Alisertib (MLN8237)

製品コードS1133

Alisertib (MLN8237)化学構造

分子量(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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JPY 27888.00
JPY 19920.00
JPY 34860.00
JPY 111220.00

文献中Selleckの製品使用例(48)

カスタマーフィードバック(12)

  • 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.

製品安全説明書

Aurora Kinase阻害剤の選択性比較

生物活性

製品説明 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.
特性 First orally available inhibitor of Aurora A.
ターゲット
Aurora A [1]
(Cell-free assay)
1.2 nM
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HCT116 NFzLSnlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MW[wMlUh|ryP MVG3NkBp NFr4[pFFVVOR Moe0TWM2OD1yLkC0JO69VQ>? NXu3No1xOjZzM{[2PFQ>
LS174T NYO0e5FWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHz6VowxNjVizszN MUO3NkBp M{T2XmROW09? MYnJR|UxRTBwMEWg{txO NXrTdYNkOjZzM{[2PFQ>
T84 NVPlZnhwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXGwMlUh|ryP NHLOTJg4OiCq NGjrb4RFVVOR NHmxWpNKSzVyPUCuNFkh|ryP MkPlNlYyOzZ4OES=
LS180 M4PYc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGH2[mExNjVizszN MVy3NkBp NG\yTJhFVVOR MWjJR|UxRTFizszN NYTh[pBWOjZzM{[2PFQ>
SW948 NIn1fGhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmTWNE42KM7:TR?= MlPpO|IhcA>? Mn\lSG1UVw>? MVzJR|UxRTFizszN M1;lU|I3OTN4Nki0
HCT15 NUPMeYtqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnPqNE42KM7:TR?= M1v5UFczKGh? MlXISG1UVw>? MUfJR|UxRDBwNDFOwG0> MU[yOlE{PjZ6NB?=
DLD-1 NH\PSoJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NULxVVdDOC53IN88US=> MUG3NkBp MXzEUXNQ NV;KO2FzUUN3MEywMlgh|ryP MmLiNlYyOzZ4OES=
MIP-101 M2XJZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnvINE42KM7:TR?= M2W3NVczKGh? MluwSG1UVw>? NHH4e5lKSzVyPUGg{txO NHv4PVMzPjF|Nk[4OC=>
SNU1544 MoqwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWCwMlUh|ryP MXe3NkBp NEPQXXRFVVOR Mlu2TWM2OD1zIN88US=> NETD[I4zPjF|Nk[4OC=>
OCI-Ly10 MYHDfZRwfG:6aXOgRZN{[Xl? MX:3NkBp NGXyV4xFVVOR MVvJR|UxRTBwMEW4JO69VQ>? Ml\YNlU5Pzh|M{G=
SU-DHL2 NES3foxEgXSxdH;4bYMhSXO|YYm= Ml7RO|IhcA>? NVvsbIM{TE2VTx?= M2rqbmlEPTB;MD6wNUDPxE1? Ml7jNlU5Pzh|M{G=
OCI-LY7 NYPkWpFpS3m2b4TvfIlkKEG|c3H5 M{S4cFczKGh? MkjQSG1UVw>? NHrqe5pKSzVyPUCuNFgyKM7:TR?= MXOyOVg4QDN|MR?=
SU-DHL6 MnnjR5l1d3SxeHnjJGF{e2G7 NETzTpk4OiCq MmLYSG1UVw>? M2K3[GlEPTB;MD60PFIh|ryP MkfNNlU5Pzh|M{G=
Jeko-1 MojmR5l1d3SxeHnjJGF{e2G7 NWmwcnJvPzJiaB?= MWHEUXNQ MVLJR|UxRTBwMEK5JO69VQ>? MYCyOVg4QDN|MR?=
JVM-2 MorqR5l1d3SxeHnjJGF{e2G7 NV3PVHN6PzJiaB?= MYPEUXNQ M4nNO2lEPTB;MD6wNUDPxE1? NWXWOIxSOjV6N{izN|E>
Rec-1 NVGzfFN2S3m2b4TvfIlkKEG|c3H5 MV63NkBp MWrEUXNQ NXjFd|dCUUN3ME2wMlA5PyEQvF2= MUGyOVg4QDN|MR?=
Z-138 M3XBdWN6fG:2b4jpZ{BCe3OjeR?= NWm3OohYPzJiaB?= Mn7lSG1UVw>? NXvvNmN7UUN3ME2wMlAyOyEQvF2= M4fleVI2QDd6M{Ox
H9 NG\JSoREgXSxdH;4bYMhSXO|YYm= NUna[2tOPzJiaB?= NVXjTZF3TE2VTx?= NH7uPIVKSzVyPUCuOkDPxE1? NXS1W401OjV6N{izN|E>
HH MkPKR5l1d3SxeHnjJGF{e2G7 M3G1SlczKGh? MYTEUXNQ NHrkUXJKSzVyPUCuO{DPxE1? NIHnfZAzPTh5OEOzNS=>
DND41 Mnv1R5l1d3SxeHnjJGF{e2G7 NUHORnlkPzJiaB?= M1jtPGROW09? M4LoTWlEPTB;MD6xJO69VQ>? MkHFNlU5Pzh|M{G=
CCL119 MYfDfZRwfG:6aXOgRZN{[Xl? M{TtV|czKGh? NHvrdWlFVVOR NF[2VFFKSzVyPUCuNFYzKM7:TR?= MUSyOVg4QDN|MR?=
J.Cam 1.6 MXfDfZRwfG:6aXOgRZN{[Xl? NWjNOGR7PzJiaB?= MnfqSG1UVw>? MlzSTWM2OD1yLkGwOUDPxE1? NUi2To1uOjV6N{izN|E>
Sup-T1 MUDDfZRwfG:6aXOgRZN{[Xl? NH;IdFI4OiCq NUnLNWV6TE2VTx?= MoDSTWM2OD1{LkG0NkDPxE1? M4LSOFI2QDd6M{Ox
Tib 152 M{\OfGN6fG:2b4jpZ{BCe3OjeR?= NEWwfXQ4OiCq NVP3fot4TE2VTx?= NYT0b5N3UUN3ME2wMlgh|ryP MWKyOVg4QDN|MR?=
MCF7 NIPXO|JHfW6ldHnvckBCe3OjeR?= MUO1JO69VQ>? MkW4NlQhcA>? MorOSG1UVw>? NUfKTWkyUW6mdXPld{BIOi:PIHHydoV{fA>? NHrQb|gzPTh|NESwNS=>
MDA-MB-231 NFzzfHZHfW6ldHnvckBCe3OjeR?= MYq1JO69VQ>? NFnDOlEzPCCq MkW5SG1UVw>? NEPHPW1KdmS3Y3XzJGc{N01iYYLy[ZN1 MmL1NlU5OzR2MEG=
MCF7 Mk\BSpVv[3Srb36gRZN{[Xl? MWm1JO69VQ>? MUOyOEBp NIDaXHFFVVOR MnHoSIVkemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|EwS0SFMh?= MkTZNlU5OzR2MEG=
MCF7 MV\GeY5kfGmxbjDBd5NigQ>? MonIOUDPxE1? NWjFW5NTOjRiaB?= NIK4ZWNFVVOR MoPuSIVkemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|I> NWnoN3J1OjV6M{S0NFE>
MCF7 NHuzb5BHfW6ldHnvckBCe3OjeR?= NX7aUFZEPSEQvF2= MlXvNlQhcA>? M37RWGROW09? NYT6PG1nTGWlcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJIN6[2yrbjDCNS=> NEj2enMzPTh|NESwNS=>
MCF7 NV\NR3RiTnWwY4Tpc44hSXO|YYm= NVHGbWtZPSEQvF2= NVzxN5JwOjRiaB?= NIDrOWNFVVOR M13VNmlv[3KnYYPld{B1cGViZYjwdoV{e2mxbjDs[ZZmdCCxZjDwNlEhX2GoMT;DbZAy Mmq0NlU5OzR2MEG=
MCF7 MUjGeY5kfGmxbjDBd5NigQ>? NVziXGd{PSEQvF2= MXGyOEBp NGLXbWJFVVOR NELNNHpKdmO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gdFI4KEurcEG= NEe5NmUzPTh|NESwNS=>
MDA-MB-231 MlXwSpVv[3Srb36gRZN{[Xl? NVzJdZZOPSEQvF2= NITITGMzPCCq NI\1OINFVVOR NEPDbHlF\WO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gR2RMOS:FRFOy MVSyOVg{PDRyMR?=
MDA-MB-231 Ml\3SpVv[3Srb36gRZN{[Xl? MWGxJO69VQ>? NXXvWopzOjRiaB?= NWrF[IF7TE2VTx?= M3Pwdmlv[3KnYYPld{B1cGViZYjwdoV{e2mxbjDs[ZZmdCCxZjDDSGsz MmPYNlU5OzR2MEG=
MDA-MB-231 NFS4PIpHfW6ldHnvckBCe3OjeR?= M4\EVFUh|ryP MkfJNlQhcA>? MXvEUXNQ M{TENWRm[3KnYYPld{B1cGViZYjwdoV{e2mxbjDs[ZZmdCCxZjDjfYNtcW5iQkG= MXqyOVg{PDRyMR?=
MDA-MB-231 MnPMSpVv[3Srb36gRZN{[Xl? NF7tRVQ2KM7:TR?= NHLwfGkzPCCq NWrvWZdETE2VTx?= M1TscWlv[3KnYYPld{B1cGViZYjwdoV{e2mxbjDs[ZZmdCCxZjDwNlEhX2GoMT;DbZAy MWWyOVg{PDRyMR?=
MDA-MB-231 M37zW2Z2dmO2aX;uJGF{e2G7 NWrTWIJJPSEQvF2= Mo\FNlQhcA>? MlvmSG1UVw>? NX3UVWN{UW6lcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJJAzPyCNaYCx NHn1UYszPTh|NESwNS=>
MDA-MB-231 MV\GeY5kfGmxbjDBd5NigQ>? MmiwOUDPxE1? M1m2UVI1KGh? NYmzWpo3TE2VTx?= M4jIfWlv[3KnYYPld{B1cGViZYjwdoV{e2mxbjDs[ZZmdCCxZjDwOVM> NGrw[lMzPTh|NESwNS=>
MCF7 MnHORZBweHSxc3nzJGF{e2G7 Mle2OUDPxE1? M4\YcFI1KGh? Mnj2SG1UVw>? NH\W[WtKdmS3Y3XzJIFxd3C2b4TpZ{Bl\WG2aB?= NHjCVXgzPTh|NESwNS=>
MDA-MB-231 MmDPRZBweHSxc3nzJGF{e2G7 M3jGXFUh|ryP NXrrNnJXOjRiaB?= MoLBSG1UVw>? NUTBd5d7UW6mdXPld{BieG:ydH;0bYMh\GWjdHi= MoO5NlU5OzR2MEG=
MCF7 MnXhSpVv[3Srb36gRZN{[Xl? M{\ENVEh|ryP M1rC[VczKGh? MnnpSG1UVw>? M1XIbmlv\HWlZYOgZZV1d3CqYXfpZ{Bl\WG2aB?= M4PkflI2QDN2NECx
MDA-MB-231 MY\GeY5kfGmxbjDBd5NigQ>? MX[xJO69VQ>? MVy3NkBp NVW2RlRZTE2VTx?= MXTJcoR2[2W|IHH1eI9xcGGpaXOg[IVifGh? MmDWNlU5OzR2MEG=
U-2 OS MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M12zV|UxKM7:TR?= NFTUZlUzPCCq MV\EUXNQ M{[zcGlEPTB;MU[uOkDPxE1? M2n0b|I2Pzl{OEGx
MG-63 MlPOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{nYTFUxKM7:TR?= M3ftSFI1KGh? MYXEUXNQ Ml3HTWM2OD17LkWg{txO NF\STHczPTd7MkixNS=>
U-2 OS NVv5fXFuSXCxcITvd4l{KEG|c3H5 M{XCV|Uh|ryP NYDy[lBnOjRiaB?= MnTNSG1UVw>? NF3ONGFKdmS3Y3XzJIFxd3C2b4TpZ{Bk\WyuIHTlZZRp MUeyOVc6OjhzMR?=
MG-63 NVjXfXdDSXCxcITvd4l{KEG|c3H5 MX21JO69VQ>? M4DYXFI1KGh? MkLTSG1UVw>? NXvjdYdVUW6mdXPld{BieG:ydH;0bYMh[2WubDDk[YF1cA>? MnvmNlU4QTJ6MUG=
U-2 OS Mn7TSpVv[3Srb36gRZN{[Xl? NX62d|VVPSEQvF2= MVyyOEBp MYfEUXNQ MmjBVJJwdW:2ZYOgZZV1d3CqYXfpZ{Bk\WyuIHTlZZRp MXGyOVc6OjhzMR?=
MG-63 MoLCSpVv[3Srb36gRZN{[Xl? NXzj[m5XPSEQvF2= NYHC[G5yOjRiaB?= NFzOWm5FVVOR MUjQdo9ud3SnczDheZRweGijZ3njJINmdGxiZHXheIg> NH7JZXgzPTd7MkixNS=>
PANC-1 MojrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHfrZmc2OCEQvF2= Mn21NlQhcA>? NFj5PJFFVVOR MWnJR|UxRTdwMTFOwG0> M3fCUlI2PjN{MkK1
BxPC-3 NYS4S5p5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX61NEDPxE1? MX:yOEBp MYLEUXNQ M3nhR2lEPTB;Nj64JO69VQ>? MViyOVY{OjJ{NR?=
PANC-1 MXHGeY5kfGmxbjDBd5NigQ>? MkewOUDPxE1? MV2yOEBp NHjue2ZFVVOR MXHJcoR2[2W|IHPlcIwh[3mlbHWgZZJz\XO2IHnuJGczN01icHjhd4U> NVexWZNsOjV4M{KyNlU>
BxPC-3 M2XVSWZ2dmO2aX;uJGF{e2G7 M2W5TVUh|ryP NVXYVXhVOjRiaB?= NYW5bmlCTE2VTx?= Mn;HTY5lfWOnczDj[YxtKGO7Y3zlJIFzemW|dDDpckBIOi:PIIDoZZNm Mn7XNlU3OzJ{MkW=
PANC-1 NYGw[IM{TnWwY4Tpc44hSXO|YYm= MXS1JO69VQ>? Ml3FNlQhcA>? NHnkfm9FVVOR NFPCfYFKdmS3Y3XzJIF2fG:yaHHnbYMh[2WubDDk[YF1cA>? MnjGNlU3OzJ{MkW=
BxPC-3 NVizNpFXTnWwY4Tpc44hSXO|YYm= MmLSOUDPxE1? M4DrWVI1KGh? NIDRN2xFVVOR NXrpblZrUW6mdXPld{BifXSxcHjh[4lkKGOnbHyg[IVifGh? MVKyOVY{OjJ{NR?=
SKOV3 NYTUfVROT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVqxNFAh|ryP M1f1[VI1KGh? NUj4fZlmTE2VTx?= Mnv0TWM2OD1{MD60PEDPxE1? M{fTOFI2PjJ2N{Ww
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SMS-SAN MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXSxNEDPxE1? MoOwPVYhcA>? NIPpS|NFVVOR NWHXeY1qUUN3ME2wMlAzOCEQvF2= MoXqNlE1PDh3OUG=
Granta-4 M1zZcWN6fG:2b4jpZ{BCe3OjeR?= M{XOWFExKM7:TR?= MYm3JIQ> Mnm4TWM2OD1yLkC0NEDPxE1? NUL2O|NOOjF{OUG4Olc>
DB NGLlfFFEgXSxdH;4bYMhSXO|YYm= MXqxNEDPxE1? Mn;lO{Bl M1XpO2lEPTB;MD6wOFIh|ryP NYD6NW1mOjF{OUG4Olc>
RL MXLDfZRwfG:6aXOgRZN{[Xl? MkXpNVAh|ryP MoHiO{Bl MYnJR|UxRTBwMEG1JO69VQ>? M{G3Z|IyOjlzOE[3
K562 M2[2SGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlWwNVAh|ryP NETSZXA6PiCq MmrjTWM2OD1yLkC4O{DPxE1? NXfO[4RNOjFyOUG2N|M>
LAMA-84 M4TrTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVPq[mpOOTBizszN NV3SfFFIQTZiaB?= NVi1U4FzUUN3ME2wMlA2PyEQvF2= MlH1NlExQTF4M{O=
MM15 NYHNcIRoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUO0JO69VQ>? MYm3NkBp M2rVN2ROW09? MXPJR|UxRTBwMUOg{txO MUGyNFM5Ojh2NB?=
OPM1 M2HiRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXLxc2hGPCEQvF2= Mlq4O|IhcA>? MYHEUXNQ M2PFZ2lEPTB;MD6wN{DPxE1? NULwdVZCOjB|OEK4OFQ>
RPM1 NGrPc25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NG\keZI1KM7:TR?= MkW0O|IhcA>? MXjEUXNQ NFzsV3hKSzVyPUGwMlMzKM7:TR?= Ml\1NlA{QDJ6NES=
INA6 M{L1c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFjwU5Q1KM7:TR?= NEHldpo4OiCq MmqwSG1UVw>? MnXnTWM2OD1yLkCwNkDPxE1? NH35U48zODN6Mki0OC=>
OPM2 M3S5Nmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NU\RRYNLPCEQvF2= NVmzbXpXPzJiaB?= NVnRR5hnTE2VTx?= M2WwbmlEPTB;ND6zO{DPxE1? MVuyNFM5Ojh2NB?=
MM1R MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH7wTZY1KM7:TR?= MVG3NkBp Mn7JSG1UVw>? NY\sU2JFUUN3ME2xMlY5KM7:TR?= M2TZflIxOzh{OES0
DOX40 NIToOoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1HieVQh|ryP NFP5R5A4OiCq Ml3ySG1UVw>? M1PKfmlEPTB;NT60PEDPxE1? NVP4fHhvOjB|OEK4OFQ>
LR5 MmC5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIPpZmg1KM7:TR?= MoPIO|IhcA>? NXrlVldnTE2VTx?= MXvJR|UxRTJwNUOg{txO NXPKXpdvOjB|OEK4OFQ>
U266 NETjVGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWG0JO69VQ>? NXXu[ndbPzJiaB?= MWPEUXNQ M3zsSGlEPTB;MT60N{DPxE1? M1\DclIxOzh{OES0
RD M1LHRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVfwTVZFOTBizszN M3G0c|k3KGh? MX7JR|UxRTBwMkK4JO69VQ>? M2\YdlIxOTB6M{O4
Rh41 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoDNNVAh|ryP NI\nSY46PiCq NEjVXXZKSzVyPUCuNFkxKM7:TR?= Mn\XNlAyODh|M{i=
Rh30 Mnv6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlTnNVAh|ryP NGe1cXY6PiCq MV3JR|UxRTBwMkOwJO69VQ>? NHLjUngzODFyOEOzPC=>
BT-12 NUDsb|lET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoTmNVAh|ryP MV[5OkBp NHjGb2tKSzVyPUCuNFYxKM7:TR?= MWSyNFExQDN|OB?=
CHLA-266 MmPWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{HJTVExKM7:TR?= NFP0RXg6PiCq MUDJR|UxRTBwMEeyJO69VQ>? NVvH[lhMOjBzMEizN|g>
TC-71 Mlv5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYSxNEDPxE1? NXXLTplJQTZiaB?= M365OWlEPTB;MD6xNFIh|ryP NVTj[|ZjOjBzMEizN|g>
SJ-GBM2 MnPRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUi0S4RvOTBizszN MnriPVYhcA>? NHfGZWZKSzVyPUCuNFUxKM7:TR?= NGWyZYkzODFyOEOzPC=>
NALM-6 M1rER2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4PFe|ExKM7:TR?= M{\kWFk3KGh? NFXmUoRKSzVyPUCuNFYzKM7:TR?= NU\zZmt5OjBzMEizN|g>
COG-LL-317 NYLL[XpyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVmxNEDPxE1? NUPPdW5CQTZiaB?= MYTJR|UxRTBwMES3JO69VQ>? NWrEdJl{OjBzMEizN|g>
RS4-11 MoPBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3\zVVExKM7:TR?= MYG5OkBp MmLrTWM2OD1yLkCxPEDPxE1? M3zJZVIxOTB6M{O4
MOLT-4 MoHyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmnVNVAh|ryP NY\wWXVDQTZiaB?= MknWTWM2OD1yLkCyOkDPxE1? MkDXNlAyODh|M{i=
CCRF-CEM MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{m3PVExKM7:TR?= NEWwU4k6PiCq NFHjbplKSzVyPUCuNFk1KM7:TR?= MUeyNFExQDN|OB?=
Kasumi-1 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVLmd4E2OTBizszN M13S[Vk3KGh? MWfJR|UxRTBwMUCzJO69VQ>? NF3JSHkzODFyOEOzPC=>
Karpas-299 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1:1fFExKM7:TR?= M2DoVVk3KGh? MVHJR|UxRTBwMEO4JO69VQ>? MVeyNFExQDN|OB?=
Ramos-RA1 NXXaTI1JT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWLNc|lyOTBizszN M{DrbVk3KGh? NE[5WFdKSzVyPUCuNVI4KM7:TR?= M1fvSlIxOTB6M{O4

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

体内試験 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]

お薦めの試験操作(参考用のみ)

キナーゼ試験:[1]
+ 展開

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.
細胞試験: [2]
+ 展開
  • 細胞株: MM1.S, MM.1R, LR5, RPMI 8226, DOX40, OPM1, OPM2, INA6, and U266
  • 濃度: Dissolved in DMSO, final concentrations ~10 μM
  • 反応時間: 24, 48, and 72 hours
  • 実験の流れ: 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.
    (参考用のみ)
動物試験:[2]
+ 展開
  • 動物モデル: Severe combined immune-deficient (SCID) mice inoculated subcutaneously with MM1.S cells
  • 製剤: Formulated in 10% 2-hydroxypropyl-β-cyclodextrin/1% sodium bicarbonate
  • 投薬量: ~30 mg/kg/day
  • 投与方法: Orally
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 27 mg/mL (52.03 mM)
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
5%DMSO+30% PEG300+5%Tween-80+ddH2O
混合させたのち直ちに使用することを推奨します。
8mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。

化学情報

分子量 518.92
化学式

C27H20ClFN4O4

CAS No. 1028486-01-2
保管
in solvent
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備するために必要な希釈率を計算してください。Selleck希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • 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):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

質量 濃度 体積 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
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
NCT02700022 Terminated Diffuse Large B-cell Lymphoma|Follicular Lymphoma|Burkitt Lymphoma UNC Lineberger Comprehensive Cancer Center|Millennium Pharmaceuticals Inc. October 2016 Phase 1
NCT02812056 Withdrawn Malignant Neoplasms of Digestive Organs|Malignant Neoplasms of Female Genital Organs|Malignant Neoplasms of Lip Oral Cavity and Pharynx|Malignant Neoplasms of Male Genital Organs M.D. Anderson Cancer Center|Millennium Pharmaceuticals Inc. September 2016 Phase 1
NCT02719691 Recruiting Metastatic Breast Cancer|Solid Tumors University of Colorado Denver May 13 2016 Phase 1
NCT02560025 Active not recruiting Acute Myeloid Leukemia Massachusetts General Hospital|Takeda December 2015 Phase 2
NCT02530619 Active not recruiting Acute Megakaryoblastic Leukemia|Myelofibrosis|Primary Myelofibrosis Northwestern University|The Leukemia and Lymphoma Society|Millennium Pharmaceuticals Inc.|National Cancer Institute (NCI) October 2015 Not Applicable

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

よくある質問(FAQ)

  • 質問1:

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

  • 回答:

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

Aurora Kinaseシグナル伝達経路

Aurora Kinase Inhibitors with Unique Features

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