Alisertib (MLN8237)

目录号:S1133

Alisertib (MLN8237) Chemical Structure

Molecular Weight(MW): 518.92

Alisertib (MLN8237)是一种选择性Aurora A抑制剂,无细胞试验中IC50为1.2 nM,作用于Aurora A比作用于Aurora B选择性强200倍以上。Phase 3。

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客户购买Selleck的此次产品后发表的文献48篇:

客户使用该产品的12个实验数据:

  • 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.

产品安全说明书

Aurora Kinase抑制剂选择性比较

生物活性

产品描述 Alisertib (MLN8237)是一种选择性Aurora A抑制剂,无细胞试验中IC50为1.2 nM,作用于Aurora A比作用于Aurora B选择性强200倍以上。Phase 3。
特性 MLN8237 是第一个口服有效的小分子Aurora A激酶选择性抑制剂。
靶点
Aurora A [1]
(Cell-free assay)
1.2 nM
体外研究

MLN8237作用于Aurora A选择性比作用于结构相关的Aurora B 高200多倍,IC50为396.5 nM, 而对205种其他激酶则没有显著活性。[1] 0.5 μM MLN8237处理MM1.S和 OPM1 细胞,抑制 Aurora A磷酸化,而不影响 Aurora B调节的组蛋白H3磷酸化。MLN8237作用于多发性骨髓瘤(MM) 细胞系,显著抑制细胞增殖,IC50为0.003-1.71 μM。在BM 基质细胞,IL-6和 IGF-1 存在时,MLN8237作用于原代MM 细胞和MM细胞系,抗增殖活性比只有MLN8237单独作用时高很多。0.5 μM MLN8237 作用于原代MM细胞和细胞系,使G2/M 期细胞提高2到6倍,且显著诱导凋亡和衰老,涉及p53, p21 和p27的上调,及 PARP,caspase 3,和 caspase 9的裂解。此外, MLN8237和 Dexamethasone联用具有协同作用,具有强抗MM 功效, 而和Doxorubicin 及Bortezomib联用则具有另外的功能。[2] 0.5 μM MLN8237处理 FLO-1, OE19, 和OE33 食管腺癌细胞系,抑制集落形成,且显著提高多倍体细胞百分数,随后提高G1期细胞百分数,而与 Cisplatin (2.5 μM)联用则效果进一步提高,与单独用药相比,诱导产生更多, TAp73β, PUMA, NOXA, cleaved caspase-3, 和cleaved PARP。[3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HCT116 MlnXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXTMOGJuOC53IN88US=> M{L3NVczKGh? MkDtSG1UVw>? Ml7QTWM2OD1yLkC0JO69VQ>? NGHwdokzPjF|Nk[4OC=>
LS174T M330Wmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoXSNE42KM7:TR?= MlO3O|IhcA>? NWOxWYp{TE2VTx?= NFnlSWRKSzVyPUCuNFUh|ryP NFvIcnQzPjF|Nk[4OC=>
T84 M4XrWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoDBNE42KM7:TR?= M2DIO|czKGh? M4\NNmROW09? MXfJR|UxRTBwMEmg{txO MnTmNlYyOzZ4OES=
LS180 NHrCcm5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWCwMlUh|ryP MnHzO|IhcA>? MVXEUXNQ NHvRUWRKSzVyPUGg{txO M3iwelI3OTN4Nki0
SW948 MlHJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4XjT|AvPSEQvF2= M1jncVczKGh? NInN[XhFVVOR MlTiTWM2OD1zIN88US=> NGS2R5IzPjF|Nk[4OC=>
HCT15 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkTBNE42KM7:TR?= MVO3NkBp M2f3bGROW09? M{C4emlEPTB:MD60JO69VQ>? NHfMc3ozPjF|Nk[4OC=>
DLD-1 NWrsUoZ6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4XHOFAvPSEQvF2= MYO3NkBp M2T2W2ROW09? NETMR|VKSzVyPECuPEDPxE1? NYnIfmY4OjZzM{[2PFQ>
MIP-101 M1vRcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFrnWZUxNjVizszN M{\oelczKGh? NWL3[pB1TE2VTx?= NEPoPFVKSzVyPUGg{txO MWiyOlE{PjZ6NB?=
SNU1544 NXjH[|NrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmX6NE42KM7:TR?= NXPmZmZrPzJiaB?= NVzEc45QTE2VTx?= M4PsVGlEPTB;MTFOwG0> MUCyOlE{PjZ6NB?=
OCI-Ly10 NVHVSG9DS3m2b4TvfIlkKEG|c3H5 MXe3NkBp NUnOR3FwTE2VTx?= MXHJR|UxRTBwMEW4JO69VQ>? MnOxNlU5Pzh|M{G=
SU-DHL2 MlfMR5l1d3SxeHnjJGF{e2G7 MmnsO|IhcA>? NYHn[4FwTE2VTx?= M2[yN2lEPTB;MD6wNUDPxE1? MlfhNlU5Pzh|M{G=
OCI-LY7 Mo\MR5l1d3SxeHnjJGF{e2G7 NInISpU4OiCq MWTEUXNQ NIDuS45KSzVyPUCuNFgyKM7:TR?= M3j4R|I2QDd6M{Ox
SU-DHL6 MYnDfZRwfG:6aXOgRZN{[Xl? M1f0elczKGh? M1\hfmROW09? MlHXTWM2OD1yLkS4NkDPxE1? M1Xh[lI2QDd6M{Ox
Jeko-1 NUm2SWdES3m2b4TvfIlkKEG|c3H5 NFPWdHg4OiCq NV:5[oJMTE2VTx?= MoPvTWM2OD1yLkCyPUDPxE1? NWDRboxoOjV6N{izN|E>
JVM-2 MYXDfZRwfG:6aXOgRZN{[Xl? M{DhXlczKGh? NV;EVXFzTE2VTx?= NYL0UpJSUUN3ME2wMlAyKM7:TR?= MYmyOVg4QDN|MR?=
Rec-1 NFvaVYJEgXSxdH;4bYMhSXO|YYm= NHnhUmQ4OiCq Mn\oSG1UVw>? NFnPOplKSzVyPUCuNFg4KM7:TR?= NUPjR5hbOjV6N{izN|E>
Z-138 MXXDfZRwfG:6aXOgRZN{[Xl? Mnr5O|IhcA>? M1izSGROW09? NUmwOZI3UUN3ME2wMlAyOyEQvF2= M{\EN|I2QDd6M{Ox
H9 NF;Q[plEgXSxdH;4bYMhSXO|YYm= NXjzPVJJPzJiaB?= NFrqboZFVVOR M33ZWWlEPTB;MD62JO69VQ>? NH22fmwzPTh5OEOzNS=>
HH NXLLeVJoS3m2b4TvfIlkKEG|c3H5 NGXkO4c4OiCq NYroRnNJTE2VTx?= MV3JR|UxRTBwNzFOwG0> NFvJWoIzPTh5OEOzNS=>
DND41 Mn\mR5l1d3SxeHnjJGF{e2G7 MmjEO|IhcA>? NYjOXWhQTE2VTx?= MmnZTWM2OD1yLkGg{txO MlPzNlU5Pzh|M{G=
CCL119 M32xVWN6fG:2b4jpZ{BCe3OjeR?= NHHKVHE4OiCq MnHrSG1UVw>? NV74OYFLUUN3ME2wMlA3OiEQvF2= MknENlU5Pzh|M{G=
J.Cam 1.6 MVzDfZRwfG:6aXOgRZN{[Xl? MVO3NkBp NUPZOpU4TE2VTx?= MXLJR|UxRTBwMUC1JO69VQ>? MUmyOVg4QDN|MR?=
Sup-T1 Mlu3R5l1d3SxeHnjJGF{e2G7 NVfVNZJwPzJiaB?= M3q1cmROW09? NYLhRow3UUN3ME2yMlE1OiEQvF2= M2Pnb|I2QDd6M{Ox
Tib 152 MXTDfZRwfG:6aXOgRZN{[Xl? MWe3NkBp M1vG[2ROW09? MVLJR|UxRTBwODFOwG0> NFrxVGIzPTh5OEOzNS=>
MCF7 MVfGeY5kfGmxbjDBd5NigQ>? MoLjOUDPxE1? NHPGc2szPCCq MUTEUXNQ NFfUUm9KdmS3Y3XzJGczN01iYYLy[ZN1 NVPvTmxmOjV6M{S0NFE>
MDA-MB-231 NEnmbXdHfW6ldHnvckBCe3OjeR?= NXS2Rmx2PSEQvF2= NWPUeIg3OjRiaB?= MlXaSG1UVw>? MUTJcoR2[2W|IFezM20h[XK{ZYP0 MkjMNlU5OzR2MEG=
MCF7 NI\IUohHfW6ldHnvckBCe3OjeR?= NUX6e3I{PSEQvF2= MV6yOEBp NFr3b3lFVVOR NXnhblhqTGWlcnXhd4V{KHSqZTDlfJBz\XO|aX;uJIxmfmWuIH;mJGNFUzFxQ1TDNi=> MXKyOVg{PDRyMR?=
MCF7 NF3qWJRHfW6ldHnvckBCe3OjeR?= Mkm0OUDPxE1? M{juT|I1KGh? NIj3NJZFVVOR Ml\4SIVkemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|I> M2KwT|I2QDN2NECx
MCF7 NH:3RWdHfW6ldHnvckBCe3OjeR?= NHfISoo2KM7:TR?= MlT1NlQhcA>? NE\TXGtFVVOR M2nwZ2Rm[3KnYYPld{B1cGViZYjwdoV{e2mxbjDs[ZZmdCCxZjDjfYNtcW5iQkG= MVSyOVg{PDRyMR?=
MCF7 MlnGSpVv[3Srb36gRZN{[Xl? NVjJTVlCPSEQvF2= NH\2N2EzPCCq Mm\pSG1UVw>? MlO5TY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIICyNUBY[WZzL1PpdFE> Ml[0NlU5OzR2MEG=
MCF7 NHPZcINHfW6ldHnvckBCe3OjeR?= MX21JO69VQ>? NUDxdZNmOjRiaB?= M{HnXmROW09? M33MNGlv[3KnYYPld{B1cGViZYjwdoV{e2mxbjDs[ZZmdCCxZjDwNlchU2myMR?= NX32d297OjV6M{S0NFE>
MDA-MB-231 MnzkSpVv[3Srb36gRZN{[Xl? NIfOeFI2KM7:TR?= Mn3PNlQhcA>? M{fXWmROW09? MX\E[YNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZiQ1TLNU9ETEN{ NYPnVZFxOjV6M{S0NFE>
MDA-MB-231 NUDydZpNTnWwY4Tpc44hSXO|YYm= MmPNNUDPxE1? MVeyOEBp MWTEUXNQ Mn\UTY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIFPET|I> NWKzUYRmOjV6M{S0NFE>
MDA-MB-231 Mo[ySpVv[3Srb36gRZN{[Xl? M3i1[|Uh|ryP M2LtTVI1KGh? M1vQUmROW09? MXvE[YNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZiY4njcIlvKEJz MkPCNlU5OzR2MEG=
MDA-MB-231 MoLWSpVv[3Srb36gRZN{[Xl? NHS1TZY2KM7:TR?= M{npUVI1KGh? NYLicnRWTE2VTx?= MVfJcoNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZicEKxJHdi\jFxQ3nwNS=> MXiyOVg{PDRyMR?=
MDA-MB-231 NHvWUnNHfW6ldHnvckBCe3OjeR?= MWK1JO69VQ>? MoXrNlQhcA>? M4HBTWROW09? Mnj5TY5kemWjc3XzJJRp\SCneIDy[ZN{cW:wIHzleoVtKG:oIICyO{BMcXBz MUGyOVg{PDRyMR?=
MDA-MB-231 NGLWNolHfW6ldHnvckBCe3OjeR?= NH7pTpg2KM7:TR?= MkHyNlQhcA>? MmH1SG1UVw>? MWrJcoNz\WG|ZYOgeIhmKGW6cILld5Nqd25ibHX2[Ywhd2ZicEWz NFHwNIwzPTh|NESwNS=>
MCF7 NWrDbI1JSXCxcITvd4l{KEG|c3H5 NEfuTI42KM7:TR?= MmLBNlQhcA>? NFzZT2hFVVOR M1\pcmlv\HWlZYOgZZBweHSxdHnjJIRm[XSq MUGyOVg{PDRyMR?=
MDA-MB-231 NYD2TIFrSXCxcITvd4l{KEG|c3H5 NHrmU2c2KM7:TR?= NFrBfo0zPCCq NYfUT3lETE2VTx?= NVLsSoY3UW6mdXPld{BieG:ydH;0bYMh\GWjdHi= MmmwNlU5OzR2MEG=
MCF7 NYrGPXV3TnWwY4Tpc44hSXO|YYm= MmjFNUDPxE1? NWPLPJlJPzJiaB?= M4HoWmROW09? MVzJcoR2[2W|IHH1eI9xcGGpaXOg[IVifGh? MoTmNlU5OzR2MEG=
MDA-MB-231 MUnGeY5kfGmxbjDBd5NigQ>? M2npSVEh|ryP M4HIVFczKGh? MVrEUXNQ M2LoOGlv\HWlZYOgZZV1d3CqYXfpZ{Bl\WG2aB?= MWiyOVg{PDRyMR?=
U-2 OS MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mnj5OVAh|ryP NITDWmEzPCCq Mn\6SG1UVw>? NX7Qc3UyUUN3ME2xOk43KM7:TR?= MnjlNlU4QTJ6MUG=
MG-63 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYe1NEDPxE1? MYeyOEBp MYrEUXNQ NWGwUY41UUN3ME25MlUh|ryP M4e0UFI2Pzl{OEGx
U-2 OS MkXRRZBweHSxc3nzJGF{e2G7 NG\neJE2KM7:TR?= Mnv2NlQhcA>? NFq4WFJFVVOR M3fjZWlv\HWlZYOgZZBweHSxdHnjJINmdGxiZHXheIg> MojqNlU4QTJ6MUG=
MG-63 MmTURZBweHSxc3nzJGF{e2G7 NIrUeGY2KM7:TR?= MoLiNlQhcA>? M4LM[mROW09? M1:4VGlv\HWlZYOgZZBweHSxdHnjJINmdGxiZHXheIg> M3nje|I2Pzl{OEGx
U-2 OS MnnQSpVv[3Srb36gRZN{[Xl? MkPPOUDPxE1? NVrDe|ZXOjRiaB?= MnO1SG1UVw>? MVjQdo9ud3SnczDheZRweGijZ3njJINmdGxiZHXheIg> M1;PdlI2Pzl{OEGx
MG-63 MXfGeY5kfGmxbjDBd5NigQ>? NYr1UGdkPSEQvF2= NEW1ZYszPCCq NU\3cFZGTE2VTx?= NIP1d3BRem:vb4Tld{BifXSxcHjh[4lkKGOnbHyg[IVifGh? Mn;xNlU4QTJ6MUG=
PANC-1 NEjK[3pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2jTU|UxKM7:TR?= NE\TcoIzPCCq NWnX[IQ1TE2VTx?= NWfPd5VSUUN3ME23MlEh|ryP NEC2XHczPTZ|MkKyOS=>
BxPC-3 M{jQUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVW0cohbPTBizszN MnjqNlQhcA>? M3XkbmROW09? MlTxTWM2OD14Lkig{txO NV\SUFk3OjV4M{KyNlU>
PANC-1 NWXOdHhuTnWwY4Tpc44hSXO|YYm= M2\3ZVUh|ryP NVrR[nc2OjRiaB?= NEDY[WhFVVOR NEjHV2ZKdmS3Y3XzJINmdGxiY4njcIUh[XK{ZYP0JIlvKEd{L12gdIhie2V? M2[4W|I2PjN{MkK1
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SMS-KAN NFfmOYxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1;WRlExKM7:TR?= MWO5OkBp NVf0PWxyTE2VTx?= M{\DTmlEPTB;MD6wN|Qh|ryP MmXMNlE1PDh3OUG=
SMS-KANR M4DqVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYCxNEDPxE1? MXW5OkBp M1[zNGROW09? NHTXZ|lKSzVyPUCuNFI3KM7:TR?= M3rOVlIyPDR6NUmx
SMS-KCN MnnuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVuxNEDPxE1? NWjWfGdyQTZiaB?= NI\nZYJFVVOR MYPJR|UxRTBwMEG5JO69VQ>? NYHoPG4{OjF2NEi1PVE>
SMS-KCNR NUTCTZJTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2rwXFExKM7:TR?= M3vKNFk3KGh? MoT2SG1UVw>? MkfiTWM2OD1yLkCxNEDPxE1? MmS2NlE1PDh3OUG=
SMS-LHN M13wS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH63RmMyOCEQvF2= MYm5OkBp NXfPR25NTE2VTx?= NGj1RWNKSzVyPUCuNFMzKM7:TR?= MkDPNlE1PDh3OUG=
SMS-MSN Mn\LS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUizUnV{OTBizszN MUK5OkBp MV7EUXNQ NFXNfphKSzVyPUCuNFIzKM7:TR?= MlK2NlE1PDh3OUG=
SMS-SAN M3\aRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUHoU5lIOTBizszN MVe5OkBp M1PzU2ROW09? MY\JR|UxRTBwMEKwJO69VQ>? MXGyNVQ1QDV7MR?=
Granta-4 MV;DfZRwfG:6aXOgRZN{[Xl? NXPmXFFHOTBizszN M4DSfVch\A>? MUnJR|UxRTBwMESwJO69VQ>? NX34[IhrOjF{OUG4Olc>
DB M{f3VGN6fG:2b4jpZ{BCe3OjeR?= NH7oe2wyOCEQvF2= NIjZWVc4KGR? M3fFfWlEPTB;MD6wOFIh|ryP NUW5T3VKOjF{OUG4Olc>
RL NYnab3h2S3m2b4TvfIlkKEG|c3H5 M{DJPFExKM7:TR?= Mo[xO{Bl MkTxTWM2OD1yLkCxOUDPxE1? NUn0TGZUOjF{OUG4Olc>
K562 M2O0[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Moq0NVAh|ryP MmjKPVYhcA>? M2HW[WlEPTB;MD6wPFch|ryP NED3bo4zOTB7MU[zNy=>
LAMA-84 NFjlc25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXHOZ5doOTBizszN MY[5OkBp NFzjc5VKSzVyPUCuNFU4KM7:TR?= MnOwNlExQTF4M{O=
MM15 NH73fI9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1;STFQh|ryP MWm3NkBp NHPIfFhFVVOR Mm\UTWM2OD1yLkGzJO69VQ>? NYHrV3hxOjB|OEK4OFQ>
OPM1 NXPGPGd{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVu0JO69VQ>? MmT5O|IhcA>? NVnjZYJETE2VTx?= M{nCXWlEPTB;MD6wN{DPxE1? NHvKb|MzODN6Mki0OC=>
RPM1 NEDkXJNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{exOFQh|ryP MnTrO|IhcA>? MVnEUXNQ M{\NRWlEPTB;MUCuN|Ih|ryP NWfN[5U2OjB|OEK4OFQ>
INA6 MnTPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXTHb5R3PCEQvF2= Mn72O|IhcA>? M2jIbGROW09? MV7JR|UxRTBwMECyJO69VQ>? NEm1eW8zODN6Mki0OC=>
OPM2 MmHSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUO0JO69VQ>? NHfYdoc4OiCq M3Hh[mROW09? Mon5TWM2OD12LkO3JO69VQ>? MoXFNlA{QDJ6NES=
MM1R NYf2c2ZkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M33hZVQh|ryP NXfBbIZ3PzJiaB?= NH\3UnFFVVOR NXLnSohjUUN3ME2xMlY5KM7:TR?= NEm0T2czODN6Mki0OC=>
DOX40 NVLycWNET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYK0JO69VQ>? MkO1O|IhcA>? MmOzSG1UVw>? NITzTlVKSzVyPUWuOFgh|ryP NYjJc5pzOjB|OEK4OFQ>
LR5 NHT0cIRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGnpZpg1KM7:TR?= NF;DdIk4OiCq M13Mb2ROW09? MXTJR|UxRTJwNUOg{txO NUP1N|lXOjB|OEK4OFQ>
U266 NGLoO5lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{jyZlQh|ryP NIjH[lI4OiCq NYDNV|Z5TE2VTx?= NIPoRYxKSzVyPUGuOFMh|ryP NXHmV5ZUOjB|OEK4OFQ>
RD NVvqcFhJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXixNEDPxE1? MX:5OkBp NHrR[3NKSzVyPUCuNlI5KM7:TR?= M1L2d|IxOTB6M{O4
Rh41 M2fDZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NG\xblMyOCEQvF2= NX3XfHU{QTZiaB?= MVPJR|UxRTBwMEmwJO69VQ>? NGi1[IQzODFyOEOzPC=>
Rh30 NYrOSlRtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NI\YRmYyOCEQvF2= MmHtPVYhcA>? NYrEN4F1UUN3ME2wMlI{OCEQvF2= NHnMSI4zODFyOEOzPC=>
BT-12 NHfqZ3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX:xNEDPxE1? M3r4elk3KGh? MUTJR|UxRTBwME[wJO69VQ>? NEi5epIzODFyOEOzPC=>
CHLA-266 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NI\qZWcyOCEQvF2= MVy5OkBp M2PiWGlEPTB;MD6wO|Ih|ryP NEmxV5UzODFyOEOzPC=>
TC-71 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWSxNEDPxE1? NVTn[WtHQTZiaB?= MlTXTWM2OD1yLkGwNkDPxE1? M4Wxc|IxOTB6M{O4
SJ-GBM2 M4flS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M32wZlExKM7:TR?= MVG5OkBp NH7KTWRKSzVyPUCuNFUxKM7:TR?= NXLMeodWOjBzMEizN|g>
NALM-6 M2rpV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmPFNVAh|ryP NWDycYRMQTZiaB?= MXHJR|UxRTBwME[yJO69VQ>? NEK1WGszODFyOEOzPC=>
COG-LL-317 M2\Qbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M371UlExKM7:TR?= NYnUWmhLQTZiaB?= MYLJR|UxRTBwMES3JO69VQ>? Mkj4NlAyODh|M{i=
RS4-11 NW\NV29zT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlzBNVAh|ryP M4ftflk3KGh? NUS4fIJbUUN3ME2wMlAyQCEQvF2= MljUNlAyODh|M{i=
MOLT-4 NHfvd4pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NW\IdphMOTBizszN MVO5OkBp MkTjTWM2OD1yLkCyOkDPxE1? NUfER4JvOjBzMEizN|g>
CCRF-CEM MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml\xNVAh|ryP MlXXPVYhcA>? MYnJR|UxRTBwMEm0JO69VQ>? NGDBR|IzODFyOEOzPC=>
Kasumi-1 NH;LOHFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1fKcVExKM7:TR?= NUe3c4ViQTZiaB?= MXzJR|UxRTBwMUCzJO69VQ>? M2T3bFIxOTB6M{O4
Karpas-299 M2fQeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2TIdVExKM7:TR?= Mn3jPVYhcA>? MVfJR|UxRTBwMEO4JO69VQ>? NX\ye3luOjBzMEizN|g>
Ramos-RA1 M4jpN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYWxNEDPxE1? MUW5OkBp MmTDTWM2OD1yLkGyO{DPxE1? Mlr0NlAyODh|M{i=

... Click to View More Cell Line Experimental Data

体内研究 MLN8237口服处理,显著降低肿瘤负担,按15 mg/kg 和30 mg/kg剂量处理肿瘤生长抑制率(TGI) 分别为42%和80%,且与对照组相比,延迟小鼠寿命。[2] MLN8237 (30 mg/kg) 与Cisplatin (2 mg/kg) 联用作用于FLO-1移植瘤,与单独用药相比,抗癌活性增强,伴随着Ki-67表达受抑制,细胞核p73蛋白和cleaved caspase 3表达增强。[3]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:[1]
+ 展开

Aurora A放射性闪光板酶实验:

进行Aurora A放射性闪光板酶实验,测定体外MLN8237抑制程度。在Sf9细胞中表达重组Aurora A,然后使用GST亲和层析进行纯化。Aurora A 肽底物与生物素联合形成生物素-GLRRASLG。在50 mM Hepes (pH 7.5), 10 mM MgCl2, 5 mM DTT, 0.05% Tween-20, 2 μM 肽底物, 3.3 μCi/mL [γ-33 P]ATP 2 μM, 和浓度不断增高的MLN8237 的混合物中进行Aurora A激酶 (5 nM)实验。
细胞实验:[2]
+ 展开
  • Cell lines: MM1.S, MM.1R, LR5, RPMI 8226, DOX40, OPM1, OPM2, INA6, 和U266
  • Concentrations: 溶于DMSO,终浓度为~10 μM
  • Incubation Time: 24, 48, 和72小时
  • Method: 使用不同浓度MLN8237处理细胞24, 48,和72小时。通过MTT实验测定细胞活力,通过测定 3[3H]-胸甘渗透而测定细胞增殖。为了分析细胞周期,使用70%乙醇在-20oC下使细胞通透,然后与50 μg/mL PI 和20 单位/mL RNase-A温育。 通过流式细胞仪使用 BDFACS-Canto II和FlowJo软件分析DNA含量。 为了测定凋亡和衰老,使用异硫氰酸荧光素-annexin V和PI对细胞进行染色。通过流式细胞仪使用 BDFACS-Canto II和FlowJo软件测定凋亡细胞。
    (Only for Reference)
动物实验:[2]
+ 展开
  • Animal Models: 皮下接种 MM1.S 细胞的SCID鼠
  • Formulation: 在10% 2-羟丙基-β-环糊精/1%碳酸氢钠中配制
  • Dosages: ~30 mg/kg/day
  • Administration: 口服处理
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 27 mg/mL (52.03 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
5%DMSO+30% PEG300+5%Tween-80+ddH2O
8mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 518.92
化学式

C27H20ClFN4O4

CAS号 1028486-01-2
稳定性 powder
in solvent
别名 N/A

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

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

技术支持

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操作手册

如果有其他问题,请给我们留言。

  • * 必填项

常见问题及建议解决方法

  • 问题 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 Signaling Pathway Map

Aurora Kinase Inhibitors with Unique Features

相关Aurora Kinase产品

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID