Volasertib (BI 6727)

Catalog No.S2235

Volasertib (BI 6727) Chemical Structure

Molecular Weight(MW): 618.81

Volasertib (BI 6727) is a highly potent Plk1 inhibitor with IC50 of 0.87 nM in a cell-free assay. It shows 6- and 65-fold greater selectivity against Plk2 and Plk3. Phase 3.

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In DMSO USD 202 In stock
USD 120 In stock

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3 Customer Reviews

  • Western blot analysis. HeLa or MCF7 cells were treated with nocodazole (noc, 50 ng/ml), paclitaxel (pacli, 50 nM), the Plk1 inhibitor BI 2536 (50 nM) or BI 6727 (50 nM) for 16 h and cellular extracts were prepared for western blot analysis with antibodies as indicated. con: cellular extracts from control cells without any treatment. β-actin served as loading control.

    Oncogene 2013 10.1038/onc.2013.518. Volasertib (BI 6727) purchased from Selleck.

    Decrease viability of Hec50 subclones after 3 days treatment with BI6727 was shown. Reduction of Cdc2 Tyr15 phosphorylation and increase Histone H3 Ser10 phosphorylation in cells treated with BI 6727 was observed.

    Dr. Xiangbing Meng from University of Iowa. Volasertib (BI 6727) purchased from Selleck.

  • Hec50 cells are arrested in mitosis after 24hours treatment with 10nM BI 6727.

    Dr. Xiangbing Meng from University of Iowa. Volasertib (BI 6727) purchased from Selleck.

Purity & Quality Control

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Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

Biological Activity

Description Volasertib (BI 6727) is a highly potent Plk1 inhibitor with IC50 of 0.87 nM in a cell-free assay. It shows 6- and 65-fold greater selectivity against Plk2 and Plk3. Phase 3.
Features A high volume of distribution, indicating good tissue penetration, and a long terminal half-life.
Targets
PLK1 [1]
(Cell-free assay)
0.87 nM
In vitro

Like BI2536, BI6727 is an ATP-competitive kinase inhibitor from the dihydropteridinone class of compounds. In addition to Plk1, BI6727 also potently inhibits two closely related kinases Plk2 and Plk3 with IC50 of 5 nM and 56 nM, respectively. BI6727 at concentrations up to 10 μM displays no inhibitory activity against a panel of >50 other kinases. BI6727 inhibits the proliferation of multiple cell lines derived from various cancer tissues, including HCT116, NCI-H460, BRO, GRANTA-519, HL-60, THP-1, and Raji cells with EC50 of 23 nM, 21 nM, 11 nM, 15 nM, 32 nM, 36 nM, and 37 nM, respectively. BI6727 treatment (100 nM) in NCI-H460 cells induces an accumulation of mitotic cells with monopolar spindles and positive staining for histone H3 phosphoserine 10, confirming that cells are arrested early in the M phase, followed by induction of apoptosis. [1] Low nanomolar concentrations of BI6727 display potent inhibitory activity against neuroblastoma (NB) tumor-initiating cells (NB TIC) with EC50 of 21 nM, whereas only micromolar concentrations of BI6727 are cytotoxic for normal pediatric neural stem cells. [2] BI6727 induces growth arrest of Daoy and ONS-76 medulloblastoma cells similar to BI 2536. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
KASUMI-1 NHvreXVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1TiVVczKGh? NH61TGNKSzVyPUG3NOKyPTFibl2= M1zFOlI2PTd4MEe0
KG-1 MnfPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NInBTZE4OiCq Mn7STWM2OD1zNUFCtVY4KG6P Ml3BNlU2PzZyN{S=
MOLM-13 NFz4OGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnTOO|IhcA>? NGLjXXJKSzVyPUW3xtE1PCCwTR?= M3nBe|I2PTd4MEe0
MV-4-11 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF[3V2Q4OiCq M{fvXGlEPTB;MUdCtVYhdk1? MXSyOVU4PjB5NB?=
NOMO-1 NV3Cb2pwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoTFO|IhcA>? M3f6bWlEPTB;MUS1xtE4KG6P MlLMNlU2PzZyN{S=
OCI-AML3 NEG4NI1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXG3NkBp NEHjbYxKSzVyPUmwxtE2OSCwTR?= M1KzT|I2PTd4MEe0
SKM-1 M3XKWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmDJO|IhcA>? MYfJR|UxRTl3wsG1NkBvVQ>? NXLiXXhZOjV3N{[wO|Q>
THP-1 NYn4TnFMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYS3NkBp NE[wfGZKSzVyPUW2xtE{QSCwTR?= MWOyOVU4PjB5NB?=
MCF7/LTED  M{Tnemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXrRVJU3Oi53LUSwJI5O MlzwOUBl MlrPbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmNWSncHXu[IVvfCCvYX7u[ZI> MnXqNlU1QDB7NEO=
HCC1428/LTED M4[4OGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoDQNk42NTRyIH7N M1e0SlUh\A>? NUf3T4VYcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? NH3KfmMzPTR6MEm0Ny=>
A431 Ml;rS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFjDbZcxNTNyIH7N M33sWVEuPCCm MXnpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCkb4ToJIRwe2VvIHHu[EB1cW2nLXTldIVv\GWwdDDtZY5v\XJ? MVKyN|g6OTB7Nh?=
FaDu  MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGPLR3cxNTFyMECgcm0> MmfvNU01KGR? M4fPSIlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHLveIgh\G:|ZT2gZY5lKHSrbXWt[IVx\W6mZX70JI1idm6nch?= M1zsWlI{QDlzMEm2
SF188 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{n1WFUxNTF3MDDuUS=> NV7nWGJbPzJiaB?= NWroR5pMTE2VTx?= NXj1RoRscW6qaXLpeJMh[2WubDDwdo9tcW[ncnH0bY9v M3nacVI{QDh5NkS1
T98G M{PqdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkXsOVAuOTVyIH7N NIXhUlc4OiCq MknQSG1UVw>? NXftbXBTcW6qaXLpeJMh[2WubDDwdo9tcW[ncnH0bY9v M3LhdFI{QDh5NkS1
DU145 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWGxNE82OC9{NUCgcm0> MnzZNlQhcA>? MnLLTWM2ODxzMDDuUS=> M2r4[|I{QDh2NEK4
LNCaP MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLvNVAwPTBxMkWwJI5O NE\KS|EzPCCq NXLhUGFCUUN3MEyxNEBvVQ>? NGLs[GEzOzh6NESyPC=>
PC3 MlXPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{HhOVExNzVyL{K1NEBvVQ>? NV[4T49JOjRiaB?= NGrIRnRKSzVy4pk8OlAxKG6P MXSyN|g5PDR{OB?=
RT4 NXK1Xmx4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkjXOFghcA>? NIXuUmRKSzVyPUGxNU4zPyCwTR?= NEH3dWYzOzd7Mk[zPS=>
5637 NH70TVFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVO0PEBp NXrQOldnUUN3ME2xNVY2NjF2IH7N MX6yN|c6OjZ|OR?=
T24 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4nUR|Q5KGh? M1;wfGlEPTB;MkC0MlkyKG6P MVuyN|c6OjZ|OR?=
KMCH-1 NYrvdlhPSXCxcITvd4l{KEG|c3H5 MoG2NlAxKG6P MnPvNlQhcA>? MVjpcoR2[2W|IHHwc5B1d3Orcx?= NHXGW5ozOzdyM{[3Ny=>
Mz-ChA-1 MYrBdI9xfG:|aYOgRZN{[Xl? MnLPNlAxKG6P MmnMNlQhcA>? MXrpcoR2[2W|IHHwc5B1d3Orcx?= MViyN|cxOzZ5Mx?=
HUCCT-1 MmTZRZBweHSxc3nzJGF{e2G7 M4nqNVIxOCCwTR?= MnPrNlQhcA>? NEPOO4RqdmS3Y3XzJIFxd3C2b4Ppdy=> M2H1PFI{PzB|Nkez
HCT 116 M1XnT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTkVG1GSzVywrC9JFI{KG6P MmfaNVk{QDN6MkO=
NCI-H460 MlPYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFW2VplGSzVywrC9JFIyKG6P MV6xPVM5Ozh{Mx?=
BRO NVLGOWF7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYLFR|UxyqB;IEGxJI5O Mln5NVk{QDN6MkO=
GRANTA-519 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWjzdIdJTUN3MNMgQUAyPSCwTR?= MmDmNVk{QDN6MkO=
HL-60 MmrsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVj6PFJmTUN3MNMgQUA{OiCwTR?= MVuxPVM5Ozh{Mx?=
THP-1 M1zWdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{\JRmVEPTBiPTCzOkBvVQ>? NVHqWHU2OTl|OEO4NlM>
Raji Ml7hS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVjFR|UxKD1iM{egcm0> MmjCNVk{QDN6MkO=

... Click to View More Cell Line Experimental Data

In vivo Administration of BI6727 significantly inhibits the growth of multiple human carcinoma xenografts including HCT116, NCI-H460, and taxane-resistant CXB1 colon carcinoma, accompanied by an increase in the mitotic index as well as an increase in apoptosis. [1] In in vivo studies, BI6727 shows better toxicity and pharmacokinetic profile compared to BI2536. [3]

Protocol

Kinase Assay:[1]
+ Expand

In vitro kinase assays:

Recombinant human Plk1 (residues 1-603) is expressed as NH2-terminal, GST-tagged fusion protein using a baculoviral expression system and purified by affinity chromatography using glutathione-agarose. Enzyme activity assays for Plk1 are done in the presence of serially diluted BI6727 using 20 ng of recombinant kinase and 10 μg casein from bovine milk as substrate. Kinase reactions are done in a final volume of 60 μL for 45 minutes at 30 °C [15 mM MgCl2, 25 mM MOPS (pH 7.0), 1 mM DTT, 1% DMSO, 7.5 μM ATP, 0.3 μCi γ-32P-ATP]. Reactions are terminated by the addition of 125 μL of ice-cold 5% TCA. After transferring the precipitates to MultiScreen mixed ester cellulose filter plates, plates are washed with 1% TCA and quantified radiometrically. Dose-response curves are used for calculating IC50 value.
Cell Research:[1]
+ Expand
  • Cell lines: HCT116, NCI-H460, BRO, GRANTA-519, HL-60, THP-1, and Raji
  • Concentrations: Dissolved in DMSO, final concentrations ~1 μM
  • Incubation Time: 24, 48, and 72 hours
  • Method: Cell proliferation assays are done by incubating cells in the presence of various concentrations of BI6727 for 24, 48, and 72 hours and cell growth is assessed by measuring Alamar blue dye conversion in a fluorescence spectrophotometer. Effective concentrations at which cellular growth is inhibited by 50% (EC50) are extrapolated from the dose-response curve fit. To determine the DNA content, cell suspensions are fixed in 80% ethanol, treated for 5 minutes with 0.25% Triton X-100 in PBS, and incubated with 0.1% RNase and 10 μg/mL propidium iodide in PBS for 20 minutes at room temperature. Cell cycle profiles are determined by flow cytometric analysis.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Female BomTac:NMRI-Foxn1nu mice grafted s.c. with HCT116, NCI-H460, or CXB1 cells
  • Formulation: Formulated in hydrochloric acid (0.1 N), and diluted with 0.9% NaCl, or suspended in 0.5% Natrosol 250 hydroxyethyl-cellulose
  • Dosages: ~25 mg/kg/day
  • Administration: Injected i.v., or given intragastrally via gavage needle
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 20 mg/mL (32.32 mM) warming
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 4% DMSO+corn oil 2mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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 618.81
Formula

C34H50N8O3

CAS No. 755038-65-4
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02722135 Withdrawn Leukemia, Myeloid, Acute Boehringer Ingelheim November 2016 Phase 1
NCT02527174 Not yet recruiting Leukemia, Myeloid, Acute|Leukemia, Monocytic, Acute|Leukemia, Myelomonocytic, Acute|Leukemia, Erythroblastic, Acute|Leukemia, Megakaryoblastic, Acute University of Alberta November 2016 Phase 1
NCT02757248 Withdrawn PTCL|CTCL Anne Beaven, MD|National Comprehensive Cancer Network|Boehringer Ingelheim|Duke University November 2016 Phase 1
NCT02875002 Not yet recruiting Relapsed and Refractory Aggressive B- and T-cell Lymphomas|Lymphoma Yale University|Massey Cancer Center|Sidney Kimmel Comprehensive Cancer Center October 2016 Phase 1
NCT02905994 Not yet recruiting AML Massachusetts General Hospital|Boehringer Ingelheim September 2016 Phase 1
NCT02861040 Withdrawn Recurrent Adult Acute Lymphoblastic Leukemia|Refractory Adult Acute Lymphoblastic Leukemia Northwestern University|National Comprehensive Cancer Network|National Cancer Institute (NCI) August 2016 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID