHH6bnNGSzVyPUG3MlTDuTFwMDDuUS=> MWexPVkyOzl|NR?=
JHH-2 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4fENlAvO+LCk{GwNFDDqG6P Mn3KO|IhcA>? M3n4cGVEPTB;MkG4MlDDuTFyLkigcm0> MWixPVkyOzl|NR?=
JHH-4 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWewMlPjiJNzMECwxsBvVQ>? Mmn3O|IhcA>? NIjS[IhGSzVyPUG1OU43yrFzNj64JI5O M1vsOVE6QTF|OUO1
HuH-1 NH7HVI5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4\PeVAvO+LCk{GwNFDDqG6P M4Dk[VczKGh? MmPHSWM2OD1{Nz6zxtE2NjBibl2= NEe5boQyQTlzM{mzOS=>
HuH-6 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1\NZlAvO+LCk{GwNFDDqG6P NHqwcFE4OiCq Mkf6SWM2OD1|LkhCtVAvPiCwTR?= M{ja[lE6QTF|OUO1
HuH-7 M4ntcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYiwMlPjiJNzMECwxsBvVQ>? NFTHSIg4OiCq MUTFR|UxRTZwONMxNE4{KG6P MYCxPVkyOzl|NR?=
HLE MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M174PFAvO+LCk{GwNFDDqG6P MWi3NkBp M2njVmVEPTB;NEWuPeKyPi52IH7N M1nUXFE6QTF|OUO1
HLF NEi4[XBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1zJeVAvO+LCk{GwNFDDqG6P MYe3NkBp M3LaTmVEPTB;MUK2MlHDuTF{LkKgcm0> NYq3WpVwOTl7MUO5N|U>
PLC/PRF/5 NUOyeHRiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGLQPI0xNjQkgKOxNFAxyqCwTR?= MYG3NkBp NX64T|ZMTUN3ME23Ok46yrF7Lkmgcm0> MmS2NVk6OTN7M{W=
SK-Hep1 MlG2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mo\wNE4{6oDVMUCwNOKhdk1? M3;VT|czKGh? NYPzd4JTTUN3ME2yNU46yrFzLkKgcm0> NXHFSXA4OTl7MUO5N|U>
Hep3B MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml;RNE4{6oDVMUCwNOKhdk1? MWS3NkBp MWfFR|UxRTdwNtMxNU4zKG6P M3fV[lE6QTF|OUO1
HepG2 MkTxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXmwMlPjiJNzMECwxsBvVQ>? MnzwO|IhcA>? NYD0OGZ4TUN3ME2xOE44yrFzLkegcm0> NWnWN5BXOTl7MUO5N|U>
Ramos MXHBdI9xfG:|aYOgRZN{[Xl? MYiyOU82OC9zMECgcm0> M1;pWVQ5KGh? M{fQdolv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> NHfjdooyQTh{M{G2PC=>
Daudi  MVfBdI9xfG:|aYOgRZN{[Xl? MYeyOU82OC9zMECgcm0> MWq0PEBp MXzpcoNz\WG|ZYOgeIhmKGyndnXsd{Bw\iC2aHWgZ4xm[X[nZDDmc5JueyCxZjDQRXJRKGGwZDDjZZNx[XOnIEO= NWnufZBEOTl6MkOxOlg>
BALM-14 MU\BdI9xfG:|aYOgRZN{[Xl? NFrwTGMyOi53L{K1M|UxKG6P MYq0PEBp Moq1bY5kemWjc3XzJJRp\SCuZY\lcJMhd2ZidHjlJINt\WG4ZXSg[o9zdXNib3[gVGFTWCCjbnSgZ4F{eGG|ZTCz M1K4OVE6QDJ|MU[4
BALM-27 M3;rN2Fxd3C2b4Ppd{BCe3OjeR?= NIDRVlUyOi53L{K1M|UxKG6P M4TPdlQ5KGh? NVvQendrcW6lcnXhd4V{KHSqZTDs[ZZmdHNib3[geIhmKGOuZXH2[YQh\m:{bYOgc4YhWEGUUDDhcoQh[2G|cHHz[UA{ M4XOO|E6QDJ|MU[4
NB4 M1HHfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn:0NE4xOS9yLkGvNUDPxE1? Mk\qOFghcA>? MV3pcohq[mm2czDj[YxtKGe{b4f0bEB{cWewaX\pZ4FvfGy7 M3vnbVE5OzZ5NEi0

... 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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    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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