Alisertib (MLN8237)

Catalog No.S1133

Alisertib (MLN8237) Chemical Structure

Molecular Weight(MW): 518.92

Alisertib (MLN8237) is a selective Aurora A inhibitor with IC50 of 1.2 nM in a cell-free assay. It has >200-fold higher selectivity for Aurora A than Aurora B. Phase 3.

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Cited by 48 Publications

12 Customer Reviews

  • Inhibition of Aurka kinase activity by MLN8237 impairs expression of pluripotency genes in CCE cells as measured by qRT-PCR. All values shown are mean ?SEM for n=3. The level of phosphorylated H3(S10) (p-H3(S10)), an Aurka phosphorylation target site, is decreased in MLN8237-treated samples.

    Cell Stem Cell 2012 11, 179-94. Alisertib (MLN8237) purchased from Selleck.

    Recruitment of clathrin to the mitotic spindle is controlled by phosphorylation of TACC3 by Aurora-A kinase. Representative micrographs of HEK293 cells incubated with 0.3 μM MLN8237 for 40 min. Cells were fixed and stained as indicated.

    EMBO J 2012 30, 906-19. Alisertib (MLN8237) purchased from Selleck.

  • Tissue levels of 53BP1, a-tubulin, IkB-a and IL-6 in an Hs294T xenograft treated with MLN8237 or vehicle control were visualized by immunofluorescence co-staining with DAPI. Representative micrographs are shown from triplicate experiments.

    EMBO Mol Med 2013 5(1), 149-66. Alisertib (MLN8237) purchased from Selleck.

    NUSAP mitotic phosphorylation at Ser 240 correlates with Aurora A activity. Protein samples of FLAG-NUSAP immunoprecipitated from I, M and MtMLN or with MtZM were analysed using LC-MS/MS, focusing on the predicted phosphorylated residue Ser 240. The histograms (A, B) show the calculated ratios based on peptides carrying the phosphorylated Ser 240 compared with all matched peptides containing this residue.

     

     

    EMBO reports 2010 11, 977-984. Alisertib (MLN8237) purchased from Selleck.

  • Aurora A inhibition rescues the PPP6C depletion phenotype. (A) HeLa cells transfected for 48 h with control and PPP6C si08 duplexes were treated with 10 or 20 nM MLN8237 or a solvent control for 15 min before lysis in phosphatase inhibitor containing buffer or fixation. Total lysates were analyzed by Western blotting. The red and black lines indicate the hosphorylated and nonphosphorylated forms of Aurora A. Fixed cells were stained using DAPI to detect DNA and antibodies to α-tubulin and Aurora A pT288. The intensity of pT288 staining was integrated using ImageJ over the spindle region defined by TPX2 staining and is plotted in the bar graph ( n = 4). Arrowheads indicate micronuclei. Bar, 5 µm. (B) HeLa cells transfected for 48 h with control and PPP6C si08 duplexes were treated with 10 nM MLN8237 or a solvent control for 24 h before fixation and staining with DAPI to detect DNA.

    J Cell Biol 2010 191, 1315-32. Alisertib (MLN8237) purchased from Selleck.

    D) Pharmacological inhibition of AURKA using alisertib led to downregulation of p-EIF4E (S209) and c-MYC proteins in FLO-1 and SK-GT-4 resistant cells, with or without RAD001 treatment.

    Clin Cancer Res, 2017, 23(14):3756-3768. Alisertib (MLN8237) purchased from Selleck.

  • Eg5 inhibition counteracts the induction of spindle pole fragmentation by Aurora-A inactivation. The protocol to inhibit Aurora-A by MLN8237 in cells progressing towards mitosis is depicted (time intervals not represented to scale). Control cultures were treated with solvent (DMSO) in the same time window. When indicated, MON was added 1 hour before harvesting. Note the absence of active phosphorylated (pThr288) Aurora-A (in red in IF panels) in cells treated with MLN8237. Upper histograms represent the percentage of all spindle and MT abnormalities in control and MLN8237-treated cultures (200 counted PM/M per condition in 2 experiments); the grey fraction of the histograms represents mitoses with spindle extrapoles, while other defects (monopolar or disorganised spindles, few and short MTs) are in white. Lower histograms and IF panels show that concomitant Eg5 inhibition by MON prevents MLN8237-induced spindle pole fragmentation (note the failure of centrosome migration reflecting Eg5 inactivation in lower IF panels). 200 PM/M per condition were counted in 2 experiments. Error bars represent s.d. **: p < 0.001, χ2 test. Red asterisks indicate significant differences with respect to DMSO controls, and black asterisks significant differences between Aurora-Ai mitoses with active or inactive Eg5. Scale bar: 10 μm

    Mol Cancer 2011 10, 131. Alisertib (MLN8237) purchased from Selleck.

    Alisertib inhibits AURKA and AURKB in a concentration-dependent manner. (a) Alisertib induces G 2 /M delay or genome reduplication. HeLa cells were exposed to buffer or the indicated concentrations of Alisertib. After 24 h, the cells were harvested and analyzed with flow cytometry. The positions of 2N, 4N and 8N DNA contents are indicated. (b) Alisertib delays mitotic exit or induces slippage. HeLa cells stably expressing histone H2B-GFP were exposed to buffer or the indicated concentrations of Alisertib. Individual cells were then tracked for 24 h with time-lapse microscopy. Each horizontal bar represents one cell (n ¼ 50). Key: light gray ¼ interphase; black ¼ mitosis (from DNA condensation to anaphase or mitotic slippage); dark gray ¼ interphase after mitotic slippage; truncated bars ¼ cell death. (c) Different concentrations of Alisertib are involved in delaying mitotic exit and inducing slippage. Live-cell imaging of cells treated with Alisertib 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 was quantified. (d) Alisertib promotes apoptosis in a concentration-dependent manner. HeLa cells were incubated with the indicated concentrations of Alisertib for 48 h. The cells were then harvested and analyzed with flow cytometry. (e) Concentration-dependent cytotoxicity of Alisertib. HeLa cells were cultured in the presence of the indicated concentrations of Alisertib for 48 h. The number of live and dead cells was analyzed with trypan blue exclusion assay. (f) Concentration-dependent suppression of long-term survival by Alisertib. HeLa cells were seeded on 60-mm culture plates and grown in the presence of 250 n M or 1 m M of Alisertib. After 24 h, the cells were washed gently and propagated in normal medium for another 10–12 days. Colonies were fixed and stained with crystal violet solution (examples of the plates are shown). Average±s.d. from three independent experiments. (g) Both AURKA and AURKB are inhibited by Alisertib.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 Alisertib for 2 h. Lysates were then prepared and activated phospho-AURKAThr288 and AURKBThr232were detected with immunoblotting. The asterisk indicates the position of an AURKB-like protein (the same throughout this study). Uniform loading was confirmed by immunoblotting for actin. In this assay, nocodazole and MG132 (a proteasome inhibitor) were added to prevent the cells from exiting mitosis. Accordingly, the total AURKA and AURKB levels remained constant throughout the experiment. (h) Alisertib prevents activation of AURKA and AURKB. HeLa cells were incubated with the indicated concentrations of Alisertib for 8 h. Nocodazole was then added for another 6 h to trap cells that entered mitosis. Lysates were prepared and analyzed with immunoblotting. Actin analysis was included to assess loading and transfer.

    Oncogene 2014 33, 3550-60. Alisertib (MLN8237) purchased from Selleck.

  • Inhibition of Aurora A (12.5 nM) by MLN8054 or MLN8237 was assessed in duplicate radiometric assays containing 100 μM [γ-32P] ATP and quantified by p81 phosphocellulose assay and scintillation counting. Kinase activity is reported as a percentage of control calculated from duplicate incubations containing 2.5% (v/v) DMSO. IC50 values represent the mean ±SEM calculated from two independent experiments.

     

     

    ACS Chem Biol 2010 5, 563-576. Alisertib (MLN8237) purchased from Selleck.

    The effects of T217D and T217N Aurora A mutations were directly compared to WT Aurora A-expressing cells. Each well was treated with either DMSO or 500 nM MLN8054 (E), or 30 nM MLN8237 (F) on day one of the experiment and cells were cultured for 8 days, at which point they were fixed. For all colony assays, an area encompassing >90 % of the colonies per dish is shown. Similar results were seen in two independent duplicate experiments.

    ACS Chem Biol 2010 5, 563-576. Alisertib (MLN8237) purchased from Selleck.

  • B, drug-treated cells were also stained with DAPI to visualize nuclear DNA and analyzed with a microscope equipped with a fluorescence digital CCD camera. Representative results are shown. Bar, 40 μm.

    J Biol Chem, 2017, 292(5):1910-1924. Alisertib (MLN8237) purchased from Selleck.

    C, Fry depletion decreases the level of Thr-210 phosphorylation of Plk1 on spindle poles. HeLa cells transfected with siRNAs were cultured in growth medium for 12 h and in thymidine-containing medium for 36 h. They were then released from thymidine arrest for 12 h before being fixed and stained with anti-Plk1 pT210 ( green) and anti-pericentrin (red) antibodies. DNA was stained with TO-PRO-3 ( blue ). For Aurora A inhibition, after release from thymidine block for 10 h, HeLa cells transfected with control siRNA were incubated for2h in medium containing MLN8237 (100 nM) and MG132 (10 μM). Magnified images of the white boxes are also shown. Scale bar ,5 μm.

    J Biol Chem 2012 287, 27670-81. Alisertib (MLN8237) purchased from Selleck.

Purity & Quality Control

Choose Selective Aurora Kinase Inhibitors

Biological Activity

Description Alisertib (MLN8237) is a selective Aurora A inhibitor with IC50 of 1.2 nM in a cell-free assay. It has >200-fold higher selectivity for Aurora A than Aurora B. Phase 3.
Features First orally available inhibitor of Aurora A.
Targets
Aurora A [1]
(Cell-free assay)
1.2 nM
In vitro

MLN8237 shows >200-fold higher selectivity for Aurora A than the structurally related Aurora B with an IC50 of 396.5 nM, and does not have any significant activity against 205 other kinases. [1] MLN8237 (0.5 μM) treatment inhibits the phosphorylation of Aurora A in MM1.S and OPM1 cells, without affecting the Aurora B mediated histone H3 phosphorylation. MLN8237 significantly inhibits cell proliferation in multiple myeloma (MM) cell lines with IC50 values of 0.003-1.71 μM. MLN8237 displays more potent anti-proliferation activity against primary MM cells and MM cell lines in the presence of BM stroma cells, as well as IL-6 and IGF-1 than against MM cells alone. MLN8237 (0.5 μM) induces 2- to 6-fold increase in G2/M phase in primary MM cells and cell lines, as well as significant apoptosis and senescence, involving the up-regulation of p53, p21 and p27, as well as PARP, caspase 3, and caspase 9 cleavage. In addition, MLN8237 shows strong synergistic anti-MM effect with dexamethasone, as well as additive effect with doxorubicin and bortezomib. [2] MLN8237 (0.5 μM) treatment causes the inhibition of colony formation of FLO-1, OE19, and OE33 esophageal adenocarinoma cell lines, and induces a significant increase in the percentage of polyploid cells, and subsequently an increase in the percentage of cells in the sub-G1 phase, which can be further enhanced in combination with cisplatin (2.5 μM), involving the higher induction of TAp73β, PUMA, NOXA, cleaved caspase-3, and cleaved PARP as compared with a single-agent treatment. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HCT116 NYfidoFYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmDkNE42KM7:TR?= MWW3NkBp NHXTXZhFVVOR MnXuTWM2OD1yLkC0JO69VQ>? MljtNlYyOzZ4OES=
LS174T NGHzSYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M13wVVAvPSEQvF2= MmrVO|IhcA>? NVLu[mxGTE2VTx?= MmjoTWM2OD1yLkC1JO69VQ>? MXKyOlE{PjZ6NB?=
T84 MlnQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{D2ZVAvPSEQvF2= MoHlO|IhcA>? MlzBSG1UVw>? MWPJR|UxRTBwMEmg{txO NV3uXFA6OjZzM{[2PFQ>
LS180 NHK3VpRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWqwMlUh|ryP M{TxTVczKGh? NVi4[YV1TE2VTx?= M3\MZmlEPTB;MTFOwG0> Ml3GNlYyOzZ4OES=
SW948 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NULzUppZOC53IN88US=> MWe3NkBp NWXh[WdMTE2VTx?= MXXJR|UxRTFizszN M3yyclI3OTN4Nki0
HCT15 NUWyNWRFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{XTRVAvPSEQvF2= MkHZO|IhcA>? M1jEVWROW09? M13pZmlEPTB:MD60JO69VQ>? MoLINlYyOzZ4OES=
DLD-1 M3LpXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmPUNE42KM7:TR?= M3vzPFczKGh? NW\yVnBKTE2VTx?= M4W3fmlEPTB:MD64JO69VQ>? NIXmd4wzPjF|Nk[4OC=>
MIP-101 NWCydmFUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3:5elAvPSEQvF2= MorrO|IhcA>? NHfrdYtFVVOR Ml[yTWM2OD1zIN88US=> MlvqNlYyOzZ4OES=
SNU1544 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mny2NE42KM7:TR?= MYq3NkBp MkLQSG1UVw>? MlLtTWM2OD1zIN88US=> NE\sSG0zPjF|Nk[4OC=>
OCI-Ly10 NGj5[phEgXSxdH;4bYMhSXO|YYm= NEfnfHo4OiCq NVfvUXcyTE2VTx?= MWrJR|UxRTBwMEW4JO69VQ>? M{TmR|I2QDd6M{Ox
SU-DHL2 NFzibYpEgXSxdH;4bYMhSXO|YYm= MlHLO|IhcA>? MXfEUXNQ M1rmSWlEPTB;MD6wNUDPxE1? NU[3Z3RxOjV6N{izN|E>
OCI-LY7 MkDCR5l1d3SxeHnjJGF{e2G7 NFjLR2I4OiCq MlraSG1UVw>? NU\TW5ZzUUN3ME2wMlA5OSEQvF2= NWnrbXhpOjV6N{izN|E>
SU-DHL6 M{LadGN6fG:2b4jpZ{BCe3OjeR?= MlzFO|IhcA>? M3P6[GROW09? NHPNPIlKSzVyPUCuOFgzKM7:TR?= NH3MVpczPTh5OEOzNS=>
Jeko-1 MkPlR5l1d3SxeHnjJGF{e2G7 MWK3NkBp NISzSo1FVVOR MlKyTWM2OD1yLkCyPUDPxE1? NFvVeHMzPTh5OEOzNS=>
JVM-2 MoXJR5l1d3SxeHnjJGF{e2G7 NInRR3M4OiCq M2S3VmROW09? MXHJR|UxRTBwMEGg{txO NWPPXlFkOjV6N{izN|E>
Rec-1 MWLDfZRwfG:6aXOgRZN{[Xl? NXzwUXFbPzJiaB?= M3THUWROW09? NH3tcldKSzVyPUCuNFg4KM7:TR?= M3f6[lI2QDd6M{Ox
Z-138 M2rOb2N6fG:2b4jpZ{BCe3OjeR?= NE\yTFE4OiCq NYfpTVBJTE2VTx?= NXjWPHE5UUN3ME2wMlAyOyEQvF2= NVP1botlOjV6N{izN|E>
H9 MX;DfZRwfG:6aXOgRZN{[Xl? NGPhNoE4OiCq M{\pOGROW09? NUnVZ5RLUUN3ME2wMlYh|ryP M4LGVlI2QDd6M{Ox
HH NVTjU|dES3m2b4TvfIlkKEG|c3H5 NX3ZfWZEPzJiaB?= MofvSG1UVw>? MnexTWM2OD1yLkeg{txO MYGyOVg4QDN|MR?=
DND41 NYHzWndGS3m2b4TvfIlkKEG|c3H5 MUC3NkBp NHvEdnhFVVOR NIjOfJFKSzVyPUCuNUDPxE1? MYOyOVg4QDN|MR?=
CCL119 NYP2WVRWS3m2b4TvfIlkKEG|c3H5 M3HYVlczKGh? M{HyU2ROW09? NF;oc4NKSzVyPUCuNFYzKM7:TR?= NXXPZ2x5OjV6N{izN|E>
J.Cam 1.6 NH63[49EgXSxdH;4bYMhSXO|YYm= MV63NkBp NIPDbI1FVVOR NGTwTldKSzVyPUCuNVA2KM7:TR?= M4DsTVI2QDd6M{Ox
Sup-T1 M2[0TmN6fG:2b4jpZ{BCe3OjeR?= M{XkZ|czKGh? NIjJeXJFVVOR NXHEW4pHUUN3ME2yMlE1OiEQvF2= NVXLcmlCOjV6N{izN|E>
Tib 152 M3n6dmN6fG:2b4jpZ{BCe3OjeR?= NX[5OGhDPzJiaB?= M4fQNGROW09? MXnJR|UxRTBwODFOwG0> M1vhXFI2QDd6M{Ox
MCF7 NXP2WZlqTnWwY4Tpc44hSXO|YYm= NYHRfnB[PSEQvF2= MUmyOEBp MlW3SG1UVw>? NVHab|lkUW6mdXPld{BIOi:PIHHydoV{fA>? M4D4WVI2QDN2NECx
MDA-MB-231 Mn\KSpVv[3Srb36gRZN{[Xl? M3fO[lUh|ryP M3jvXlI1KGh? NV7XTpdyTE2VTx?= NIPXSJZKdmS3Y3XzJGc{N01iYYLy[ZN1 MoTLNlU5OzR2MEG=
MCF7 MXLGeY5kfGmxbjDBd5NigQ>? M4TIU|Uh|ryP M2rK[|I1KGh? NYnpW2F3TE2VTx?= Mnv0SIVkemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|EwS0SFMh?= NI\qW|AzPTh|NESwNS=>
MCF7 NV;RclRzTnWwY4Tpc44hSXO|YYm= M4DZeVUh|ryP NITBcpQzPCCq NWrKVHdrTE2VTx?= NHTpbJBF\WO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gR2RMOg>? MYSyOVg{PDRyMR?=
MCF7 NX\s[WV[TnWwY4Tpc44hSXO|YYm= NGT6RW82KM7:TR?= NXHldJh4OjRiaB?= M4S1T2ROW09? MXTE[YNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZiY4njcIlvKEJz NH74NHgzPTh|NESwNS=>
MCF7 MYDGeY5kfGmxbjDBd5NigQ>? MWm1JO69VQ>? M4LZc|I1KGh? NYX4SmFHTE2VTx?= NXLxSWd5UW6lcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJJAzOSCZYX[xM2NqeDF? MljRNlU5OzR2MEG=
MCF7 M3:wZ2Z2dmO2aX;uJGF{e2G7 NVf3VlB6PSEQvF2= M4G5UVI1KGh? MY\EUXNQ MnPBTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIICyO{BMcXBz NEPXWHAzPTh|NESwNS=>
MDA-MB-231 NIC1XY9HfW6ldHnvckBCe3OjeR?= NXnLdGRQPSEQvF2= NF3tNFczPCCq M1\iXWROW09? NGDPPZBF\WO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gR2RMOS:FRFOy NX7Zc5JHOjV6M{S0NFE>
MDA-MB-231 MlT5SpVv[3Srb36gRZN{[Xl? NF6wO3UyKM7:TR?= NVrPfG1vOjRiaB?= MoO5SG1UVw>? Ml6xTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|I> NGTDUmIzPTh|NESwNS=>
MDA-MB-231 NV7FZZo3TnWwY4Tpc44hSXO|YYm= MXK1JO69VQ>? NXL2d2JROjRiaB?= NUPTb4EzTE2VTx?= NYj4RY9STGWlcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJIN6[2yrbjDCNS=> NV74[G5vOjV6M{S0NFE>
MDA-MB-231 M4SxOGZ2dmO2aX;uJGF{e2G7 MmjNOUDPxE1? Moq0NlQhcA>? MmH0SG1UVw>? NHO2WohKdmO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gdFIyKFejZkGvR4lxOQ>? NFH3OnIzPTh|NESwNS=>
MDA-MB-231 NIHmbGVHfW6ldHnvckBCe3OjeR?= Mnj1OUDPxE1? NXTCXnZZOjRiaB?= NIXmeFRFVVOR MUnJcoNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZicEK3JGtqeDF? M{fWZlI2QDN2NECx
MDA-MB-231 Mn71SpVv[3Srb36gRZN{[Xl? M2PiclUh|ryP Ml\JNlQhcA>? NVP4dJh1TE2VTx?= Ml3YTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIIC1Ny=> M33sclI2QDN2NECx
MCF7 NH\xd3lCeG:ydH;zbZMhSXO|YYm= NF70foQ2KM7:TR?= MlLONlQhcA>? NHn0PYRFVVOR MYLJcoR2[2W|IHHwc5B1d3SrYzDk[YF1cA>? NIjySGYzPTh|NESwNS=>
MDA-MB-231 NHHYV|NCeG:ydH;zbZMhSXO|YYm= NIjsZWk2KM7:TR?= MVKyOEBp M1;2ZWROW09? NU\3PVRJUW6mdXPld{BieG:ydH;0bYMh\GWjdHi= M1zUdVI2QDN2NECx
MCF7 MYfGeY5kfGmxbjDBd5NigQ>? NIO3bVkyKM7:TR?= NUex[ZlCPzJiaB?= MmLLSG1UVw>? M1jhSmlv\HWlZYOgZZV1d3CqYXfpZ{Bl\WG2aB?= NU\B[plQOjV6M{S0NFE>
MDA-MB-231 NVP2bG5kTnWwY4Tpc44hSXO|YYm= M{LCdVEh|ryP NGnoeZk4OiCq NXryeZV2TE2VTx?= M321XGlv\HWlZYOgZZV1d3CqYXfpZ{Bl\WG2aB?= NHe3PWwzPTh|NESwNS=>
U-2 OS MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4nPRlUxKM7:TR?= NGfYenAzPCCq MWnEUXNQ M3LLT2lEPTB;MU[uOkDPxE1? NGDEN4QzPTd7MkixNS=>
MG-63 NXW0SIQ5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYO1NEDPxE1? M{jYVlI1KGh? NHTUfGZFVVOR NEjRXoNKSzVyPUmuOUDPxE1? M{e2Z|I2Pzl{OEGx
U-2 OS MV3BdI9xfG:|aYOgRZN{[Xl? Ml7sOUDPxE1? NED3TFAzPCCq MUHEUXNQ M4nR[mlv\HWlZYOgZZBweHSxdHnjJINmdGxiZHXheIg> NWrUbFFVOjV5OUK4NVE>
MG-63 MX7BdI9xfG:|aYOgRZN{[Xl? MkfZOUDPxE1? MXyyOEBp NF:3dmpFVVOR NX23SHlYUW6mdXPld{BieG:ydH;0bYMh[2WubDDk[YF1cA>? M17Cc|I2Pzl{OEGx
U-2 OS NYO1XZdwTnWwY4Tpc44hSXO|YYm= MmrpOUDPxE1? MWqyOEBp NVPMTI1oTE2VTx?= NH;ibZVRem:vb4Tld{BifXSxcHjh[4lkKGOnbHyg[IVifGh? M4nCXFI2Pzl{OEGx
MG-63 NY\CVGtKTnWwY4Tpc44hSXO|YYm= NGrVelM2KM7:TR?= M3jqOFI1KGh? MmfDSG1UVw>? M1i2RXBzd22xdHXzJIF2fG:yaHHnbYMh[2WubDDk[YF1cA>? NFniRWYzPTd7MkixNS=>
PANC-1 M3LCXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX21NEDPxE1? NXXC[Fk{OjRiaB?= NVf4T4ZUTE2VTx?= MmfyTWM2OD15LkGg{txO M2qzcVI2PjN{MkK1
BxPC-3 MnHCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoXCOVAh|ryP NWDsfmFCOjRiaB?= NGX3c4pFVVOR M3zKRWlEPTB;Nj64JO69VQ>? MYGyOVY{OjJ{NR?=
PANC-1 M3Lz[WZ2dmO2aX;uJGF{e2G7 MYm1JO69VQ>? MmD2NlQhcA>? MoC3SG1UVw>? MV3JcoR2[2W|IHPlcIwh[3mlbHWgZZJz\XO2IHnuJGczN01icHjhd4U> MXWyOVY{OjJ{NR?=
BxPC-3 MlTKSpVv[3Srb36gRZN{[Xl? M4rKdFUh|ryP MXKyOEBp NIDM[VhFVVOR NXnjVm5MUW6mdXPld{Bk\WyuIHP5Z4xmKGG{cnXzeEBqdiCJMj;NJJBp[XOn M4T0VlI2PjN{MkK1
PANC-1 NEnJRo1HfW6ldHnvckBCe3OjeR?= M{D3eVUh|ryP M1\0cFI1KGh? MkW0SG1UVw>? NETRWmZKdmS3Y3XzJIF2fG:yaHHnbYMh[2WubDDk[YF1cA>? MmWyNlU3OzJ{MkW=
BxPC-3 Mn;1SpVv[3Srb36gRZN{[Xl? MV61JO69VQ>? Mny2NlQhcA>? M4rBbGROW09? M3fUVmlv\HWlZYOgZZV1d3CqYXfpZ{Bk\WyuIHTlZZRp MVmyOVY{OjJ{NR?=
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SMS-SAN M{jJ[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MW[xNEDPxE1? MknkPVYhcA>? MkP0SG1UVw>? NHL5SVRKSzVyPUCuNFIxKM7:TR?= NXj1NWRSOjF2NEi1PVE>
Granta-4 NHTEN41EgXSxdH;4bYMhSXO|YYm= MoD6NVAh|ryP MkXnO{Bl M1H6[WlEPTB;MD6wOFAh|ryP NXHZ[ZVJOjF{OUG4Olc>
DB MX;DfZRwfG:6aXOgRZN{[Xl? Mo[yNVAh|ryP NVr0[5lKPyCm MWXJR|UxRTBwMESyJO69VQ>? M4OxflIyOjlzOE[3
RL Ml;TR5l1d3SxeHnjJGF{e2G7 Mn[zNVAh|ryP NUfPSW8yPyCm MYHJR|UxRTBwMEG1JO69VQ>? M3jVTVIyOjlzOE[3
K562 M2X6Umdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIXmZXcyOCEQvF2= NFf3[2k6PiCq MYTJR|UxRTBwMEi3JO69VQ>? NV20XYFnOjFyOUG2N|M>
LAMA-84 M4XxWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NITz[m8yOCEQvF2= NF\0b486PiCq M1jaWmlEPTB;MD6wOVch|ryP M4L4bFIyODlzNkOz
MM15 M37UVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MojuOEDPxE1? NHPSVYo4OiCq MW\EUXNQ M37QVWlEPTB;MD6xN{DPxE1? MWCyNFM5Ojh2NB?=
OPM1 M2nkbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3fNOVQh|ryP NWfoN3NiPzJiaB?= NEPEXVRFVVOR MUPJR|UxRTBwMEOg{txO NX\ufFc5OjB|OEK4OFQ>
RPM1 NVvmNpozT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1vIdFQh|ryP MX63NkBp MVfEUXNQ NIf3eY9KSzVyPUGwMlMzKM7:TR?= MnHKNlA{QDJ6NES=
INA6 NYO4ZWdZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlG5OEDPxE1? MlHhO|IhcA>? MXrEUXNQ NGS0XVVKSzVyPUCuNFAzKM7:TR?= M3TzN|IxOzh{OES0
OPM2 NV;lS5pMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlPFOEDPxE1? MnjKO|IhcA>? MkXtSG1UVw>? NEXTOYRKSzVyPUSuN|ch|ryP MoGwNlA{QDJ6NES=
MM1R MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1\Y[FQh|ryP MV23NkBp Ml\rSG1UVw>? MYTJR|UxRTFwNkig{txO NGiyXIkzODN6Mki0OC=>
DOX40 MmTTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoDWOEDPxE1? MmLsO|IhcA>? NV;wPZNoTE2VTx?= MUDJR|UxRTVwNEig{txO M2TaflIxOzh{OES0
LR5 Ml3US5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mlz1OEDPxE1? NGTLN3M4OiCq MXrEUXNQ NVT5XWh5UUN3ME2yMlU{KM7:TR?= MnLnNlA{QDJ6NES=
U266 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV3HTYpJPCEQvF2= MUi3NkBp NEDmVGJFVVOR NEH4d5ZKSzVyPUGuOFMh|ryP MWmyNFM5Ojh2NB?=
RD Mo\XS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmTENVAh|ryP MlvkPVYhcA>? M1vhcmlEPTB;MD6yNlgh|ryP NHnUToIzODFyOEOzPC=>
Rh41 NGn4NXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVnYSlJ6OTBizszN NIG2cWs6PiCq MoPFTWM2OD1yLkC5NEDPxE1? MV6yNFExQDN|OB?=
Rh30 MlHVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYHuWZNiOTBizszN NYTDcXlkQTZiaB?= MlPETWM2OD1yLkKzNEDPxE1? MlG0NlAyODh|M{i=
BT-12 NICz[lBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2HucVExKM7:TR?= M4e0elk3KGh? NH7nZXhKSzVyPUCuNFYxKM7:TR?= MYGyNFExQDN|OB?=
CHLA-266 M4roRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlnVNVAh|ryP MV:5OkBp NHO0bWtKSzVyPUCuNFczKM7:TR?= NW\WOppOOjBzMEizN|g>
TC-71 NVvscHhLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2fQXVExKM7:TR?= MmD4PVYhcA>? NGm0ZpJKSzVyPUCuNVAzKM7:TR?= MUWyNFExQDN|OB?=
SJ-GBM2 Ml:yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX2xNEDPxE1? MoXWPVYhcA>? Mm\zTWM2OD1yLkC1NEDPxE1? M3;EUFIxOTB6M{O4
NALM-6 MoX3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2j3W|ExKM7:TR?= Mnz6PVYhcA>? Ml7TTWM2OD1yLkC2NkDPxE1? NX\QSHdvOjBzMEizN|g>
COG-LL-317 MnfNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWrtOmVJOTBizszN NYDrWHptQTZiaB?= MlzYTWM2OD1yLkC0O{DPxE1? NIr0fJozODFyOEOzPC=>
RS4-11 M2LkVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rnVFExKM7:TR?= NVTacVVGQTZiaB?= MoTlTWM2OD1yLkCxPEDPxE1? MkP3NlAyODh|M{i=
MOLT-4 NXzLU5BZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3[3[FExKM7:TR?= MUe5OkBp MXPJR|UxRTBwMEK2JO69VQ>? NWnkbWRSOjBzMEizN|g>
CCRF-CEM MlfzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnezNVAh|ryP M13qSVk3KGh? MWfJR|UxRTBwMEm0JO69VQ>? MlXyNlAyODh|M{i=
Kasumi-1 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MljWNVAh|ryP MlO0PVYhcA>? NXO0XlN2UUN3ME2wMlExOyEQvF2= MVGyNFExQDN|OB?=
Karpas-299 NXnQS2ttT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXy5ZnZqOTBizszN MUW5OkBp M37iSWlEPTB;MD6wN|gh|ryP NF3SU4EzODFyOEOzPC=>
Ramos-RA1 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3rLb|ExKM7:TR?= Ml7YPVYhcA>? MVjJR|UxRTBwMUK3JO69VQ>? MnTYNlAyODh|M{i=

... Click to View More Cell Line Experimental Data

In vivo MLN8237 significantly reduces the tumor burden with tumor growth inhibition (TGI) of 42% and 80% at 15 mg/kg and 30 mg/kg, respectively, and prolongs the survival of mice compared with the control. [2]

Protocol

Kinase Assay:[1]
+ Expand

Aurora A radioactive Flashplate enzyme assay:

Aurora A radioactive Flashplate enzyme assay is conducted to determine the nature and degree of MLN8237-mediated inhibition in vitro. Recombinant Aurora A is expressed in Sf9 cells and purified with GST affinity chromatography. The peptide substrate for Aurora A is conjugated with biotin (Biotin-GLRRASLG). Aurora A kinase (5 nM) is assayed in 50 mM Hepes (pH 7.5), 10 mM MgCl2, 5 mM DTT, 0.05% Tween 20, 2 μM peptide substrate, 3.3 μCi/mL [γ-33P]ATP at 2 μM, and increasing concentrations of MLN8237 by using Image FlashPlates.
Cell Research:[2]
+ Expand
  • Cell lines: MM1.S, MM.1R, LR5, RPMI 8226, DOX40, OPM1, OPM2, INA6, and U266
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 24, 48, and 72 hours
  • Method: Cells are exposed to various concentrations of MLN8237 for 24, 48, and 72 hours. Cells viability is measured using MTT assay, and cell proliferation is measured using 3[H]-thymidine incorporation. For cell cycle analysis, cells are permeabilized by 70% ethanol at -20 °C, and incubated with 50 μg/mL PI and 20 units/mL RNase-A. DNA content is analyzed by flow cytometry using BDFACS-Canto II and FlowJo software. For the detection of apoptosis and senescence, cells are stained with fluorescein isothiocyanate-annexin V and PI. Apoptotic cells are determined by flow cytometric analysis using BDFACS-Canto II and FlowJo software.
    (Only for Reference)
Animal Research:[2]
+ Expand
  • Animal Models: Severe combined immune-deficient (SCID) mice inoculated subcutaneously with MM1.S cells
  • Formulation: Formulated in 10% 2-hydroxypropyl-β-cyclodextrin/1% sodium bicarbonate
  • Dosages: ~30 mg/kg/day
  • Administration: Orally
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 27 mg/mL (52.03 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5%DMSO+30% PEG300+5%Tween-80+ddH2O
For best results, use promptly after mixing.
8mg/mL

* 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 518.92
Formula

C27H20ClFN4O4

CAS No. 1028486-01-2
Storage powder
in solvent
Synonyms N/A

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
    Concentration
    Volume
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*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

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01924260 Active not recruiting Acinar Cell Adenocarcinoma of the Pancreas|Duct Cell Adenocarcinoma of the Pancreas|Recurrent Pancreatic Cancer|Stage III Pancreatic Cancer|Stage IV Pancreatic Cancer|Unspecified Adult Solid Tumor Protocol Specific University of California Davis|National Cancer Institute (NCI)|Takeda August 9 2013 Phase 1
NCT01397825 Completed Diffuse Large B-Cell Lymphoma|Transformed Follicular Lymphoma|Mantle Cell Lymphoma|Burkitt''s Lymphoma Millennium Pharmaceuticals Inc.|Takeda August 9 2011 Phase 1|Phase 2
NCT01677559 Completed Adenocarcinoma|Pancreatic Neoplasms Washington University School of Medicine May 7 2013 Phase 1
NCT00697346 Completed B-cell Follicular Lymphoma|B-cell Marginal Zone Lymphoma|Diffuse Large B-cell Lymphoma|B-cell Mantle Cell Lymphoma|B-cell Small Lymphocytic Lymphoma (SLL)|B-Cell Chronic Lymphocytic Leukemia (B-CLL)|Multiple Myeloma|Waldenstrom''s Macroglobulinemia|Noncutaneous Peripheral T-cell Lymphoma Not Otherwise Specified (PTCL-NOS)|Angioimmunoblastic T-cell Lymphoma (AITL)|Anaplastic Large Cell Lymphoma|Enteropathy Associated T-cell Lymphoma (EATCL)|NK Lymphoma (NKL) Millennium Pharmaceuticals Inc.|Takeda October 7 2008 Phase 1
NCT02860000 Recruiting Estrogen Receptor Status|HER2/Neu Negative|Invasive Breast Carcinoma|Postmenopausal|Stage III Breast Cancer|Stage IIIA Breast Cancer|Stage IIIB Breast Cancer|Stage IIIC Breast Cancer|Stage IV Breast Cancer Mayo Clinic|National Cancer Institute (NCI) July 6 2017 Phase 2
NCT01695941 Active not recruiting Recurrent B-Cell Non-Hodgkin Lymphoma|Recurrent Mantle Cell Lymphoma|Refractory B-Cell Non-Hodgkin Lymphoma|Refractory Mantle Cell Lymphoma National Cancer Institute (NCI) August 31 2012 Phase 1

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:

    What is the suggested formulation of this compound for mouse injection(i.p.)?

  • Answer:

    It can be dissolved in 6% DMSO/50% PEG 300/5% Tween 80/ddH2O at 10 mg/ml as a clear solution.

Aurora Kinase Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID