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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文献中Selleckの製品使用例(49)

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 MkDhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEPY[nQxNjVizszN M2O2eVczKGh? NHLtRndFVVOR NH3MZldKSzVyPUCuNFQh|ryP MXqyOlE{PjZ6NB?=
LS174T NGr6OGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3XMdVAvPSEQvF2= M2\tOVczKGh? MWDEUXNQ MX3JR|UxRTBwMEWg{txO MXmyOlE{PjZ6NB?=
T84 M3KxTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWGwMlUh|ryP M2L1Z|czKGh? Ml70SG1UVw>? NFvGZ3dKSzVyPUCuNFkh|ryP MnrvNlYyOzZ4OES=
LS180 M4roUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUGwMlUh|ryP NXO1dGFjPzJiaB?= M2r4T2ROW09? MWHJR|UxRTFizszN MXOyOlE{PjZ6NB?=
SW948 NXvqVZVwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoDYNE42KM7:TR?= NFu4Wmo4OiCq M2OxS2ROW09? MYTJR|UxRTFizszN NFLoW|AzPjF|Nk[4OC=>
HCT15 NEj4ZoNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlLFNE42KM7:TR?= MXi3NkBp NGOz[GtFVVOR NIf4eGpKSzVyPECuOEDPxE1? MYqyOlE{PjZ6NB?=
DLD-1 NH3rdppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGW0ZmMxNjVizszN NXq3OnlLPzJiaB?= NUHYS|NQTE2VTx?= Mnv4TWM2ODxyLkig{txO M2X3N|I3OTN4Nki0
MIP-101 MkW4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoDUNE42KM7:TR?= NIPlVZg4OiCq MojhSG1UVw>? NELtPY5KSzVyPUGg{txO NFXEWYgzPjF|Nk[4OC=>
SNU1544 M3rMN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYCwMlUh|ryP MknPO|IhcA>? NUn1OWJmTE2VTx?= NV;Ic|ZtUUN3ME2xJO69VQ>? NY\mWlJbOjZzM{[2PFQ>
OCI-Ly10 NVXsXWEyS3m2b4TvfIlkKEG|c3H5 MlTJO|IhcA>? NVnYW5p[TE2VTx?= Mlj1TWM2OD1yLkC1PEDPxE1? M2LIbFI2QDd6M{Ox
SU-DHL2 MnznR5l1d3SxeHnjJGF{e2G7 NYnaRZcyPzJiaB?= M4LJfWROW09? MVnJR|UxRTBwMEGg{txO NH7vWGwzPTh5OEOzNS=>
OCI-LY7 MkTvR5l1d3SxeHnjJGF{e2G7 NULiR3o5PzJiaB?= NFLDcG5FVVOR MWnJR|UxRTBwMEixJO69VQ>? MWqyOVg4QDN|MR?=
SU-DHL6 MlHDR5l1d3SxeHnjJGF{e2G7 NVPCVWVwPzJiaB?= NXHwTpF2TE2VTx?= Mn\ETWM2OD1yLkS4NkDPxE1? MYeyOVg4QDN|MR?=
Jeko-1 MoizR5l1d3SxeHnjJGF{e2G7 NXnHbWtPPzJiaB?= M4jBUWROW09? NUL6NZlbUUN3ME2wMlAzQSEQvF2= NE\mPWMzPTh5OEOzNS=>
JVM-2 NYPtbVdVS3m2b4TvfIlkKEG|c3H5 MmfQO|IhcA>? MYDEUXNQ NHzPPGtKSzVyPUCuNFEh|ryP NIPlOWYzPTh5OEOzNS=>
Rec-1 NX;WOVBrS3m2b4TvfIlkKEG|c3H5 NUTGNJNbPzJiaB?= NEX4fmhFVVOR NVHPUVdtUUN3ME2wMlA5PyEQvF2= NXexPYJ{OjV6N{izN|E>
Z-138 M13ne2N6fG:2b4jpZ{BCe3OjeR?= NH;qO4g4OiCq M1nJT2ROW09? NV\YcHFHUUN3ME2wMlAyOyEQvF2= M{\xflI2QDd6M{Ox
H9 NYfVZ2V5S3m2b4TvfIlkKEG|c3H5 NEnCS3I4OiCq NX:3T4xOTE2VTx?= M3zIUGlEPTB;MD62JO69VQ>? MlLTNlU5Pzh|M{G=
HH Ml;FR5l1d3SxeHnjJGF{e2G7 MVO3NkBp NHjjPIlFVVOR MYLJR|UxRTBwNzFOwG0> M1S5eVI2QDd6M{Ox
DND41 M4XRN2N6fG:2b4jpZ{BCe3OjeR?= MWi3NkBp MnPiSG1UVw>? MmLxTWM2OD1yLkGg{txO MoLsNlU5Pzh|M{G=
CCL119 Mn:4R5l1d3SxeHnjJGF{e2G7 M{DRUlczKGh? M{jG[mROW09? M1O4NWlEPTB;MD6wOlIh|ryP NUO5cnZZOjV6N{izN|E>
J.Cam 1.6 NEHpWpFEgXSxdH;4bYMhSXO|YYm= M13iTVczKGh? NI\uRVhFVVOR NVPaSW9rUUN3ME2wMlExPSEQvF2= MXiyOVg4QDN|MR?=
Sup-T1 M{fpTGN6fG:2b4jpZ{BCe3OjeR?= M3vNXVczKGh? M37ZS2ROW09? M1jFNWlEPTB;Mj6xOFIh|ryP NXf5TmxvOjV6N{izN|E>
Tib 152 M4GxcmN6fG:2b4jpZ{BCe3OjeR?= NHW4W4E4OiCq NGfRbmhFVVOR M2jZV2lEPTB;MD64JO69VQ>? M1TGUVI2QDd6M{Ox
MCF7 Mn;pSpVv[3Srb36gRZN{[Xl? MlPHOUDPxE1? NX[1XoNrOjRiaB?= NWTSXo5iTE2VTx?= MXnJcoR2[2W|IFeyM20h[XK{ZYP0 MoK0NlU5OzR2MEG=
MDA-MB-231 NGj1O2ZHfW6ldHnvckBCe3OjeR?= MnfpOUDPxE1? NYXWUod5OjRiaB?= NY\LVlF7TE2VTx?= M2\ndmlv\HWlZYOgS|MwVSCjcoLld5Q> MUGyOVg{PDRyMR?=
MCF7 M4XTN2Z2dmO2aX;uJGF{e2G7 NEPNcHM2KM7:TR?= NVLSbFQxOjRiaB?= NI\1ZWdFVVOR NWOxW41DTGWlcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJGNFUzFxQ1TDNi=> NX\nU3UzOjV6M{S0NFE>
MCF7 NXXxdodGTnWwY4Tpc44hSXO|YYm= Mn7MOUDPxE1? NIrVfWMzPCCq NILmcXFFVVOR MV;E[YNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZiQ1TLNi=> MY[yOVg{PDRyMR?=
MCF7 M{TxXWZ2dmO2aX;uJGF{e2G7 NXPHV4hRPSEQvF2= MWGyOEBp M{\mNWROW09? MoLKSIVkemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIHP5Z4xqdiCEMR?= MmDzNlU5OzR2MEG=
MCF7 NITV[3ZHfW6ldHnvckBCe3OjeR?= Ml72OUDPxE1? M4WxVlI1KGh? MU\EUXNQ MlLwTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIICyNUBY[WZzL1PpdFE> NUHNcmxmOjV6M{S0NFE>
MCF7 NIPIe2dHfW6ldHnvckBCe3OjeR?= MlHYOUDPxE1? MkXxNlQhcA>? NHvPcphFVVOR MWnJcoNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZicEK3JGtqeDF? Ml;6NlU5OzR2MEG=
MDA-MB-231 Mn:4SpVv[3Srb36gRZN{[Xl? NH;NdVQ2KM7:TR?= M{jlVVI1KGh? M{nMcGROW09? NVPTcIJJTGWlcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJGNFUzFxQ1TDNi=> NEXROpQzPTh|NESwNS=>
MDA-MB-231 NULKNHV6TnWwY4Tpc44hSXO|YYm= MlX2NUDPxE1? NF3xbZQzPCCq M17mZ2ROW09? MmXRTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|I> MXWyOVg{PDRyMR?=
MDA-MB-231 MmHnSpVv[3Srb36gRZN{[Xl? MkPzOUDPxE1? M{DlN|I1KGh? MnrtSG1UVw>? NWjMZnI5TGWlcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJIN6[2yrbjDCNS=> M{HnTVI2QDN2NECx
MDA-MB-231 Mmq4SpVv[3Srb36gRZN{[Xl? M1LiSlUh|ryP MUmyOEBp MnfQSG1UVw>? NFXhW5ZKdmO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gdFIyKFejZkGvR4lxOQ>? NILvTYszPTh|NESwNS=>
MDA-MB-231 M2\4SGZ2dmO2aX;uJGF{e2G7 M{np[|Uh|ryP MXWyOEBp MVvEUXNQ MlvDTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIICyO{BMcXBz M1vDUFI2QDN2NECx
MDA-MB-231 M1PxV2Z2dmO2aX;uJGF{e2G7 NV;kSG06PSEQvF2= M1r2VVI1KGh? NGG5WJJFVVOR MlXPTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIIC1Ny=> M3TqbVI2QDN2NECx
MCF7 NGeyVXFCeG:ydH;zbZMhSXO|YYm= NG\nR4s2KM7:TR?= MXKyOEBp M{HOc2ROW09? NVnzW4NqUW6mdXPld{BieG:ydH;0bYMh\GWjdHi= Mmn3NlU5OzR2MEG=
MDA-MB-231 NIDBZYhCeG:ydH;zbZMhSXO|YYm= MkPWOUDPxE1? NEPWVYEzPCCq M1LKNWROW09? MXTJcoR2[2W|IHHwc5B1d3SrYzDk[YF1cA>? NYTiNoplOjV6M{S0NFE>
MCF7 MnzhSpVv[3Srb36gRZN{[Xl? MmLMNUDPxE1? NGTG[ow4OiCq NFjNSXVFVVOR NXnmbZdrUW6mdXPld{BifXSxcHjh[4lkKGSnYYTo M4LYXFI2QDN2NECx
MDA-MB-231 M1W0Z2Z2dmO2aX;uJGF{e2G7 MlyxNUDPxE1? MkXFO|IhcA>? M13ZUGROW09? MoTwTY5lfWOnczDheZRweGijZ3njJIRm[XSq MYmyOVg{PDRyMR?=
U-2 OS NVXyPY5UT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX\U[HlPPTBizszN MnLkNlQhcA>? NFLsVY1FVVOR M1LYZ2lEPTB;MU[uOkDPxE1? M2G5cVI2Pzl{OEGx
MG-63 MlzKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M17RUlUxKM7:TR?= NFnoZVgzPCCq MoDjSG1UVw>? MV\JR|UxRTlwNTFOwG0> MV:yOVc6OjhzMR?=
U-2 OS MX7BdI9xfG:|aYOgRZN{[Xl? MUW1JO69VQ>? NHzydGkzPCCq M3rZWGROW09? M1HoNmlv\HWlZYOgZZBweHSxdHnjJINmdGxiZHXheIg> NX\kflZ3OjV5OUK4NVE>
MG-63 MkH4RZBweHSxc3nzJGF{e2G7 MYO1JO69VQ>? M{jaPFI1KGh? NV74[5VyTE2VTx?= MVfJcoR2[2W|IHHwc5B1d3SrYzDj[YxtKGSnYYTo MonNNlU4QTJ6MUG=
U-2 OS NVPTdZRUTnWwY4Tpc44hSXO|YYm= NFTpelA2KM7:TR?= NGrY[pozPCCq NF\FUYlFVVOR NWi2emM3WHKxbX;0[ZMh[XW2b4DoZYdq[yClZXzsJIRm[XSq MUeyOVc6OjhzMR?=
MG-63 MmDlSpVv[3Srb36gRZN{[Xl? M2XrNlUh|ryP NUHCfnhLOjRiaB?= Mlm0SG1UVw>? MVrQdo9ud3SnczDheZRweGijZ3njJINmdGxiZHXheIg> MW[yOVc6OjhzMR?=
PANC-1 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mo\sOVAh|ryP MX2yOEBp NGjzNHpFVVOR M4jJeWlEPTB;Nz6xJO69VQ>? MUmyOVY{OjJ{NR?=
BxPC-3 NEjjb2ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUm1NEDPxE1? NH;lPIwzPCCq Ml\HSG1UVw>? M{PFd2lEPTB;Nj64JO69VQ>? MY[yOVY{OjJ{NR?=
PANC-1 M4j2S2Z2dmO2aX;uJGF{e2G7 NV\aW2NkPSEQvF2= MVuyOEBp Mom2SG1UVw>? MWXJcoR2[2W|IHPlcIwh[3mlbHWgZZJz\XO2IHnuJGczN01icHjhd4U> MXeyOVY{OjJ{NR?=
BxPC-3 MYnGeY5kfGmxbjDBd5NigQ>? MVq1JO69VQ>? MXWyOEBp MnzFSG1UVw>? MmPuTY5lfWOnczDj[YxtKGO7Y3zlJIFzemW|dDDpckBIOi:PIIDoZZNm MWqyOVY{OjJ{NR?=
PANC-1 NXTIeWhHTnWwY4Tpc44hSXO|YYm= NVP3fGJuPSEQvF2= Mlv5NlQhcA>? NYr4doJWTE2VTx?= MVnJcoR2[2W|IHH1eI9xcGGpaXOgZ4VtdCCmZXH0bC=> NFKwVngzPTZ|MkKyOS=>
BxPC-3 NUPzTFBITnWwY4Tpc44hSXO|YYm= NYPjb5dLPSEQvF2= M1fJV|I1KGh? MXXEUXNQ NFq0OXdKdmS3Y3XzJIF2fG:yaHHnbYMh[2WubDDk[YF1cA>? Mmf0NlU3OzJ{MkW=
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CHLA-258 NV3XOVdpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIPGTWkyOCEQvF2= M2fRN|k3KGh? M3u5U2ROW09? NH7wZ4dKSzVyPUCuNVMzKM7:TR?= MX2yNVQ1QDV7MR?=
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SMS-MSN MnTKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPWWnhjOTBizszN MlfIPVYhcA>? NXiyS2RxTE2VTx?= NHvOUotKSzVyPUCuNFIzKM7:TR?= NG\HNYkzOTR2OEW5NS=>
SMS-SAN M1zpbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUTxdlZoOTBizszN NWnTc5RMQTZiaB?= NWO1bJQ4TE2VTx?= MVfJR|UxRTBwMEKwJO69VQ>? M1Xic|IyPDR6NUmx
Granta-4 MV7DfZRwfG:6aXOgRZN{[Xl? NGTmbXIyOCEQvF2= MnfqO{Bl NGnicIJKSzVyPUCuNFQxKM7:TR?= MmTINlEzQTF6Nke=
DB MkjHR5l1d3SxeHnjJGF{e2G7 M1O4dFExKM7:TR?= Mly3O{Bl NUHkcFQxUUN3ME2wMlA1OiEQvF2= NH\LOIczOTJ7MUi2Oy=>
RL NXXw[YNMS3m2b4TvfIlkKEG|c3H5 MlXINVAh|ryP MmjxO{Bl MWfJR|UxRTBwMEG1JO69VQ>? MXiyNVI6OTh4Nx?=
K562 NInRbohIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2rFS|ExKM7:TR?= NYfxSHRUQTZiaB?= NEP3eGVKSzVyPUCuNFg4KM7:TR?= NUn4VmZyOjFyOUG2N|M>
LAMA-84 MofiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGrIVIEyOCEQvF2= NHfK[HA6PiCq NIf3ZXhKSzVyPUCuNFU4KM7:TR?= MVyyNVA6OTZ|Mx?=
MM15 M{L1Zmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3HNOVQh|ryP M2nHeFczKGh? MXvEUXNQ M2PlemlEPTB;MD6xN{DPxE1? MUGyNFM5Ojh2NB?=
OPM1 NFO3RYhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXi0ZnI2PCEQvF2= NXS0dJR1PzJiaB?= M4D4dmROW09? NIn6dGhKSzVyPUCuNFMh|ryP MonpNlA{QDJ6NES=
RPM1 M1XsV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mo\5OEDPxE1? MV[3NkBp NVnwXmJ[TE2VTx?= NGrwSopKSzVyPUGwMlMzKM7:TR?= M1jvVFIxOzh{OES0
INA6 NXrRXFV[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVvGTVQ2PCEQvF2= M1TXbFczKGh? NELKOI5FVVOR NXXDTHVXUUN3ME2wMlAxOiEQvF2= MnLiNlA{QDJ6NES=
OPM2 NW\wNHVkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2j0dFQh|ryP NYfKe|U{PzJiaB?= MUTEUXNQ MWPJR|UxRTRwM{eg{txO NETWdZczODN6Mki0OC=>
MM1R NXT1[pZmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXLNUWI4PCEQvF2= M1LCWlczKGh? NF\SfJZFVVOR NEG1eFhKSzVyPUGuOlgh|ryP M33aZVIxOzh{OES0
DOX40 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmfHOEDPxE1? M1PqV|czKGh? M1XMfGROW09? Mlf2TWM2OD13LkS4JO69VQ>? M1\tUlIxOzh{OES0
LR5 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2XGSFQh|ryP NID3VXQ4OiCq M1zhXGROW09? MYPJR|UxRTJwNUOg{txO MYmyNFM5Ojh2NB?=
U266 M2PtcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWq0JO69VQ>? M{K5ZlczKGh? M4qxN2ROW09? NEL3d4pKSzVyPUGuOFMh|ryP MX[yNFM5Ojh2NB?=
RD MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYDCe5hrOTBizszN MV65OkBp MlK5TWM2OD1yLkKyPEDPxE1? NXXnUFdTOjBzMEizN|g>
Rh41 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4nsTlExKM7:TR?= NHn4VlI6PiCq NIHWOm5KSzVyPUCuNFkxKM7:TR?= M4LNPFIxOTB6M{O4
Rh30 MnyzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoL6NVAh|ryP M4fMbFk3KGh? NGTTXVdKSzVyPUCuNlMxKM7:TR?= M{\QUlIxOTB6M{O4
BT-12 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGH3UmwyOCEQvF2= MUm5OkBp NGTLfGtKSzVyPUCuNFYxKM7:TR?= MVKyNFExQDN|OB?=
CHLA-266 MmHIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXYcI95OTBizszN M2\Ielk3KGh? NYTSNWw2UUN3ME2wMlA4OiEQvF2= Ml7tNlAyODh|M{i=
TC-71 M{TwVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3zBWVExKM7:TR?= MVy5OkBp NWDG[pZtUUN3ME2wMlExOiEQvF2= MXWyNFExQDN|OB?=
SJ-GBM2 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXfuVmtPOTBizszN NXHFUY5HQTZiaB?= MnTZTWM2OD1yLkC1NEDPxE1? NFnnfGYzODFyOEOzPC=>
NALM-6 MkPlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGC2N3MyOCEQvF2= M1v4blk3KGh? NFPDeINKSzVyPUCuNFYzKM7:TR?= NV:1PZhMOjBzMEizN|g>
COG-LL-317 NU\WdFRET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUOzSoFrOTBizszN NUPUSYx3QTZiaB?= MVLJR|UxRTBwMES3JO69VQ>? M2fJb|IxOTB6M{O4
RS4-11 MlTpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1\YN|ExKM7:TR?= MUK5OkBp NIH6OYpKSzVyPUCuNFE5KM7:TR?= NYHuTGxOOjBzMEizN|g>
MOLT-4 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnzVNVAh|ryP NFLlPYw6PiCq NIP1[GdKSzVyPUCuNFI3KM7:TR?= MUmyNFExQDN|OB?=
CCRF-CEM Mn7aS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M17oVlExKM7:TR?= NIH3cYk6PiCq NIP2XYJKSzVyPUCuNFk1KM7:TR?= NGXucXgzODFyOEOzPC=>
Kasumi-1 NGf1elBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVmxNEDPxE1? MlK3PVYhcA>? M1O5bGlEPTB;MD6xNFMh|ryP NV;PdYJvOjBzMEizN|g>
Karpas-299 M4fz[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M37BVVExKM7:TR?= M4rQ[Vk3KGh? M4WyfmlEPTB;MD6wN|gh|ryP M3rOO|IxOTB6M{O4
Ramos-RA1 NUXBXXpvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{DBU|ExKM7:TR?= NWPHc5lGQTZiaB?= M4m0dWlEPTB;MD6xNlch|ryP NHTYPZAzODFyOEOzPC=>

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
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
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
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

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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