Alisertib (MLN8237)

製品コードS1133

Alisertib (MLN8237)化学構造

分子量(MW):518.92

Alisertib (MLN8237)は一種の選択性オーロラ(Aurora )A阻害剤で、無細胞試験でIC50値が1.2 nMです。Alisertib (MLN8237)はオーロラAに作用する選択性はオーロラ Bに作用する選択性より200倍以上が高くなります。臨床3期。

サイズ 価格(税別)  
JPY 27888.00
JPY 19920.00
JPY 34860.00
JPY 111220.00

文献中の使用例(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.

  • 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.

    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.

  • 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.. 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.

  • 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.

    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.

  • 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.

    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.

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)は一種の選択性オーロラ(Aurora )A阻害剤で、無細胞試験でIC50値が1.2 nMです。Alisertib (MLN8237)はオーロラAに作用する選択性はオーロラ Bに作用する選択性より200倍以上が高くなります。臨床3期。
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 MmnvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVmwMlUh|ryP MXG3NkBp NWftdGN6TE2VTx?= NVTGSlMxUUN3ME2wMlA1KM7:TR?= MmfQNlYyOzZ4OES=
LS174T M{TofGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUewMlUh|ryP NXPsO3dSPzJiaB?= NHnvfFhFVVOR NFnFZWlKSzVyPUCuNFUh|ryP MUSyOlE{PjZ6NB?=
T84 M{nK[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVXsXIVsOC53IN88US=> M3O1[FczKGh? M16xRmROW09? NYHBcWVyUUN3ME2wMlA6KM7:TR?= M4fMTlI3OTN4Nki0
LS180 M1Pobmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlrJNE42KM7:TR?= NVPLSnRvPzJiaB?= MlnXSG1UVw>? NUmwN4lpUUN3ME2xJO69VQ>? Ml:2NlYyOzZ4OES=
SW948 NHmyWWpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYKwMlUh|ryP NXzJSJgyPzJiaB?= Ml7TSG1UVw>? MVHJR|UxRTFizszN NFr5S5czPjF|Nk[4OC=>
HCT15 Moe3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoT2NE42KM7:TR?= MYm3NkBp NXrQepoxTE2VTx?= MnTHTWM2ODxyLkSg{txO MkLkNlYyOzZ4OES=
DLD-1 NH;OSWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHHMdXAxNjVizszN MUe3NkBp MXvEUXNQ MnjXTWM2ODxyLkig{txO NHX4NZgzPjF|Nk[4OC=>
MIP-101 M3T4R2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUPjcHVxOC53IN88US=> NGS5VoI4OiCq M3HxOWROW09? NWqzVnoxUUN3ME2xJO69VQ>? Ml3aNlYyOzZ4OES=
SNU1544 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHfSeJExNjVizszN MYe3NkBp M3T0T2ROW09? MmG2TWM2OD1zIN88US=> NYn4W2N4OjZzM{[2PFQ>
OCI-Ly10 NF\hOJdEgXSxdH;4bYMhSXO|YYm= NYq0e3pXPzJiaB?= NX\qRVd5TE2VTx?= NInzdY9KSzVyPUCuNFU5KM7:TR?= M37rcFI2QDd6M{Ox
SU-DHL2 M4XvXmN6fG:2b4jpZ{BCe3OjeR?= M4Lk[FczKGh? M4XnOGROW09? MWjJR|UxRTBwMEGg{txO NUi1d25iOjV6N{izN|E>
OCI-LY7 MkiwR5l1d3SxeHnjJGF{e2G7 M3LMc|czKGh? Mn:3SG1UVw>? NVrEc415UUN3ME2wMlA5OSEQvF2= MYSyOVg4QDN|MR?=
SU-DHL6 NYL6OZVuS3m2b4TvfIlkKEG|c3H5 MUi3NkBp NXnHcJRtTE2VTx?= NEjT[|hKSzVyPUCuOFgzKM7:TR?= M3rHdlI2QDd6M{Ox
Jeko-1 NEiwO4JEgXSxdH;4bYMhSXO|YYm= MWq3NkBp Ml\PSG1UVw>? NW\6dnFXUUN3ME2wMlAzQSEQvF2= M{PGcFI2QDd6M{Ox
JVM-2 M4TIU2N6fG:2b4jpZ{BCe3OjeR?= M3LS[|czKGh? M3S2eWROW09? M{DpTWlEPTB;MD6wNUDPxE1? MWeyOVg4QDN|MR?=
Rec-1 M2KzTGN6fG:2b4jpZ{BCe3OjeR?= M3TQb|czKGh? NXXoU|h5TE2VTx?= NVLpbZEyUUN3ME2wMlA5PyEQvF2= NF73NYYzPTh5OEOzNS=>
Z-138 NVfxb3Q6S3m2b4TvfIlkKEG|c3H5 MWG3NkBp NGLQ[21FVVOR NYLG[JhlUUN3ME2wMlAyOyEQvF2= Ml;LNlU5Pzh|M{G=
H9 NHTmfpdEgXSxdH;4bYMhSXO|YYm= M3TmWFczKGh? NF:x[odFVVOR MXzJR|UxRTBwNjFOwG0> MoqzNlU5Pzh|M{G=
HH NHjKUIVEgXSxdH;4bYMhSXO|YYm= M3z4NlczKGh? NHW0VVVFVVOR NF7u[oFKSzVyPUCuO{DPxE1? MYOyOVg4QDN|MR?=
DND41 M3\MR2N6fG:2b4jpZ{BCe3OjeR?= NHHISXg4OiCq NEPVbI1FVVOR NEHqNVJKSzVyPUCuNUDPxE1? NU\re5RmOjV6N{izN|E>
CCL119 M1rV[WN6fG:2b4jpZ{BCe3OjeR?= Mk[xO|IhcA>? NIfqNIRFVVOR NGHYU|hKSzVyPUCuNFYzKM7:TR?= NUjqfZNQOjV6N{izN|E>
J.Cam 1.6 NUn4[nhDS3m2b4TvfIlkKEG|c3H5 NVXtcmhIPzJiaB?= NYX0RWFjTE2VTx?= MW\JR|UxRTBwMUC1JO69VQ>? NETKWnYzPTh5OEOzNS=>
Sup-T1 MkfZR5l1d3SxeHnjJGF{e2G7 NH7EO2Q4OiCq MYPEUXNQ NVzJZ2ZLUUN3ME2yMlE1OiEQvF2= Mn;JNlU5Pzh|M{G=
Tib 152 NUnJcnVMS3m2b4TvfIlkKEG|c3H5 M{PGc|czKGh? NYXhPHlsTE2VTx?= MmX5TWM2OD1yLkig{txO MnrYNlU5Pzh|M{G=
MCF7 NYXBfpFZTnWwY4Tpc44hSXO|YYm= M3fX[lUh|ryP MUeyOEBp M17SZmROW09? MXrJcoR2[2W|IFeyM20h[XK{ZYP0 Ml7aNlU5OzR2MEG=
MDA-MB-231 MmP5SpVv[3Srb36gRZN{[Xl? MVu1JO69VQ>? NFfsZ4UzPCCq NIjXVoJFVVOR NHf2SodKdmS3Y3XzJGc{N01iYYLy[ZN1 MmjoNlU5OzR2MEG=
MCF7 NFXNXIVHfW6ldHnvckBCe3OjeR?= NGjEepg2KM7:TR?= NWDYbXMxOjRiaB?= NX70[ZJ4TE2VTx?= MnXsSIVkemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|EwS0SFMh?= MUCyOVg{PDRyMR?=
MCF7 M4P0bmZ2dmO2aX;uJGF{e2G7 M4r6fVUh|ryP NEXHNo0zPCCq M1PU[2ROW09? MVrE[YNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZiQ1TLNi=> NWnLOJNkOjV6M{S0NFE>
MCF7 M3zWZmZ2dmO2aX;uJGF{e2G7 MVi1JO69VQ>? M4LVd|I1KGh? NUTn[IF3TE2VTx?= NEHFR49F\WO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gZ5lkdGmwIFKx MkC5NlU5OzR2MEG=
MCF7 MkLSSpVv[3Srb36gRZN{[Xl? NIG5fHE2KM7:TR?= NVLpOmpROjRiaB?= NGnpc2VFVVOR MXvJcoNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZicEKxJHdi\jFxQ3nwNS=> M2X0PVI2QDN2NECx
MCF7 NUDOPXZiTnWwY4Tpc44hSXO|YYm= MnjYOUDPxE1? M3TzOlI1KGh? M1HjWmROW09? NH25RXFKdmO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gdFI4KEurcEG= MXKyOVg{PDRyMR?=
MDA-MB-231 MVnGeY5kfGmxbjDBd5NigQ>? NG\WXHI2KM7:TR?= Ml\aNlQhcA>? M1zGOGROW09? NGDNb3VF\WO{ZXHz[ZMhfGinIHX4dJJme3Orb36gcIV3\Wxib3[gR2RMOS:FRFOy NEfrbVEzPTh|NESwNS=>
MDA-MB-231 NWHZfHBQTnWwY4Tpc44hSXO|YYm= M3iwNlEh|ryP M{S5blI1KGh? NGHwXFZFVVOR MVPJcoNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZiQ1TLNi=> MoXLNlU5OzR2MEG=
MDA-MB-231 M{LPeWZ2dmO2aX;uJGF{e2G7 NWnBdHAyPSEQvF2= NXu0dZFEOjRiaB?= M3rFUGROW09? NUL5XlQ3TGWlcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJIN6[2yrbjDCNS=> NV[5OJF7OjV6M{S0NFE>
MDA-MB-231 NGC4WXVHfW6ldHnvckBCe3OjeR?= NH73dHE2KM7:TR?= NXy3NoJPOjRiaB?= NG\wTVdFVVOR MYDJcoNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZicEKxJHdi\jFxQ3nwNS=> MWOyOVg{PDRyMR?=
MDA-MB-231 MlnFSpVv[3Srb36gRZN{[Xl? NHKyZ3Q2KM7:TR?= MUOyOEBp NEDDN4pFVVOR Mn[1TY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIICyO{BMcXBz M3zXWVI2QDN2NECx
MDA-MB-231 MoD6SpVv[3Srb36gRZN{[Xl? M4iyfVUh|ryP M4[xb|I1KGh? MYjEUXNQ NYTxfoU1UW6lcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJJA2Ow>? MnznNlU5OzR2MEG=
MCF7 MWjBdI9xfG:|aYOgRZN{[Xl? MV21JO69VQ>? M1PabFI1KGh? NYiwblIzTE2VTx?= M3\KeGlv\HWlZYOgZZBweHSxdHnjJIRm[XSq M1Ttc|I2QDN2NECx
MDA-MB-231 MnfZRZBweHSxc3nzJGF{e2G7 NITtOnY2KM7:TR?= M4HYO|I1KGh? NV7IS3E6TE2VTx?= MXnJcoR2[2W|IHHwc5B1d3SrYzDk[YF1cA>? NYTxUVZEOjV6M{S0NFE>
MCF7 NYPWN5NMTnWwY4Tpc44hSXO|YYm= NHX4[5gyKM7:TR?= MkG5O|IhcA>? MWHEUXNQ MkC2TY5lfWOnczDheZRweGijZ3njJIRm[XSq MXOyOVg{PDRyMR?=
MDA-MB-231 NGDEdVJHfW6ldHnvckBCe3OjeR?= MljNNUDPxE1? NFjtbWk4OiCq NIjjZYNFVVOR MUHJcoR2[2W|IHH1eI9xcGGpaXOg[IVifGh? MWiyOVg{PDRyMR?=
U-2 OS MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXT1dnp7PTBizszN MoPINlQhcA>? MmDNSG1UVw>? MU\JR|UxRTF4Lk[g{txO NWLhWIl[OjV5OUK4NVE>
MG-63 NY\mN4ZMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFP3cXQ2OCEQvF2= NGi5eZUzPCCq M{n6RWROW09? M{W2WWlEPTB;OT61JO69VQ>? MnjmNlU4QTJ6MUG=
U-2 OS Ml7RRZBweHSxc3nzJGF{e2G7 NFTpbVI2KM7:TR?= NYfoTFJROjRiaB?= MWnEUXNQ M2fuOGlv\HWlZYOgZZBweHSxdHnjJINmdGxiZHXheIg> M2fJOFI2Pzl{OEGx
MG-63 M4[yeWFxd3C2b4Ppd{BCe3OjeR?= MlvjOUDPxE1? MlTONlQhcA>? M3voNGROW09? MVvJcoR2[2W|IHHwc5B1d3SrYzDj[YxtKGSnYYTo NFLvc4wzPTd7MkixNS=>
U-2 OS MXHGeY5kfGmxbjDBd5NigQ>? M1LNNlUh|ryP MofQNlQhcA>? MoHjSG1UVw>? MnSwVJJwdW:2ZYOgZZV1d3CqYXfpZ{Bk\WyuIHTlZZRp MU[yOVc6OjhzMR?=
MG-63 MlTySpVv[3Srb36gRZN{[Xl? MX[1JO69VQ>? NEf5c2kzPCCq NGjBWnpFVVOR MYHQdo9ud3SnczDheZRweGijZ3njJINmdGxiZHXheIg> NYXhdZd7OjV5OUK4NVE>
PANC-1 M2fvNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXm1NEDPxE1? MY[yOEBp M3K0SmROW09? NXfMTlNQUUN3ME23MlEh|ryP NIrHOZozPTZ|MkKyOS=>
BxPC-3 Ml\HS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXK1NEDPxE1? MV2yOEBp MYnEUXNQ MojMTWM2OD14Lkig{txO M1jpeVI2PjN{MkK1
PANC-1 MlqySpVv[3Srb36gRZN{[Xl? MVO1JO69VQ>? NEXaOWwzPCCq MYXEUXNQ MXHJcoR2[2W|IHPlcIwh[3mlbHWgZZJz\XO2IHnuJGczN01icHjhd4U> NWO4cYJ1OjV4M{KyNlU>
BxPC-3 MnrZSpVv[3Srb36gRZN{[Xl? NICwTlg2KM7:TR?= M2H2VFI1KGh? M3WxeWROW09? NYHp[phxUW6mdXPld{Bk\WyuIHP5Z4xmKGG{cnXzeEBqdiCJMj;NJJBp[XOn NFHwSYEzPTZ|MkKyOS=>
PANC-1 NWL0clFVTnWwY4Tpc44hSXO|YYm= M{DjVVUh|ryP Mn\VNlQhcA>? M17EVGROW09? M2DTdGlv\HWlZYOgZZV1d3CqYXfpZ{Bk\WyuIHTlZZRp M3\ufFI2PjN{MkK1
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SMS-KCN NYq2d2RHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF\kcYEyOCEQvF2= M3v6b|k3KGh? NIG5V4VFVVOR NYDYdndjUUN3ME2wMlAyQSEQvF2= NWS3bFU1OjF2NEi1PVE>
SMS-KCNR NELpb2xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NISxbVMyOCEQvF2= M2LSPFk3KGh? NUK0SZlzTE2VTx?= MnnyTWM2OD1yLkCxNEDPxE1? MkTRNlE1PDh3OUG=
SMS-LHN MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NILt[VYyOCEQvF2= M2TQVlk3KGh? M1PzXGROW09? NGP1WpVKSzVyPUCuNFMzKM7:TR?= NIrjUI4zOTR2OEW5NS=>
SMS-MSN NGXofXJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIfGPYsyOCEQvF2= NFHEPJU6PiCq MnziSG1UVw>? M3XCTWlEPTB;MD6wNlIh|ryP NWnV[JdwOjF2NEi1PVE>
SMS-SAN M{XESmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVr2T2xKOTBizszN M3PVPFk3KGh? M4ftSWROW09? NVK3VmVIUUN3ME2wMlAzOCEQvF2= MUeyNVQ1QDV7MR?=
Granta-4 NHP2[FBEgXSxdH;4bYMhSXO|YYm= NEOzT|MyOCEQvF2= NXSzSIc2PyCm M3XndWlEPTB;MD6wOFAh|ryP NFfjfXUzOTJ7MUi2Oy=>
DB Ml7sR5l1d3SxeHnjJGF{e2G7 MWexNEDPxE1? NWPwXoV7PyCm M2XaPGlEPTB;MD6wOFIh|ryP MUiyNVI6OTh4Nx?=
RL NFvhPIJEgXSxdH;4bYMhSXO|YYm= NVnUdYpsOTBizszN MmrWO{Bl M2LmdmlEPTB;MD6wNVUh|ryP MYWyNVI6OTh4Nx?=
K562 NWHaZ3dET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\CNVAh|ryP M1XUZlk3KGh? M3jFeWlEPTB;MD6wPFch|ryP MkXzNlExQTF4M{O=
LAMA-84 MlTZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoTxNVAh|ryP NI\FUY06PiCq NIS5T|RKSzVyPUCuNFU4KM7:TR?= NV3oW3h7OjFyOUG2N|M>
MM15 NHvWcnFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnrGOEDPxE1? MoHkO|IhcA>? MWfEUXNQ MkHFTWM2OD1yLkGzJO69VQ>? MnyxNlA{QDJ6NES=
OPM1 NXjHUXdMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmL3OEDPxE1? Mnj6O|IhcA>? NULr[oFbTE2VTx?= MlO2TWM2OD1yLkCzJO69VQ>? NYfVUpl[OjB|OEK4OFQ>
RPM1 NWnVVIZ[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEO0PIo1KM7:TR?= MVS3NkBp M2LkPWROW09? Ml3aTWM2OD1zMD6zNkDPxE1? Mk\PNlA{QDJ6NES=
INA6 MnPtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M374[|Qh|ryP NGf5PY04OiCq NW\xfJRJTE2VTx?= M2rjNmlEPTB;MD6wNFIh|ryP NHfVS5ozODN6Mki0OC=>
OPM2 NF;1cFBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXWyTIlHPCEQvF2= Mn3JO|IhcA>? MkfBSG1UVw>? MVXJR|UxRTRwM{eg{txO M3vqdFIxOzh{OES0
MM1R M2LnOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M37aPFQh|ryP NFTP[FQ4OiCq MWjEUXNQ NH65TFZKSzVyPUGuOlgh|ryP MmewNlA{QDJ6NES=
DOX40 MonNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXu0JO69VQ>? NFf0W5g4OiCq NYHkRZBmTE2VTx?= NHjDPHNKSzVyPUWuOFgh|ryP NX\NTVFyOjB|OEK4OFQ>
LR5 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX20JO69VQ>? MYi3NkBp MXPEUXNQ NUHYW4VQUUN3ME2yMlU{KM7:TR?= NWLFcmVSOjB|OEK4OFQ>
U266 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUm0JO69VQ>? M3\jR|czKGh? NH;COnpFVVOR MX3JR|UxRTFwNEOg{txO NFfHZXYzODN6Mki0OC=>
RD NHPHNZpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXHqdnVyOTBizszN MlHqPVYhcA>? NYfMb3JOUUN3ME2wMlIzQCEQvF2= MofGNlAyODh|M{i=
Rh41 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX2xNEDPxE1? MlryPVYhcA>? NGfYfJJKSzVyPUCuNFkxKM7:TR?= MUeyNFExQDN|OB?=
Rh30 MmC5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHr0Um0yOCEQvF2= NXPOOYdvQTZiaB?= M2njRmlEPTB;MD6yN|Ah|ryP MUSyNFExQDN|OB?=
BT-12 M4HjfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEPkdIgyOCEQvF2= MWG5OkBp M{m1[WlEPTB;MD6wOlAh|ryP MoXLNlAyODh|M{i=
CHLA-266 M{K3VGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXWxNEDPxE1? M{ThbFk3KGh? MmnnTWM2OD1yLkC3NkDPxE1? NV7sfW1oOjBzMEizN|g>
TC-71 MmflS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1S5XFExKM7:TR?= M4X1flk3KGh? MWTJR|UxRTBwMUCyJO69VQ>? NY\N[mp5OjBzMEizN|g>
SJ-GBM2 Mlf3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlTONVAh|ryP NF\DWoI6PiCq MUHJR|UxRTBwMEWwJO69VQ>? MVyyNFExQDN|OB?=
NALM-6 MkjtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWCxNEDPxE1? MlL5PVYhcA>? Moj2TWM2OD1yLkC2NkDPxE1? MlvPNlAyODh|M{i=
COG-LL-317 M1vqN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFXRdlQyOCEQvF2= MWm5OkBp NEXNRopKSzVyPUCuNFQ4KM7:TR?= NV\3Om4zOjBzMEizN|g>
RS4-11 NFTQUZFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2TKTFExKM7:TR?= NV3SeJFZQTZiaB?= MYHJR|UxRTBwMEG4JO69VQ>? NFPrWYYzODFyOEOzPC=>
MOLT-4 MlPHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3\E[FExKM7:TR?= M4naUVk3KGh? NVnDTmV6UUN3ME2wMlAzPiEQvF2= NHG2dpEzODFyOEOzPC=>
CCRF-CEM MoXRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVPTbGV4OTBizszN M4H2V|k3KGh? NHfDUWpKSzVyPUCuNFk1KM7:TR?= MVeyNFExQDN|OB?=
Kasumi-1 MnvHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVXOS2h3OTBizszN NYrOOYdHQTZiaB?= M1e4SGlEPTB;MD6xNFMh|ryP NV7VdY5VOjBzMEizN|g>
Karpas-299 NIHPd4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkDUNVAh|ryP Mk\mPVYhcA>? NVLtNIJ3UUN3ME2wMlA{QCEQvF2= MnvCNlAyODh|M{i=
Ramos-RA1 M3nKfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlvrNVAh|ryP MoXPPVYhcA>? NEjmXXRKSzVyPUCuNVI4KM7:TR?= MnXBNlAyODh|M{i=

多くの細胞株試験データを見る場合、クリックしてください

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 順序で溶剤を入れること:
15% Captisol
30 mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)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
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    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

貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、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 ( 輸入 輸出 )

  • 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

マス 濃度 ボリューム 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02860000 Not yet recruiting Estrogen Receptor Negative|Estrogen Receptor Positive|HER2/Neu Negative|Postmenopausal|Stage IIIA Breast Cancer|Stage IIIB Breast Cancer|Stage IIIC Breast Cancer|Stage IV Breast Cancer Mayo Clinic|National Cancer Institute (NCI) December 2016 Phase 2
NCT02812056 Not yet recruiting 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
NCT02700022 Recruiting Diffuse Large B-cell Lymphoma|Follicular Lymphoma|Burkitt Lymphoma UNC Lineberger Comprehensive Cancer Center|Millennium Pharmaceuticals, Inc. July 2016 Phase 1
NCT02719691 Recruiting Metastatic Breast Cancer|Solid Tumors University of Colorado, Denver May 2016 Phase 1
NCT02560025 Recruiting Acute Myeloid Leukemia Massachusetts General Hospital|Takeda December 2015 Phase 2
NCT02551055 Active, not recruiting Neoplasms, Advanced or Metastatic Millennium Pharmaceuticals, Inc.|Takeda October 2015 Phase 1

技術サポート

ストックの作り方、阻害剤の保管する方法、細胞実験や動物実験に注意すべきな点を全部含めており、製品を取扱う時よくあった質問に対して取扱説明書でお答えいたします。

Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

  • * 必須

よくある質問(FAQ)

  • 問題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.

Related Antibodies

Aurora Kinase信号経路図

Aurora Kinase Inhibitors with Unique Features

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