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.

    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.

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)
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 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3r2TFAuPTByIH7N Mnu5OFjDqGh? MV;JR|UxRTJ3IH7N NWPNN2hZOjV{N{e2OVk>
LNCaP NVjGb5VoSXCxcITvd4l{KEG|c3H5 NVr0XmNPOC13MECgcm0> MmLZOFjDqGh? NV22epBzcW6mdXPld{BieG:ydH;0bYMh[2WubDDk[YF1cCC2aILveYdpKGOjc4Dhd4UuOyC3cILl[5Vt[XSrb36= M1W3[lI2Ojd5NkW5
LNCaP NIDLdoZHfW6ldHnvckBCe3OjeR?= M2LGWlUxKG6P NWLKe2pUPDhiaB?= NEfBWGhqdmS3Y3XzJI1q[3KxboXjcIVqKHerdHigZY5mfWenbnnjJI1m[2ijbnnzcS=> NFrOW2wzPTJ5N{[1PS=>
Ramos NV;V[pdRTnWwY4Tpc44hSXO|YYm= NVLwb4V3PTByIH7N M4LE[VAuPzJiaB?= NYixOI4{cW6qaXLpeJMhSXW{b4LhJGIhc2mwYYPl Ml\INlE{PzF2NE[=
Daudi  MknxSpVv[3Srb36gRZN{[Xl? MVG1NFAhdk1? M3HTcFAuPzJiaB?= MYfpcohq[mm2czDBeZJwemFiQjDrbY5ie2V? MXOyNVM4OTR2Nh?=
L540 NHLD[3BHfW6ldHnvckBCe3OjeR?= MUi1NFAhdk1? M1XlO|AuPzJiaB?= NG[yZnhqdmirYnn0d{BCfXKxcnGgRkBscW6jc3W= NX\0cFBCOjF|N{G0OFY>
BJAJ MnLFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3\OWlUxOCCwTR?= MkTJNE04OiCq M2jKb4lvcGmkaYTzJINmdGxiZ4Lve5RpKHOrZ37p[olk[W62bIm= M3XMTVIyOzdzNES2
Ramos M1;4dGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3PGUFUxOCCwTR?= MWiwMVczKGh? M1:4XolvcGmkaYTzJINmdGxiZ4Lve5RpKHOrZ37p[olk[W62bIm= NYHTeFF2OjF|N{G0OFY>
Raji M1yzcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUC1NFAhdk1? MXmwMVczKGh? NH\Zb3lqdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 NH;JUXYzOTN5MUS0Oi=>
Daudi  NHX5U5VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn7OOVAxKG6P MYCwMVczKGh? NFzLNZJqdmirYnn0d{Bk\WyuIHfyc5d1cCC|aXfubYZq[2GwdHz5 M17mSFIyOzdzNES2
L428 M1r3W2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoXGOVAxKG6P MUSwMVczKGh? MVHpcohq[mm2czDj[YxtKGe{b4f0bC=> NX\HN4QyOjF|N{G0OFY>
KM-H2 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlfQOVAxKG6P NYfZOpN2OC15MjDo NEjSb5NqdmirYnn0d{Bk\WyuIHfyc5d1cA>? NWTVfJZ6OjF|N{G0OFY>
HDLM-2 Ml\3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1HnXFUxOCCwTR?= M4j6eVAuPzJiaB?= MnPjbY5pcWKrdIOgZ4VtdCCpcn;3eIg> NV\qZWZJOjF|N{G0OFY>
L450 NX:yT41CT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGLueWk2ODBibl2= NWrXO|NkOC15MjDo NUHEd5RRcW6qaXLpeJMh[2WubDDndo94fGh? MU[yNVM4OTR2Nh?=
BJAJ Ml\aRZBweHSxc3nzJGF{e2G7 M3v4XFUxOCCwTR?= MkDKNE04OiCq NHHrbIxqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> MnK0NlE{PzF2NE[=
Ramos M4fWU2Fxd3C2b4Ppd{BCe3OjeR?= M2fTWFUxOCCwTR?= NWqxNm85OC15MjDo M4rhb4lv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy M2DoXVIyOzdzNES2
Raji NXO2R3FsSXCxcITvd4l{KEG|c3H5 MYq1NFAhdk1? MlW1NE04OiCq MnntbY5lfWOnczDhdI9xfG:|aYOgbY4h[SC2aX3lMYRmeGWwZHXueEBu[W6wZYK= NGTwVpczOTN5MUS0Oi=>
Daudi  M1rPRWFxd3C2b4Ppd{BCe3OjeR?= MlXYOVAxKG6P NYi3V5RlOC15MjDo M2jiWYlv\HWlZYOgZZBweHSxc3nzJIlvKGFidHnt[U1l\XCnbnTlcpQhdWGwbnXy MYWyNVM4OTR2Nh?=
L428 MX7BdI9xfG:|aYOgRZN{[Xl? MoLrOVAxKG6P MWOwMVczKGh? MVHpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= NU\KXWRmOjF|N{G0OFY>
KM-H2 M3ju[2Fxd3C2b4Ppd{BCe3OjeR?= M2fjZ|UxOCCwTR?= MWOwMVczKGh? NETWXXJqdmS3Y3XzJIFxd3C2b4Ppd{BqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> MmHXNlE{PzF2NE[=
HDLM-2 M1HxVWFxd3C2b4Ppd{BCe3OjeR?= NX;aUnlXPTByIH7N MVSwMVczKGh? MYLpcoR2[2W|IHHwc5B1d3OrczDpckBiKHSrbXWt[IVx\W6mZX70JI1idm6nch?= M1\wUVIyOzdzNES2
L450 MVnBdI9xfG:|aYOgRZN{[Xl? NIDWZoI2ODBibl2= MXuwMVczKGh? NWjTZVZpcW6mdXPld{BieG:ydH;zbZMhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> MVWyNVM4OTR2Nh?=
SW620 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYjFR|UxRTFywsGyMlEhdk1? MViyNVI1PTB7MB?=
HCT116 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX3FR|UxRTFzwsGzMlMhdk1? MoXXNlEzPDVyOUC=
BT474 M{npOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NI[5dIsxNTFyMECwJI5O Mn36Nk02KGR? MlrQSG1UVw>? NVnxXVVZUUN3ME24JI5O M{TiVVIxOTd3OUK2
HER18 NX7CcGJlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3[zd|AuOTByMECgcm0> NV6xS4dLOi13IHS= Ml3USG1UVw>? MXHJR|UxRTJyIH7N NHWwSFkzODF5NUmyOi=>
HER18 M1j1V2Fxd3C2b4Ppd{BCe3OjeR?= M3TueFExOCCwTR?= MlToNE8zPC92ODDo NEi0d5dFVVOR MmDYbY5lfWOnczDhdI9xfG:|aYOgZY5lKHKnZIXj[ZMh[2yxbn;n[Y5q[yCyb4TlcpRq[Wx? NH7ieXEzODF5NUmyOi=>
MDA-MB-231 MofIRZBweHSxc3nzJGF{e2G7 M4fa[FExPSCwTR?= NWXMWpo{OC9{ND:0PEBp M1Xhe2ROW09? NGXKPFJqdmS3Y3XzJIFxd3C2b4Ppd{BidmRicnXkeYNmeyClbH;uc4dmdmmlIIDveIVvfGmjbB?= NGnaNYEzODF5NUmyOi=>
JHH-1 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEfKNJcxNjQkgKOxNFAxyqCwTR?= Mn3RO|IhcA>? MXzFR|UxRTF5LkVCtVEvOCCwTR?= M4\5RlE6QTF|OUO1
JHH-2 MkTOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGT2UHgxNjQkgKOxNFAxyqCwTR?= MUe3NkBp MlrQSWM2OD1{MUiuNOKyOTBwODDuUS=> M2nrc|E6QTF|OUO1
JHH-4 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXOwMlPjiJNzMECwxsBvVQ>? NVzMbGFFPzJiaB?= MXLFR|UxRTF3NT62xtEyPi56IH7N NI\LclgyQTlzM{mzOS=>
HuH-1 NGPqZmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{nlZVAvO+LCk{GwNFDDqG6P NYTBNYhlPzJiaB?= NEDNWoxGSzVyPUK3MlPDuTVwMDDuUS=> NV;5e41LOTl7MUO5N|U>
HuH-7 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHW1UVYxNjQkgKOxNFAxyqCwTR?= MY[3NkBp NHHWd3NGSzVyPU[uPOKyOC5|IH7N NHnSUJQyQTlzM{mzOS=>
HLE MnnQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWTGXnZJOC5|4pETNVAxOMLibl2= NUi4PXNPPzJiaB?= NVPSdGZ3TUN3ME20OU46yrF4LkSgcm0> MlvnNVk6OTN7M{W=
HLF NHexNIxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWnm[nJZOC5|4pETNVAxOMLibl2= Mmj5O|IhcA>? NXv4dFdCTUN3ME2xNlYvOcLzMUKuNkBvVQ>? NU\QVVdWOTl7MUO5N|U>
PLC/PRF/5 MlK0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1f6bVAvO+LCk{GwNFDDqG6P MnWzO|IhcA>? NHP4OJdGSzVyPUe2MlnDuTlwOTDuUS=> MUixPVkyOzl|NR?=
SK-Hep1 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX\RbG5qOC5|4pETNVAxOMLibl2= NH3i[oY4OiCq NYTVc5FpTUN3ME2yNU46yrFzLkKgcm0> NVjwRXg5OTl7MUO5N|U>
Hep3B MlzNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M33QT|AvO+LCk{GwNFDDqG6P MVS3NkBp MVzFR|UxRTdwNtMxNU4zKG6P NV:2VW02OTl7MUO5N|U>
HepG2 NW\lb5ZJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXS1VYcxOC5|4pETNVAxOMLibl2= NHj5b|Q4OiCq MVPFR|UxRTF2LkhCtVEvPyCwTR?= NXrGZ5JiOTl7MUO5N|U>
Ramos MXXBdI9xfG:|aYOgRZN{[Xl? NWjyTY9tOjVxNUCvNVAxKG6P NUDOO|ZGPDhiaB?= M1LiV4lv[3KnYYPld{B1cGVibHX2[Yx{KG:oIITo[UBkdGWjdnXkJIZwem2|IH;mJHBCWlBiYX7kJINie3Cjc3WgNy=> NGH0fYEyQTh{M{G2PC=>
Daudi  NGrnVm5CeG:ydH;zbZMhSXO|YYm= NVfBRotEOjVxNUCvNVAxKG6P MnjHOFghcA>? MnvsbY5kemWjc3XzJJRp\SCuZY\lcJMhd2ZidHjlJINt\WG4ZXSg[o9zdXNib3[gVGFTWCCjbnSgZ4F{eGG|ZTCz NEnxXZYyQTh{M{G2PC=>
BALM-14 MmCwRZBweHSxc3nzJGF{e2G7 MWKxNk42NzJ3L{WwJI5O M2CwVFQ5KGh? NI\jeGRqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> NV75[GRHOTl6MkOxOlg>
BALM-27 NVzrb|BTSXCxcITvd4l{KEG|c3H5 M4jGe|EzNjVxMkWvOVAhdk1? MknUOFghcA>? NFjyUGVqdmO{ZXHz[ZMhfGinIHzleoVteyCxZjD0bIUh[2ynYY\l[EBnd3KvczDv[kBRSVKSIHHu[EBk[XOyYYPlJFM> NWjXcYl2OTl6MkOxOlg>
NB4 NFKwOIJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYewMlAyNzBwMT:xJO69VQ>? MmTTOFghcA>? M3y5U4lvcGmkaYTzJINmdGxiZ4Lve5RpKHOrZ37p[olk[W62bIm= NEOwfIEyQDN4N{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 slightly soluble or insoluble
In vivo Add solvents individually and in order:
30% PEG 400+0.5% Tween 80+5% Propylene glycol

* 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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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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID