Volasertib (BI 6727)


Volasertib (BI 6727)化学構造


Volasertib (BI 6727)は一種の高度有効なPlk1阻害剤で、無細胞試験でこのIC50値が0.87nMですが、Plk1に作用する選択性はPlk2とPlk3に作用する選択性より6倍と65倍がそれぞれ高くなります。臨床3期。

サイズ 価格 在庫  
USD 254 あり
USD 151 あり


  • 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.

    immunoblot analyses were performed in A375 xenografted melanoma tissues treated with BI 6727 (10 and 25 mg/kg body weight) or vehicle alone to determine the effect of PLK1 knockdown using (D) PCK1 and (E) FBP1 antibodies. The blots were re-probed with b-actin for loading control. Data is representative of three individual experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article)

    Cancer Lett, 2017, 394:13-21. Volasertib (BI 6727) purchased from Selleck.

  • HNSCC cell-cycle stages determined according to 7-aminoactinomycin D and BrdU incorporation.

    Cancer Lett, 2017, 392:71-82. 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.




製品説明 Volasertib (BI 6727)は一種の高度有効なPlk1阻害剤で、無細胞試験でこのIC50値が0.87nMですが、Plk1に作用する選択性はPlk2とPlk3に作用する選択性より6倍と65倍がそれぞれ高くなります。臨床3期。
特性 A high volume of distribution, indicating good tissue penetration, and a long terminal half-life.
PLK1 [1]
(Cell-free assay)
0.87 nM

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 Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
KASUMI-1 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2\yN|czKGh? MUDJR|UxRTF5MNMxOVEhdk1? NV7hWWN[OjV3N{[wO|Q>
KG-1 NWPIZ|h{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHnUT|M4OiCq M2\NVWlEPTB;MUWwxtE3PyCwTR?= NWTEcJB6OjV3N{[wO|Q>
MOLM-13 MoH4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHzMOnU4OiCq M2PWO2lEPTB;NUhCtVQ1KG6P MoHqNlU2PzZyN{S=
MV-4-11 NH\WN4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXrpRXV5PzJiaB?= MXzJR|UxRTF4wsG2JI5O Mkj0NlU2PzZyN{S=
NOMO-1 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYjj[mtrPzJiaB?= MmK1TWM2OD1zNEZCtVchdk1? NX;CXHRzOjV3N{[wO|Q>
OCI-AML3 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mk\2O|IhcA>? MU\JR|UxRTlywsG1NUBvVQ>? NUjIXFd[OjV3N{[wO|Q>
SKM-1 M{HU[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4nxfVczKGh? NI[yN5JKSzVyPUm1xtE2OiCwTR?= Ml\UNlU2PzZyN{S=
THP-1 M3S3VWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVTsfYVsPzJiaB?= MYfJR|UxRTV4wsGzPUBvVQ>? NVnpNJRLOjV3N{[wO|Q>
MCF7/LTED  NXLxcnNoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWiyMlUuPDBibl2= MmDOOUBl MmD0bY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmNWSncHXu[IVvfCCvYX7u[ZI> MoPHNlU1QDB7NEO=
HCC1428/LTED MnnrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MW[yMlUuPDBibl2= NGDnR2I2KGR? Mn;mbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmNWSncHXu[IVvfCCvYX7u[ZI> Mn;oNlU1QDB7NEO=
A431 NEm5Wm9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV\wZmlFOC1|MDDuUS=> M2P3dVEuPCCm MnzhbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYn;0bEBld3OnLTDhcoQhfGmvZT3k[ZBmdmSnboSgcYFvdmW{ NEnqcGQzOzh7MUC5Oi=>
FaDu  NGrtZmdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWrxUYJIOC1zMECwJI5O NHq1XJgyNTRiZB?= MoK0bY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYn;0bEBld3OnLTDhcoQhfGmvZT3k[ZBmdmSnboSgcYFvdmW{ MUmyN|g6OTB7Nh?=
SF188 NIfQdJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX:1NE0yPTBibl2= M3vleFczKGh? MmPlSG1UVw>? NG\sXXVqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44> NVXuXHNmOjN6OEe2OFU>
T98G NYTOXVJsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{flc|UxNTF3MDDuUS=> Mm\DO|IhcA>? MW\EUXNQ NFfidmdqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44> MUmyN|g5PzZ2NR?=
DU145 MkHnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NE[4NYEyOC93MD:yOVAhdk1? M2O0[VI1KGh? NEXmVFBKSzVyPEGwJI5O M3i1cFI{QDh2NEK4
LNCaP NID1dnNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mmf6NVAwPTBxMkWwJI5O MYmyOEBp MYTJR|UxRDFyIH7N Mk\6NlM5QDR2Mki=
PC3 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHuzV3oyOC93MD:yOVAhdk1? NWnrSo14OjRiaB?= MmThTWM2OOLKvE[wNEBvVQ>? NInHN44zOzh6NESyPC=>
RT4 NXnaVHJ5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUi0PEBp MorDTWM2OD1zMUGuNlchdk1? NUGxRZFyOjN5OUK2N|k>
5637 M2\udmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV23[4hWPDhiaB?= MYjJR|UxRTFzNkWuNVQhdk1? MUSyN|c6OjZ|OR?=
T24 NGLPfIlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn:wOFghcA>? NFi2flZKSzVyPUKwOE46OSCwTR?= MorINlM4QTJ4M{m=
KMCH-1 NFLGUI5CeG:ydH;zbZMhSXO|YYm= MUeyNFAhdk1? NWq4UHhbOjRiaB?= NIfqXo9qdmS3Y3XzJIFxd3C2b4Ppdy=> NWjEVYhYOjN5MEO2O|M>
Mz-ChA-1 M4LvRmFxd3C2b4Ppd{BCe3OjeR?= M1j2NVIxOCCwTR?= MUmyOEBp M3Pye4lv\HWlZYOgZZBweHSxc3nz Mn3GNlM4ODN4N{O=
HUCCT-1 NYLyTZZlSXCxcITvd4l{KEG|c3H5 MYGyNFAhdk1? MnW5NlQhcA>? M2LmT4lv\HWlZYOgZZBweHSxc3nz MUSyN|cxOzZ5Mx?=
HCT 116 M{nPdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml3ESWM2OMLiPTCyN{BvVQ>? MmfBNVk{QDN6MkO=
BRO M{jabWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGjWXoJGSzVywrC9JFEyKG6P M2D5e|E6Ozh|OEKz
GRANTA-519 Mke5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF7jUpdGSzVywrC9JFE2KG6P M3;6R|E6Ozh|OEKz
HL-60 M4Ow[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4WycGVEPTEEoE2gN|Ihdk1? NXK5[G5QOTl|OEO4NlM>
THP-1 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn3xSWM2OCB;IEO2JI5O MVyxPVM5Ozh{Mx?=
Raji MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoLwSWM2OCB;IEO3JI5O MXixPVM5Ozh{Mx?=


体内試験 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]


+ 展開

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.
細胞試験: [1]
+ 展開
  • 細胞株: HCT116, NCI-H460, BRO, GRANTA-519, HL-60, THP-1, and Raji
  • 濃度: Dissolved in DMSO, final concentrations ~1 μM
  • 反応時間: 24, 48, and 72 hours
  • 実験の流れ: 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.
+ 展開
  • 動物モデル: Female BomTac:NMRI-Foxn1nu mice grafted s.c. with HCT116, NCI-H460, or CXB1 cells
  • 製剤: Formulated in hydrochloric acid (0.1 N), and diluted with 0.9% NaCl, or suspended in 0.5% Natrosol 250 hydroxyethyl-cellulose
  • 投薬量: ~25 mg/kg/day
  • 投与方法: Injected i.v., or given intragastrally via gavage needle

溶解度 (25°C)

体外 DMSO 20 mg/mL (32.32 mM) warming
Water slightly soluble or insoluble
Ethanol slightly soluble or insoluble
体内 順序で溶剤を入れること:
4% DMSO+corn oil

* 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。


分子量 618.81


CAS No. 755038-65-4
in solvent
別名 N/A





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


  • マス




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


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1



  • 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):




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


マス 濃度 ボリューム 分子量


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



Handling Instructions


  • * 必須


  • 問題1:

    I wonder how to reconstitute the inhibitor for in vivo studies?

  • 回答:

    Volasertib can be dissolved in 4% DMSO+Corn oil at 2mg/ml for i.p. injection in mice. For oral administration, it can be formulated in hydrochloric acid (0.1 N), and diluted with 0.9% NaCl, or suspended in 0.5% Natrosol 250 hydroxyethyl-cellulose as indicated in the publications. We also suggest the vehicle 30% PEG400/0.5% Tween80/5% propylene glycol for a suspension which we tested in house.


PLK Inhibitors with Unique Features


Tags: Volasertib (BI 6727)を買う | Volasertib (BI 6727) ic50 | Volasertib (BI 6727)供給者 | Volasertib (BI 6727)を購入する | Volasertib (BI 6727)費用 | Volasertib (BI 6727)生産者 | オーダーVolasertib (BI 6727) | Volasertib (BI 6727)化学構造 | Volasertib (BI 6727)分子量 | Volasertib (BI 6727)代理店
細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID