Tozasertib (VX-680, MK-0457)

Catalog No.S1048

Tozasertib (VX-680, MK-0457) Chemical Structure

Molecular Weight(MW): 464.59

Tozasertib (VX-680, MK-0457) is a pan-Aurora inhibitor, mostly against Aurora A with Kiapp of 0.6 nM in a cell-free assay, less potent towards Aurora B/Aurora C and 100-fold more selective for Aurora A than 55 other kinases. Phase 2.

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Cited by 37 Publications

16 Customer Reviews

  • (G) Nocodazole-arrested HeLa cells were treated with VX-680 and MG132 and stained for CENP-E (Green), pT422 (Red) and DNA (Blue). (H) pT422 fluorescence intensity was normalized to the total CENP-E fluorescence. Plots show the mean of > 15 cells per condition from two independent experiments.

    Cell 2010 142, 444–455. Tozasertib (VX-680, MK-0457) purchased from Selleck.

    Senescence induction upon PKCι depletion combined with aurora kinase inhibition. ( a) MCF7 cells were transfected as above to deplete PKCι . Two days after transfection, cells were treated for the indicated time period with 400 n M VX-680. Medium with VX-680 was then removed and fresh medium was added. Cells were stained for SA-b -gal activity 5 days after the start of transfection.* indicates a P value <0.05. ( b) MCF7 cells were treated as above. Five days after transfection, cells were fixed and assessed for the presence of gH2AX foci by immunofluorescence microscopy. (c, d) MCF7 cells were treated with dimethyl sulfoxide (DMSO) control or 400 n M VX-680 for the indicated time periods. Total cell lysates were then analyzed by western blotting for levels of p21 and GAPDH (as loading control). A representative blot is shown in panel c. Quantitation of changes in p21 levels (normalized to vehicle-treated controls) is shown in panel d. The data shown are the means ±s.e. of three independent experiments.

    Oncogene 2012 31, 3584-96. Tozasertib (VX-680, MK-0457) purchased from Selleck.

  • Senescence induction upon PKCι depletion combined with aurora kinase inhibition in glioblastoma cells. (a, b) U87MG cells were transfected as above to deplete PKCι. Two days after transfection, cells were treated for 72 ( a)or24h (b) with 400 nM VX-680. Medium with VX-680 was then removed and fresh medium was added. Cells were stained for SA-b-gal activity 5 days after the start of transfection. * indicates a P value <0.05. (c) U87MG cells were treated as described in panel a above. Five days after transfection, cells were fixed and assessed for the presence of gH2AX foci by immunofluorescence microscopy. (d) U87MG cells were treated with the dimethyl sulfoxide (DMSO) control or 400 n M VX-680 for the indicated time periods. Total cell lysates were then analyzed by western blotting for levels of p21. The bar graph shows quantitation of p21 levels (normalized to vehicle-treated controls) from three independent experiments. A representative blot is also shown, with lanes aligned to correspond to the labels on the graph.

    Oncogene 2012 31, 3584-96. Tozasertib (VX-680, MK-0457) purchased from Selleck.

    MTT assay reveals a dose-dependent decrease in cell viability in mouse derived brainstem glioma cells treated with VX-680 ( P < 0.001) after 72 h of treatment. The error bars represent the standard deviation. Propidium iodide based cell sorting of mouse derived brainstem glioma cells after 72 h treatment with 5 μM reversine or 100 nM VX-680 respectively reveals increased cell populations with 4N and 8N DNA content as compared to vehicle control.

    Brain Pathol 2012 23, 244-53. Tozasertib (VX-680, MK-0457) purchased from Selleck.

  • Treatment of mouse derived brainstem glioma cells for 72 h with 5 μM reversine or 100 nM VX-680 increases cell size compared with vehicle-treated control and leads to irregular-shaped nuclei and micronuclei (F–H). Images F–H represent immunofluorescent staining for GFAP (green) with DAPI counter-stain (blue) and were taken at 400 ×magnification.

    Brain Pathol 2012 23, 244-53. Tozasertib (VX-680, MK-0457) purchased from Selleck.

     

    Aurora-A inhibitors severely impair neuronal migration. Migration of granular neurons after treatment of Aurora-A inhibitors was examined. a, Western blotting analysis of proteins or phosphorylated proteins. Aurora-A and NDEL1 displayed similar expression levels, whereas phosphorylated Aurora-A and NDEL1 proteins were decreased during treatment with Aurora-A inhibitors. Relative intensities of the bands of Western blotting are displayed at the bottom.

    J Neurosci 2012 32, 11050-11066. Tozasertib (VX-680, MK-0457) purchased from Selleck.

  • B, BLQ1 and UCSF02 cells were treated with increasing concentrations of VX-680 for 48 hours. The percentage of apoptotic cells was determined by fluorescence-activated cell sorting analysis. C, BLQ1 cells were treated with 1 μmol/L VX-680 and cell cycle distribution was determined by flow cytometry at time points of 24 and 48 hours.

    Mol Cancer Ther 2010 9, 1318–1327. Tozasertib (VX-680, MK-0457) purchased from Selleck.

    VX-680 eliminates Bcr/Abl kinase activities. BLQ1 (T315I mutation) and TXL2 (no mutation) cells were treated with the indicated concentrations of VX-680 with or without 100 nmol/L dasatinib for 24 hours. Western blot analysis was done on total lysates with the antibodies indicated to the left. Blots were stripped and reprobed with Bcr (N-20), Src, and GAPDH antibodies as loading controls.

    Mol Cancer Ther 2010 9, 1318–1327. Tozasertib (VX-680, MK-0457) purchased from Selleck.

  • Responses of human ALL cells to short-term VX-680 treatment. A, BLQ1 cells were treated with 1 μmol/L VX-680 for 3 days. After 3 days, the drug was removed from the medium and cells were cultured without VX-680. During this period (days 3-21) without drug, viability (top left), cell numbers (bottom left), and cell cycle distribution (right) of BLQ1 cells were assessed. B, BLQ1 and BLQ1-VX-Tx cells were cytospun onto glass slides and fixed, dried, and stained with Wright-Giemsa on day 21. All images are at ×63 magnification. C, BLQ1 and BLQ1-VX-Tx cells were treated with 1.5 μmol/L VX-680 or 5 nmol/L vincristine for 72 hours. Cell viability was measured by trypan blue exclusion. *, P < 0.05, vincristine-treated BLQ1 compared with vincristine-treated BLQ1-VX-Tx.

    Mol Cancer Ther 2010 9, 1318–1327. Tozasertib (VX-680, MK-0457) purchased from Selleck.

    VX-680 and dasatinib synergize to induce cytotoxic activity in wild-type Bcr/Abl-positive human ALL cells. A, TXL2 and UCSF02 cells were exposed to 1 μmol/L VX-680 with or without 100 nmol/L dasatinib for 24 to 72 hours as indicated, after which the percentage of viable cells was determined by trypan blue exclusion. B, TXL2 cells were treated with or without VX-680 and dasatinib for 48 hours in triplicate. **, P < 0.001, VX-680 and dasatinib cotreated TXL2 compared with VX-680-treated or dasatinib alone-treated TXL2 cells. Apoptotic cells were defined by flow cytometry as Annexin V and propidium iodide (PI) double-positive cells. C, TXL2 cells were exposed to VX-680 and/or dasatinib and cell cycle distribution was assessed by flow cytometry.

    Mol Cancer Ther 2010 9, 1318–1327. Tozasertib (VX-680, MK-0457) purchased from Selleck.

  • C, E: Expression of Aur-A and phosphorylated histone H3 in TPC-1 cells after VX-680 treatment. D, F: Expression of phosphorylated histone H3 in PTC tumor tissues after VX-680 treatment.

    Biochem Biophys Res Commun, 2016, 473(1):212-8. Tozasertib (VX-680, MK-0457) purchased from Selleck.

    Apoptosis induction in HB cells treated with a combination of VX-680. HUH6 (a) and HepT1 ( b ) were incubated with VX-680 (6 and 12.5 μM). Caspase-3 activation was detected with the NucView- 488 substrate 24 h later. Green fluorescent cells denote apoptotic cells.Scale bar represents 50 μm.

    Pediatr Surg Int 2012 28, 579-89. Tozasertib (VX-680, MK-0457) purchased from Selleck.

  • Morphological changes and histone H3 phosphorylation of HB cells treated with a combination of VX-680 and SAHA. HUH6 and HepT1 were incubated with VX-680 (6 μM) and SAHA (0.5 μM). Nuclei diameter (a) and cell diameter (b) were determined 72 h later by DAPI staining and microscopy. Data represent mean±SD of the diameters from 20 cells in each experiment. (* Two-way ANOVA, Bonferroni test, p \0.05). c Western blot analysis on HUH6 and HepT1 cells were carried out with an anti-phospho-Histone H3 (Ser 10) antibody (p-H3) 24 h after incubation with VX-680 (10 μM), SAHA (0.2 μM) or a combination of both. Controls were left untreated. Western blot analysis showed a decrease in p–H3 after treatment with VX-680 ( lane 2 ) relative to controls ( lane 1 ) and an increase when SAHA was added ( lane 3 ). For the combination of VX-680 and SAHA (lane 4 ) no p-H3 was detected.

    Pediatr Surg Int 2012 28, 579-89. Tozasertib (VX-680, MK-0457) purchased from Selleck.

    ENMD-2076 has benn tested it on two different neurobiastoma cell lines(SK-N-BE(2) and CHP-134),being calculated the IC50 by a WST-1(Roche) proliferation assay, as shown in the table below. Its in vitro activity is in the micromolar range and has a comparable effect on both lines.VX-680 was used as standard, and it proved more potent on CHP-134 cells.

    Dr. Antonino Maria Sparta ,University of Trento. Tozasertib (VX-680, MK-0457) purchased from Selleck.

  • SDS-PAGE of CHP-134 cells extracts after 24 h exposure to the indicated drug and concentration. N-myc levels were evaluated and compared to beta actin used as house-keeping protein. Aurora A blockade seems to diminish N-myc expression or stability.

    Dr. Antonino Maria Sparta ,University of Trento. Tozasertib (VX-680, MK-0457) purchased from Selleck.

    Western blot analysis of Histone and Aurora kinase. 0-10μM MK0457 was added.

    Dr. Zhang of Tianjin Medical University. Tozasertib (VX-680, MK-0457) purchased from Selleck.

Purity & Quality Control

Choose Selective Aurora Kinase Inhibitors

Biological Activity

Description Tozasertib (VX-680, MK-0457) is a pan-Aurora inhibitor, mostly against Aurora A with Kiapp of 0.6 nM in a cell-free assay, less potent towards Aurora B/Aurora C and 100-fold more selective for Aurora A than 55 other kinases. Phase 2.
Targets
Aurora A [1]
(Cell-free assay)
Aurora C [1]
(Cell-free assay)
Aurora B [1]
(Cell-free assay)
FLT3 [4]
(Cell-free assay)
Bcr-Abl [4]
(Cell-free assay)
0.6 nM(Ki app) 4.6 nM(Ki app) 18 nM(Ki app) 30 nM(Ki) 30 nM(Ki)
In vitro

Although its multi-kinase profile, VX-680 induces similar cytotoxicity with IC50 of approximately 300 nM and exhibits an AUR B-like inhibitory phenotype of G2/M arrest, endoreduplication and apoptosis in BaF3 cells transfected with ABL or FLT-3 (mutant and wild type) kinases. VX-680 prevents the CAL-62 proliferation in a time-dependent manner. VX-680 treatment for 14 days significantly decreases the number and size of colonies by approximately 70% in the 8305C and 90% in the CAL-62, 8505C and BHT-101. Treatment of the different ATC cells with VX-680 inhibits proliferation with the IC50 between 25 and 150  nM. The VX-680 significantly impairs the ability of the different cell lines to form colonies in soft agar. Analysis of caspase-3 activity indicates that VX-680 induces apoptosis in the different cell lines. CAL-62 cells exposed for 12  hours to VX-680 showed an accumulation of cells with ≥4N DNA content. Time-lapse analysis demonstrates that VX-680-treated CAL-62 cells exit metaphase without dividing. Moreover, histone H3 phosphorylation is abrogated following VX-680 treatment. [2] VX-680 has significant inhibitory activity against BCR-Abl bearing the T315I mutation in patient-derived samples. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BE-13 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1jUSWlEPTB;MD6wNFM{QCEQvF2= NXHSZWR5W0GQR2LFVi=>
RS4-11 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYDp[3dEUUN3ME2wMlAxPDB2IN88US=> MmjFV2FPT1KHUh?=
MFH-ino NFy2XWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTBwMEC5PUDPxE1? NHL0[otUSU6JUlXS
NTERA-S-cl-D1 MnXJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnL2TWM2OD1yLkCxOFM1KM7:TR?= MYDTRW5IWkWU
697 M1HER2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH;FOYpKSzVyPUCuNFI1PzFizszN M1jHc3NCVkeURWK=
NALM-6 NFfUbnlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnPsTWM2OD1yLkCyOVUzKM7:TR?= M3fpc3NCVkeURWK=
ES8 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYjJR|UxRTBwMES2NVMh|ryP M3e2OXNCVkeURWK=
HUTU-80 M2nhXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF7vUpRKSzVyPUCuNFUzQTlizszN NFPweJRUSU6JUlXS
MV-4-11 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1\FUGlEPTB;MD6wO|c5OiEQvF2= MWXTRW5IWkWU
MONO-MAC-6 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX;JR|UxRTBwMEe4O|kh|ryP M1v4d3NCVkeURWK=
LC-2-ad M{TEOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFOwZ|FKSzVyPUCuNFg4QDlizszN MnrlV2FPT1KHUh?=
BL-41 NET1VnBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{XqVmlEPTB;MD6xNFQ1PSEQvF2= MonvV2FPT1KHUh?=
A4-Fuk MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFjCR4xKSzVyPUCuNVE2PjNizszN M3jtT3NCVkeURWK=
SW954 NXzJOmcxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlP2TWM2OD1yLkGyNlI6KM7:TR?= M3PhenNCVkeURWK=
BV-173 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4mxfGlEPTB;MD6xNlY1OSEQvF2= M{HkdHNCVkeURWK=
TE-11 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVjJR|UxRTBwMUS5PFIh|ryP M4K3fnNCVkeURWK=
SK-UT-1 NHnER|VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWLJR|UxRTBwMUW5OlUh|ryP NXLHSHMyW0GQR2LFVi=>
SIG-M5 Mn\BS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXnJR|UxRTBwMU[3NFch|ryP NWPoe2d2W0GQR2LFVi=>
OCUB-M M3fGfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{XuPGlEPTB;MD6xOlk5OyEQvF2= Moi5V2FPT1KHUh?=
K052 MojvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVjRfpdCUUN3ME2wMlE6PDhizszN NVnlOYxLW0GQR2LFVi=>
VA-ES-BJ NILpbHhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIDIZpNKSzVyPUCuNlAxQDZizszN MVHTRW5IWkWU
SW982 NYnEeGtPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXvJR|UxRTBwMkGzPEDPxE1? M3n6[XNCVkeURWK=
LB647-SCLC NHzRN2dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEP4OVFKSzVyPUCuNlE2OjNizszN NEDRTGdUSU6JUlXS
PSN1 MkPyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXTJR|UxRTBwMkKwNlYh|ryP Ml3UV2FPT1KHUh?=
BB30-HNC NVXRRnp3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4ew[2lEPTB;MD6yNlU6OSEQvF2= MkTJV2FPT1KHUh?=
ST486 MlrxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2rNUWlEPTB;MD6yN|A5PyEQvF2= MX;TRW5IWkWU
MOLT-4 MnPNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2\3[WlEPTB;MD6yN|M{PyEQvF2= M{P5S3NCVkeURWK=
EW-16 NG\y[4JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NG\yfYRKSzVyPUCuNlM4PjhizszN MnLrV2FPT1KHUh?=
KS-1 NY\0dm5OT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXzzUG9bUUN3ME2wMlI{Pzh3IN88US=> M2LYUnNCVkeURWK=
SR MoX5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2juPGlEPTB;MD6yOFU3PCEQvF2= NVLu[GJ7W0GQR2LFVi=>
KM12 Mn\mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlL4TWM2OD1yLkK2N|Yh|ryP MoPuV2FPT1KHUh?=
EM-2 NYSzeGhqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{The2lEPTB;MD6yOlY1OSEQvF2= MVrTRW5IWkWU
MEG-01 Mm\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXzkelZUUUN3ME2wMlI4QDR7IN88US=> MlvmV2FPT1KHUh?=
NB13 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NW\vPGJwUUN3ME2wMlI4QTh2IN88US=> NV3lOGFHW0GQR2LFVi=>
RKO MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2DnWWlEPTB;MD6zNFgyOyEQvF2= MV3TRW5IWkWU
CESS M4DMbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVjkS|FkUUN3ME2wMlMyOzJ6IN88US=> M4DjU3NCVkeURWK=
EoL-1-cell NFTJfnhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3z1[mlEPTB;MD6zN|Q2QSEQvF2= MlzsV2FPT1KHUh?=
DOHH-2 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVHJSnZNUUN3ME2wMlM{PzhzIN88US=> M1G0enNCVkeURWK=
A388 Ml3nS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlXETWM2OD1yLkO0NFg3KM7:TR?= NGLLZXBUSU6JUlXS
LAMA-84 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NW\4[2tDUUN3ME2wMlM2OTd6IN88US=> M2S1N3NCVkeURWK=
IMR-5 NV:ybFlsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NU[zW|FHUUN3ME2wMlM2PTRizszN NIOxcpdUSU6JUlXS
KARPAS-422 M3TuZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoK1TWM2OD1yLkO3NlczKM7:TR?= M1K5T3NCVkeURWK=
MRK-nu-1 M3nUfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXLJR|UxRTBwM{ixN{DPxE1? M37yS3NCVkeURWK=
BL-70 M2Ljdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVnJR|UxRTBwM{i5O|Qh|ryP Ml[2V2FPT1KHUh?=
LXF-289 M{Xz[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHjOclBKSzVyPUCuOFA1ODZizszN Mli0V2FPT1KHUh?=
RL95-2 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXHKWVd[UUN3ME2wMlQxPTZ5IN88US=> NH[3NI5USU6JUlXS
QIMR-WIL MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXHre3JlUUN3ME2wMlQzPjd4IN88US=> NEX6NYZUSU6JUlXS
K-562 NY\TOVZuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV\JR|UxRTBwNEO0O|Ih|ryP MlTTV2FPT1KHUh?=
NCI-H510A MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIDuOoFKSzVyPUCuOFM5OjNizszN MVXTRW5IWkWU
NCI-H524 M37HdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3;3RWlEPTB;MD61NVE1PyEQvF2= Mn34V2FPT1KHUh?=
KE-37 NH;iSYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGPHdm1KSzVyPUCuOVIyODJizszN M1\OVXNCVkeURWK=
KP-N-YS M{TKTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV\JR|UxRTBwNUSzPVIh|ryP NFXXcJpUSU6JUlXS
LS-411N NHq3cFhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M336cmlEPTB;MD61O|c2OiEQvF2= MXnTRW5IWkWU
CTV-1 NWm5WnU3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVTIUXA4UUN3ME2wMlU5Pzd|IN88US=> Mn\aV2FPT1KHUh?=
NCI-SNU-16 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{OxcmlEPTB;MD62N|U4OSEQvF2= MW\TRW5IWkWU
HT-144 NUi3XWN3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX;JR|UxRTBwNkO3PVgh|ryP M2X2bXNCVkeURWK=
NCI-H187 M1rYO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHvIVIFKSzVyPUCuOlQyOyEQvF2= NV;mdoNJW0GQR2LFVi=>
OCI-AML2 M1z4Rmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmDjTWM2OD1yLk[0OFA{KM7:TR?= M{fQWXNCVkeURWK=
CCRF-CEM NESwT5lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4LhVWlEPTB;MD62OVM1PiEQvF2= M4Xkc3NCVkeURWK=
ONS-76 M2HVVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXnJR|UxRTBwNk[0OVgh|ryP MYfTRW5IWkWU
IST-SL2 NXnwU5o4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2rkOmlEPTB;MD63NVk5OiEQvF2= Mo\vV2FPT1KHUh?=
NB6 NU\ldGhwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWG0[JRiUUN3ME2wMlc4OjV2IN88US=> M{CwdnNCVkeURWK=
SK-PN-DW NWGwS3JkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlnBTWM2OD1yLke5NVQh|ryP NXf1Z2VLW0GQR2LFVi=>
HCC1599 MofhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NULnPHhtUUN3ME2wMlgxQDd2IN88US=> MVrTRW5IWkWU
MC116 M{XvOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXvUXoJmUUN3ME2wMlg2ODFzIN88US=> NH23emJUSU6JUlXS
TE-15 NFyw[GlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYLJR|UxRTBwOEWwPVgh|ryP NXnjZ29qW0GQR2LFVi=>
HOP-62 MkjzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXHocGNIUUN3ME2wMlg3OzJ7IN88US=> MXnTRW5IWkWU
TGBC24TKB MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYXCenVkUUN3ME2wMlg3Ozh3IN88US=> NILhXFdUSU6JUlXS
HCE-4 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkCwTWM2OD1yLki4NFY{KM7:TR?= NGHtVI1USU6JUlXS
ALL-PO NH;JWm9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWnUfVlXUUN3ME2wMlg5OTd3IN88US=> M{G2WHNCVkeURWK=
KGN MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1y4SWlEPTB;MD64PVk6PSEQvF2= NEj4bGNUSU6JUlXS
ML-2 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoXuTWM2OD1yLkmwNlU6KM7:TR?= MUTTRW5IWkWU
ES4 M1PWc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MY\JR|UxRTBwOUGxNlgh|ryP NUT6dWRqW0GQR2LFVi=>
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NCI-H2107 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1Wzd2lEPTB;Mj64N|cyOSEQvF2= M2PpWnNCVkeURWK=
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RPMI-8402 NVjP[XVFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmS4TWM2OD1|LkW4OlA{KM7:TR?= MXXTRW5IWkWU
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ES1 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIThe|ZKSzVyPUOuPVIzQTNizszN NV\HO5hyW0GQR2LFVi=>
NCI-H2171 MomyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWjwSXZTUUN3ME2zMlkzPDJ|IN88US=> M2\xcHNCVkeURWK=
NCI-H747 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY\JR|UxRTNwOUSyNlEh|ryP Mnu1V2FPT1KHUh?=
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TE-12 NH3NTYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkK2TWM2OD12LkW2N|k1KM7:TR?= MWLTRW5IWkWU
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COR-L279 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4nPZWlEPTB;ND63OVg6OSEQvF2= MVnTRW5IWkWU
SF268 MoPUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV\JR|UxRTRwN{m5NVYh|ryP NVLpTGxnW0GQR2LFVi=>
MC-CAR M1\1T2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGfvNXpKSzVyPUWuNFY4PTdizszN M4H4OHNCVkeURWK=
TK10 Mo\SS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGfhbVNKSzVyPUWuN|U1PjlizszN NXrlSmh{W0GQR2LFVi=>
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NCI-H2126 NIfWZ3ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXPJR|UxRTVwNkS1O|Qh|ryP NF\GUZRUSU6JUlXS
Daudi M4TBXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4nFR2lEPTB;NT62PVEzKM7:TR?= Mm\EV2FPT1KHUh?=
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NCI-H1581 MlfSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mkj1TWM2OD14Lke4OFA2KM7:TR?= M3rQTHNCVkeURWK=
UACC-257 NIm5XHFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXrVV5RPUUN3ME23MlA1PTF{IN88US=> MYrTRW5IWkWU
KM-H2 M1HjO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkG0TWM2OD15LkG4OFU4KM7:TR?= MX\TRW5IWkWU
NCI-H1436 Ml;wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1vyWGlEPTB;Nz62PVk{OiEQvF2= MnvsV2FPT1KHUh?=
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NCI-H526 NIfMZ3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn7BTWM2OD16LkK1OlM4KM7:TR?= MVHTRW5IWkWU
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8-MG-BA MlfhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWXzWHdlUUN3ME25MlMzQDR2IN88US=> MWPTRW5IWkWU
KY821 NH7iS3NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYfJR|UxRTlwN{e0PFQh|ryP MYfTRW5IWkWU
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NB69 MlvhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUKwfZpvUUN3ME2xNU44PzB3IN88US=> MnnHV2FPT1KHUh?=
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DMS-153 MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH35PWNKSzVyPUGyMlA1OjZizszN NYnXZoVxW0GQR2LFVi=>
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NCI-H1882 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3\WOGlEPTB;MUKuOFA3PiEQvF2= MWXTRW5IWkWU
KG-1 NVe1cnRNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWHQSJBzUUN3ME2xNk43PTR3IN88US=> MWPTRW5IWkWU
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NCI-H1417 NHP4NnBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MY\JR|UxRTF2LkOwOVIh|ryP MYHTRW5IWkWU
MZ7-mel M3:yRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnXxTWM2OD1zND60OFM{KM7:TR?= MUHTRW5IWkWU
JiyoyeP-2003 MnWyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmPnTWM2OD1zNT62N|I3KM7:TR?= MkLQV2FPT1KHUh?=
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SF539 MlT0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnHlTWM2OD1zNz65PVIzKM7:TR?= NHnGVmJUSU6JUlXS
Calu-6 NVz3OXBjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkixTWM2OD1zOT6yN|kh|ryP MX;TRW5IWkWU
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CAL-148 NH7CTVRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV7JR|UxRTJyLkm5N|Qh|ryP NInKWW9USU6JUlXS
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KLE NH;6ZW1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUK1NlZ7UUN3ME2yNk4yQTB|IN88US=> M1n2PXNCVkeURWK=
LB831-BLC MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWjJR|UxRTJ3LkG1NlYh|ryP NHrDU|hUSU6JUlXS
NCI-H889 NF3DT41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXrJR|UxRTJ3LkG5N|Eh|ryP NIi1Z21USU6JUlXS
REH NEPZdWJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWC1SXRvUUN3ME2yOU41PjdzIN88US=> NWjGb5JsW0GQR2LFVi=>
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MPP-89 NGHBT4pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUPtTXNsUUN3ME2yOU42OzF2IN88US=> NFTtUphUSU6JUlXS
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NCI-H748 NH63NlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUPJR|UxRTJ3Lke2Nlch|ryP NIXqPItUSU6JUlXS
LB2518-MEL MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmDkTWM2OD1{Nz6xO|c{KM7:TR?= MVnTRW5IWkWU
TGBC1TKB NUXWemdJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmS2TWM2OD1{Nz61OVg2KM7:TR?= Mkf4V2FPT1KHUh?=
MHH-PREB-1 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoLrTWM2OD1{OD6wO|M1KM7:TR?= NUDjdZFjW0GQR2LFVi=>
MZ2-MEL Ml;5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2fETGlEPTB;MkiuOlE1OyEQvF2= MV\TRW5IWkWU
U-266 NXrV[XFET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NE\tbGlKSzVyPUK4MlY{PjZizszN MW\TRW5IWkWU
SNU-C1 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{\2ZmlEPTB;MkiuPVQ{KM7:TR?= NG\aVHBUSU6JUlXS
SW962 M{DWZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEG1RmZKSzVyPUOwMlI4PDdizszN M2izeXNCVkeURWK=
Raji MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXzJR|UxRTNyLkW1PVIh|ryP MkjXV2FPT1KHUh?=
KNS-42 NHO0[|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIX0Wo5KSzVyPUOwMlg6PTZizszN MXvTRW5IWkWU
LB996-RCC MmS1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVLLfGRlUUN3ME2zNU4yPzB{IN88US=> M3vaRXNCVkeURWK=
CHP-126 MoLYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoHCTWM2OD1|MT6xPVg1KM7:TR?= MYLTRW5IWkWU
RXF393 NITS[ppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXvJR|UxRTN{LkS5O{DPxE1? NUnre2FnW0GQR2LFVi=>
COLO-684 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIK4NolKSzVyPUOyMlY1OzhizszN M4PP[XNCVkeURWK=
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A253 NGrR[3JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV\JR|UxRTN|LkW4OVIh|ryP Mn7TV2FPT1KHUh?=
KNS-81-FD M{XqOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUPJR|UxRTN2LkW0OVYh|ryP MYPTRW5IWkWU
TE-441-T MnfwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2LzWWlEPTB;M{SuOlM4OSEQvF2= M4nnenNCVkeURWK=
HCC2157 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NULHTZdwUUN3ME2zOU41PjF7IN88US=> NUjwToNSW0GQR2LFVi=>
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KU812 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MknZTWM2OD12MT61NFch|ryP NXvVeZl2W0GQR2LFVi=>
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DG-75 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M33m[2lEPTB;NEWuNVU4PyEQvF2= NUiyToZmW0GQR2LFVi=>
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LS-513 MljtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUXJR|UxRTR3LkmxOVYh|ryP MXzTRW5IWkWU
HD-MY-Z NHX3ZphIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVnocIxWUUN3ME20Ok41PjF{IN88US=> NGHF[WJUSU6JUlXS
L-363 Mn3ZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1uyVWlEPTB;NE[uPFgyKM7:TR?= MlLDV2FPT1KHUh?=
TE-6 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn7JTWM2OD12OD60OFYh|ryP NYnQXo0yW0GQR2LFVi=>
NCI-H345 NYXufo9LT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX;mTo83UUN3ME20PE41PjhizszN MYTTRW5IWkWU
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... Click to View More Cell Line Experimental Data

In vivo VX-680 gives rise to a marked decrease in tumor size in a human AML (HL-60) xenograft model. In mude mice treateed with VX-680 at 75 mg/kg, twice a day intraperitoneally (b.i.d. i.p.) for 13 days, mean tumor volumes are reduced by 98%. Tumor growth decrease is dose dependent and significant at a dose of 12.5 mg/kg b.i.d. VX-680 is well tolerated, with a small decrease in body weight observed only at the highest dose. VX-680 also triggers tumor regresson in pancreatic and colon xenograft models. VX-680 also displays potent antitumor activity when infused i.v. in mude rats bearing established HCT116 tumors. A higher dose of VX-680 (2 mg/kg/h) improves efficacy with a 56% decrease in mean tumor volume. [1]

Protocol

Kinase Assay:

[3]

+ Expand

Kinase inhibition assays:

The consumption of ATP is coupled via the pyruvate kinase/lactic dehydrogenase enzyme pair to the oxidation of NADH, which can be monitored through the decrease in absorption at 340 nm. Reactions contains 100 mM Tris (pH 8), 10 mM MgCl2, 2.2 mM ATP, 1 mM phosphoenolpyruvate, 0.6 mg/mL NADH, 75 units/mL pyruvate kinase, 105 units/mL lactate dehydrogenase, and 0.5 mM substrate peptide (sequence: EAIYAAPFAKKK). Reactions (75 μL) are started by adding sufficient kinase to bring the reactions to 30 nM kinase concentration and the decrease in absorbance is monitored over 30 minutes at 30°C in a microtiter plate spectrophotometer. Inhibitory constants are obtained through addition of 3.75 μL VX-680 in 100% DMSO or DMSO alone. Ki values are calculated as follows, K i = IC50 / (1 + [S]/Kd), where [S] = [ATP] = 2.2 mM, and Kd (of ATP to Abl) = 70 μM. These values are calculated assuming a Kd (ATP) of 70 μM for wild type and H396P Abl kinase domain.
Cell Research:

[2]

+ Expand
  • Cell lines: CAL-62 cells
  • Concentrations: 5-500 nM
  • Incubation Time: 4 days
  • Method:

    The CAL-62 cells are cultured in the absence (dimethyl sulfoxide, DMSO) or the presence of 500  nM VX-680 for different periods of time (1-5 days). The dose-dependent effects of VX-680 on cell proliferation are evaluated by treating the different ATC cells for 4 days with different concentrations of the Aurora inhibitor (5–500  nM). The cells are pulse labeled with 30  mM BrdU for 2  hours before the end of the incubation time. The BrdU incorporation is analyzed by means of a colorimetric immunoassay using the cell proliferation ELISA kit. The results from VX-680-treated cells are compared with those observed in control cells and expressed as a fold of variation versus control.


    (Only for Reference)
Animal Research:

[1]

+ Expand
  • Animal Models: Female athymic NCr-nu mice bearing HL-60 leukemia cells
  • Formulation: 50% PEG300 in 50 mM phosphate buffer
  • Dosages: 50 mg/kg, 75 mg/kg
  • Administration: Administered via i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 93 mg/mL (200.17 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
15mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 464.59
Formula

C23H28N8OS

CAS No. 639089-54-6
Storage powder
in solvent
Synonyms N/A

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

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  • Computed Result

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    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
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    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

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Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00405054 Terminated Leukemia Merck Sharp & Dohme Corp. December 2006 Phase 2
NCT00290550 Terminated Carcinoma Non-Small-Cell Lung Merck Sharp & Dohme Corp. June 2006 Phase 2
NCT00111683 Completed Chronic Myelogenous Leukemia in Blast Crisis|Lymphocytic Leukemia B Cell Acute|Myelodysplastic Syndromes|Myelogenous Leukemia Chronic Merck Sharp & Dohme Corp. June 2005 Phase 1
NCT02532868 Terminated Cancer Merck Sharp & Dohme Corp. May 2005 Phase 1
NCT00099346 Terminated Colorectal Cancer|Advanced Solid Tumors Merck Sharp & Dohme Corp. January 2005 Phase 1

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

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Aurora Kinase Signaling Pathway Map

Aurora Kinase Inhibitors with Unique Features

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID