Linifanib (ABT-869)

For research use only. Not for use in humans.

製品コードS1003 別名:AL39324,RG3635

Linifanib (ABT-869)化学構造


Linifanib (ABT-869) is a novel, potent ATP-competitive VEGFR/PDGFR inhibitor for KDR, CSF-1R, Flt-1/3 and PDGFRβ with IC50 of 4 nM, 3 nM, 3 nM/4 nM and 66 nM respectively, mostly effective in mutant kinase-dependent cancer cells (i.e. FLT3). Linifanib (ABT-869) induces autophagy and apoptosis. Phase 3.

サイズ 価格(税別) 在庫  
10mM (1mL in DMSO) JPY 31800 あり
JPY 21900 あり
JPY 36800 あり
JPY 96600 あり

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  • (B and C) KMCH-1 cells were plated alone (monoculture) or together with PDGF-BB-secreting LX-2 cells (co-culture) in a transwell insert co-culture system (KMCH-1 cells in the bottom wells and LX-2 cells in the inserts; 1:1 ratio) for 2 days. Cells were treated as indicated with vehicle, rhTRAIL (10 ng/ml for 6 h on day 2), rhTRAIL plus imatinib [rhTRAIL:10 ng/ml for 6 h on day 2; Imatinib: 5 μmol/L for 24 h (day2)], or rhTRAIL plus linifanib [rhTRAIL: 10 ng/ml for 6 h on day 2; Linifanib:0.5 μmol/L for 24 h (day2)]. After rhTRAIL treatment for 6 h,KMCH-1 cells were analysed for apoptotic nuclear morphology by DAPI-staining (B) and for DNA fragmentation by transferasemediated dUTP nick end labelling assay (C) with quantification of apoptotic nuclei by fluorescence microscopy.

    Liver Int 2011 32, 400-409. Linifanib (ABT-869) purchased from Selleck.

  • T47D breast cancer cells were pretreated with indicated concentrations of ABT-869



    Dr. Zhang of Tianjin Medical University. Linifanib (ABT-869) purchased from Selleck.

  • Effect of the anti-vascular agents Linifanib (100 nM) in the VMO(vascularized micro-organ). VMOs were exposed to the drug at day 5 and cultured for an additional 96 h.

    Sci Rep, 2016, 6:31589.. Linifanib (ABT-869) purchased from Selleck.




製品説明 Linifanib (ABT-869) is a novel, potent ATP-competitive VEGFR/PDGFR inhibitor for KDR, CSF-1R, Flt-1/3 and PDGFRβ with IC50 of 4 nM, 3 nM, 3 nM/4 nM and 66 nM respectively, mostly effective in mutant kinase-dependent cancer cells (i.e. FLT3). Linifanib (ABT-869) induces autophagy and apoptosis. Phase 3.
(Cell-free assay)
CSF-1R [1]
(Cell-free assay)
(Cell-free assay)
FLT3 [1]
(Cell-free assay)
Kit [1]
(Cell-free assay)
3 nM 3 nM 4 nM 4 nM 14 nM

Linifanib shows inhibitory to Kit, PDGFRβ and Flt4 with IC50 of 14 nM, 66 nM and 190 nM in kinases assay. Linifanib also inhibits ligand-induced KDR, PDGFRβ, Kit, and CSF-1R phosphorylation with IC50 of 2 nM, 2 nM, 31 nM and 10 nM at cellular level and this cellular potency could be affected by serum protein. Linifanib suppresses VEGF-stimulated HUAEC proliferation with IC50 of 0.2 nM. While Linifanib has weak activity against tumor cells which are not induced by VEGF or PDGF, except for MV4-11 leukemia cells (with constitutively active form of Flt3) with IC50 of 4 nM. Linifanib could cause a decrease in S and G2-M phases with a corresponding increase in the sub-G0-G1 apoptotic population in MV4-11 cells. [1] Linifanib binds to the ATP-binding site of CSF-1R with Ki of 3 nM. [2] Linifanib (10 nM) exhibits a reduced phosphorylation of Akt at Ser473 and decreased phosphorylation of GSK3βat Ser9 in Ba/F3 FLT3 ITD cell lines. [3]

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
mouse 3T3 cells MlXVSpVv[3Srb36gZZN{[Xl? M3:1NmlvcGmkaYTpc44hd2ZiVlXHSk1qdmS3Y3XkJIh2dWGwIFvEVkBxcG:|cHjvdplt[XSrb36gbY4hdW:3c3WgN3Q{KGOnbHzzJIJ6KEWOSWPBMEBKSzVyPUCuNFA1KM7:TR?= M4GxNFE4OzR|M{ey
Sf9 insect cells NXP0SmVxTnWwY4Tpc44h[XO|YYm= MVixNlAhdWmwcx?= NH;R[oRKdmirYnn0bY9vKG:oIILlZ49u[mmwYX70JGdUXC22YXfn[YQhXkWJRmKyJIV5eHKnc4Pl[EBqdiCVZkmgbY5{\WO2IHPlcIx{KGGodHXyJFEzOCCvaX7zJIJ6KEurbnHz[U1IdG9iYYPzZZktKEmFNUC9OUBvVQ>? NHXrc|gzOTdyOES2PC=>
human MOLM13 cells MnnDR5l1d3SxeHnjbZR6KGG|c3H5 NXrQZolDPzJiaB?= Ml;XR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUW9NVTF|IHPlcIx{KGijcnLvdolv\yCvdYThcpQhTkyWMzDh[pRmeiB5MjDodpMh[nliTWTTJIF{e2G7LDDHTVUxRTBwMEO3JO69VQ>? MW[yN|YyQDdyOR?=
human MV4-11 cells MmTYVJJwdGmoZYLheIlwdiCjc4PhfS=> M3HkUVczKGh? NYPJcIp1SW62aYDyc4xq\mW{YYTpc44h[WO2aY\peJkh[WejaX7zeEBHVFR|L1nUSEBp[XKkb4LpcochcHWvYX6gUXY1NTFzIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFNibXX0bI9lNCCJSUWwQVAvODRizszN MVeyNVcxQDR4OB?=
human MOLT4 cells NH3jPJpRem:uaX\ldoF1cW:wIHHzd4F6 MnjHO|IhcA>? MkW3RY51cXC{b3zp[oVz[XSrb36gZYN1cX[rdImgZYdicW6|dDDoeY1idiCPT1zUOEBi\nSncjC3NkBpenNiYomgUXRUKG2ndHjv[EwhT0l3ME22Mlch|ryP M3fPR|IyPzB6NE[4
RS4:11 cells M37OSXBzd2yrZnXyZZRqd25iYYPzZZk> M2r6dlczKGh? MmLHRY51cXC{b3zp[oVz[XSrb36gZYN1cX[rdImgZYdicW6|dDDoeY1idiCUU{S6NVEh[2WubIOg[ZhxemW|c3nu[{B4cWymIIT5dIUhTkyWMzDh[pRmeiB5MjDodpMh[nliTWTTJI1mfGixZDygS2k2OD17LkKg{rxu MV2yNVcxQDR4OB?=
U937 cells M3\JUHBzd2yrZnXyZZRqd25iYYPzZZk> NETlUZc4OiCq M2fOR2FvfGmycn;sbYZmemG2aX;uJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iRlzUN{Bo\W6nLXTl[olkcWWwdDDVPVM4KGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDNWHMhdWW2aH;kMEBIUTVyPUG5JO69VQ>? MYSyNVcxQDR4OB?=


Methods Test Index PMID
Western blot
phospho-FLT3 / FLT3 ; 

PubMed: 21471285     

Ba/F3 FLT3 ITD cells were treated for 15, 30 or 60 minutes with 10nM Linifanib or vehicle control (DMSO). Cell lysates were immunoprecipitated (IP) with anti-FLT3 polyclonal antisera or anti-AKT(Pan) monoclonal antisera and sepharose beads. 

Beclin-1 / ATG5 / ATG7 / p62 ; 

PubMed: 25327881     

Immunoblotting for Beclin-1, ATG5, ATG7, and p62 using lysates from cells treated with linifanib for 24 h. 

p-PDGFRβ / PDGFRβ/ p-AKT / AKT / p-mTOR / mTOR / p-S6K ; 

PubMed: 25327881     

Immunoblotting for phospho- or total PDGFR-ß, Akt, mTOR and S6Kin cells treated with linifanib for 24 h.

21471285 25327881
LC3 ; 

PubMed: 25327881     

Relative quantity of LC3-II was calculated by ImageJ densitometric analysis and normalized by GAPDH. (C). Cells were treated with DMSO or 2.5 μM linifanib for 24 h before they were labeled with fluorescence and imaged by fluorescence microscope. Green: FITC-labeled LC3; Red: lyso-tracker-labeled lysosome; Blue: DAPI-labeled nucleus.

体内試験 Linifanib (0.3 mg/kg) results in complete inhibition of KDR phosphorylation in lung tissue. Linifanib also inhibits the edema response with ED50 of 0.5 mg/kg. Linifanib (7.5 and 15 mg/kg, bid) significantly inhibits both bFGF- and VEGF-induced angiogenesis in the cornea. Linifanib inhibits tumor growth in flank xenograft models including HT1080, H526, MX-1 and DLD-1 with ED75 from 4.5-12 mg/kg. Linifanib also shows efficacy in A431 and MV4-11 xenografts at low dose levels. Linifanib (12.5 mg/kg bid) reveals a decrease of microvasculure density in MDA-231 xenograft. Linifanib shows a Cmax and AUC24 hours with 0.4 μg/mL and 2.7 μg•hour/mL in HT1080 fibrosarcoma model. [1]


- 合併

Kinase assays:

Potencies (IC50 values) are determined by assays of active kinase domains cloned and expressed in baculovirus using the FastBacbaculovirus expression system or obtained commercially. For tyrosine kinase assays, a biotinylated peptide substrate containing a single tyrosine is used with 1 mM ATP, anEu-cryptate–labeled anti-phosphotyrosine antibody (PT66), and Strepavidin-APC in a homogeneous time-resolved fluorescence assay. Serine/threonine kinases are assayed using 5 μM ATP, [33P]ATP, and a biotinylated peptide substrate with peptide capture and incorporation of 33P determined using a SA-Flashplate. Linifanib is assayed at multiple concentrations prepared by serial dilution of a DMSO stock solution of Linifanib. The concentration resulting in 50% inhibition of activity is calculated using nonlinear regression analysis of the concentration response data.
細胞試験: [1]
- 合併
  • 細胞株: HUAEC, HT-29, HT1080, A431, MDA-435, MDA-231, H526, DLD-1, 9L and MV4-11 cells
  • 濃度: 0-100 μM
  • 反応時間: 72 hours
  • 実験の流れ: Cells are seeded into 96-well plates at 2.5 × 103 per well and incubated with serum-free medium for 24 hours. Linifanib and VEGF (final, 10 ng/mL) are added and incubated for 72 hours in serum-free medium. For carcinoma cell lines, 3 × 103 cells/well are plated overnight in full growth medium. Linifanib is added to the cells in full growth medium and incubated for 72 hours. For leukemia cells, generally 5 × 104 per well are plated in full growth medium, Linifanib is added, and incubated for 72 hours. The effects on proliferation are determined by addition of Alamar Blue (final solution, 10%), incubation for 4 hours at 37 °C in a CO2 incubator and analysis in a fluorescence plate reader (544 nm, excitation: 590 nm, emission
- 合併
  • 動物モデル: H526, DLD-1, MDA-231, MDA-435LM, HCT-116, H526, DLD-1, MDA-231, MDA-435LM, MV4-11 and MX-1 xenografts are established in mice.
  • 投薬量: ~ 10 mg/kg
  • 投与方法: Oral administration

溶解度 (25°C)

体外 DMSO 75 mg/mL (199.78 mM)
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
5%DMSO+40%PEG 300+5%Tween80+50%ddH2O
10 mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。


分子量 375.41


CAS No. 796967-16-3
Storage powder
in solvent
別名 AL39324,RG3635
Smiles CC1=CC(=C(F)C=C1)NC(=O)NC2=CC=C(C=C2)C3=C4C(=N[NH]C4=CC=C3)N


投与量 mg/kg 動物平均体重 g 投与体積(動物毎) ul 動物数
% DMSO % % Tween 80 % ddH2O





質量 (mg) = 濃度 (mM) x 体積 (mL) x 分子量 (g/mol)


  • 質量





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 ( 入力 出力 )

  • 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


質量 濃度 体積 分子量



Handling Instructions


  • * 必須


VEGFR Inhibitors with Unique Features


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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID