Foretinib (GSK1363089)

Catalog No.S1111 Synonyms: EXEL-2880,XL-880

Foretinib (GSK1363089) Chemical Structure

Molecular Weight(MW): 632.65

Foretinib (GSK1363089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit, PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.

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In DMSO USD 286 In stock
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3 Customer Reviews

  • D. Effects of erlotinib and inhibitors of PI3K, MEK, MET or IGF-1R on phosphorylation of AKT and ERK in ER3 cells.

    Theranostics, 2016, 6(8):1232-43. Foretinib (GSK1363089) purchased from Selleck.

    c-MET/RON inhibitors restore sensitivity to lapatinib in SK-BR-3-LR cells. Cell growth was determined using the sulforhodamine B assay. The concentration used was 0.1 uM for crizotinib, MGCD-265, XL880, sunitinib, dasatinib, and TAE-684I. The phosphorylation of HER2, AKT and ERK1/2 was determined by Western blotting.

    Cancer Lett 2013 340(1), 43-50. Foretinib (GSK1363089) purchased from Selleck.

  • After starved in serum-free medium for 24h, MDA-MB-231 cells incubated with the indicated concentrations of XL-880 for 3h,followed by 20-minute stimolation of 100ng/ml EGF

     

     

    Dr. Zhang of Tianjin Medical University. Foretinib (GSK1363089) purchased from Selleck.

Purity & Quality Control

Choose Selective c-Met Inhibitors

Biological Activity

Description Foretinib (GSK1363089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit, PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.
Targets
Met [1]
(Cell-free assay)
KDR [1]
(Cell-free assay)
Tie-2 [1]
(Cell-free assay)
VEGFR3/FLT4 [1]
(Cell-free assay)
RON [1]
(Cell-free assay)
0.4 nM 0.86 nM 1.1 nM 2.8 nM 3 nM
In vitro

XL880 inhibits HGF receptor family tyrosine kinases with IC50 values of 0.4 nM for Met and 3 nM for Ron. XL880 also inhibits KDR, Flt-1, and Flt-4 with IC50 values of 0.9 nM, 6.8 nM and 2.8 nM, respectively. XL880 inhibits colony growth of B16F10, A549 and HT29 cells with IC50 of 40 nM, 29 nM and 165 nM, respectively. [1] A recent study indicates XL880 affects cell growth differently in gastric cancer cell lines MKN-45 and KATO-III. XL880 inhibits phosphorylation of MET and downstream signaling molecules in MKN-45 cells, while targets GFGR2 in KATO-III cells. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Daoy  NHTsfG9HfW6ldHnvckBCe3OjeR?= NUDCNIpJOC53L{GvNk42KM7:TR?= NH7DSlkzPCCq NEfuTZhFVVOR Mn74bY5pcWKrdIOgeIhmKEiJRj3pcoR2[2WmIHPNSXQheGG2aIfhfUBi[3SrdnH0bY9v MkHhNlU{QTF{NEG=
ONS76 NWH3Wo5tTnWwY4Tpc44hSXO|YYm= MnTBNE42NzFxMj61JO69VQ>? MVyyOEBp NWnDe5cyTE2VTx?= MYjpcohq[mm2czD0bIUhUEeILXnu[JVk\WRiY13FWEBx[XSqd3H5JIFkfGm4YYTpc44> M4jxNlI2OzlzMkSx
Daoy  NGPPXXBHfW6ldHnvckBCe3OjeR?= MorlNE42NzFxMj61JO69VQ>? NH7BZVAzPCCq M2m4RWROW09? MVnpcohq[mm2czDIS2YudWWmaXH0[YQhdWmpcnH0bY9vKGGwZDDpcpZie2mxbh?= MkfYNlU{QTF{NEG=
ONS76 M1O1[GZ2dmO2aX;uJGF{e2G7 NGTaVYQxNjVxMT:yMlUh|ryP M3SyOVI1KGh? NH7yeYlFVVOR MkPHbY5pcWKrdIOgTGdHNW2nZHnheIVlKG2rZ4LheIlwdiCjbnSgbY53[XOrb36= M1Wyd|I2OzlzMkSx
Daoy  NYK0WXR2SXCxcITvd4l{KEG|c3H5 MVuxJO69VQ>? M2LJOVI1KGh? NEnXRZZFVVOR NWDEdXZMcW6mdXPld{BieG:ydH;zbZM> M1HVb|I2OzlzMkSx
Daoy  NILpR2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3e3e|AvPS9zL{KuOUDPxE1? MX[yOE06PiCq MoL3SG1UVw>? NH\4cG5qdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NXzlT4RmOjV|OUGyOFE>
U251 M2DpN2Z2dmO2aX;uJGF{e2G7 Mn2zNVAxNzNyMD:5NFAhdk1? NYewb4w3OSCq NYW3TFhnTE2VTx?= MmK2bY5pcWKrdIOgeIhmKHCqb4PwbI9zgWyjdHnvckBw\iCPZYLUT:Kh MVWyOFY2QDN{Nh?=
A172 M333cGZ2dmO2aX;uJGF{e2G7 Mn:zNVAxNzNyMD:5NFAhdk1? MofnNUBp M4[4PGROW09? MnK0bY5pcWKrdIOgeIhmKHCqb4PwbI9zgWyjdHnvckBw\iCPZYLUT:Kh NEHGWVIzPDZ3OEOyOi=>
SF188 M17lemZ2dmO2aX;uJGF{e2G7 MWGxNFAwOzByL{mwNEBvVQ>? NXvTZpZuOSCq NWTmRXhTTE2VTx?= MVnpcohq[mm2czD0bIUheGixc4Doc5J6dGG2aX;uJI9nKE2ncmTLxsA> M{fSRlI1PjV6M{K2
U251 M4XoWGZ2dmO2aX;uJGF{e2G7 MXyxNFAwOzByL{mwNEBvVQ>? MXKxJIg> M3:yW2ROW09? MmHJbY5pcWKrdIOgeIhmKGGldHn2bZR6KG:oIFH4cEwhXHm{b{O= MnL6NlQ3PTh|Mk[=
A172 M3LqTWZ2dmO2aX;uJGF{e2G7 MoDCNVAxNzNyMD:5NFAhdk1? M1;C[VEhcA>? NXnjU29CTE2VTx?= NIPqO4tqdmirYnn0d{B1cGViYXP0bZZqfHlib3[gRZhtNCCWeYLvNy=> M2K5bFI1PjV6M{K2
SF188 MnvZSpVv[3Srb36gRZN{[Xl? M2XFRVExOC9|MECvPVAxKG6P MoCwNUBp NF\6cVhFVVOR MUXpcohq[mm2czD0bIUh[WO2aY\peJkhd2ZiQYjsMEBVgXKxMx?= M33pOlI1PjV6M{K2
U251 MUHGeY5kfGmxbjDBd5NigQ>? MWixNFAwOzByL{mwNEBvVQ>? MWGxJIg> MkfYSG1UVw>? NYnrdYtK\GWlcnXhd4V{KEGtdDDwbI9{eGixconsZZRqd25iaX6gZUBkd26lZX70doF1cW:wIHTldIVv\GWwdDDtZY5v\XJ? NV63cGVxOjR4NUizNlY>
A172 NYq3VJRHTnWwY4Tpc44hSXO|YYm= NVHZO2xnOTByL{OwNE86ODBibl2= MlvkNUBp MULEUXNQ MmTG[IVkemWjc3XzJGFsfCCyaH;zdIhwenmuYYTpc44hcW5iYTDjc45k\W62cnH0bY9vKGSncHXu[IVvfCCvYX7u[ZI> NXzGcGNIOjR4NUizNlY>
SF188 M1HZOWZ2dmO2aX;uJGF{e2G7 MYqxNFAwOzByL{mwNEBvVQ>? NF\CeWgyKGh? M4HITWROW09? NHHTSZdl\WO{ZXHz[ZMhSWu2IIDoc5NxcG:{eXzheIlwdiCrbjDhJINwdmOnboTyZZRqd25iZHXw[Y5l\W62IH3hco5meg>? NIHnSIkzPDZ3OEOyOi=>
U251 NF[4SIVHfW6ldHnvckBCe3OjeR?= MWCxNFAwOzByL{mwNEBvVQ>? M1O1fVI5KGh? NXzlfJk4TE2VTx?= MXnpcoR2[2W|IGDBVnAh[2ynYY\h[4U> M3vLSlI1PjV6M{K2
SF188 NX7XUoRZTnWwY4Tpc44hSXO|YYm= M1m0SlExOC9|MECvPVAxKG6P MkK4NlghcA>? NFPKO5hFVVOR MXTpcoR2[2W|IGDBVnAh[2ynYY\h[4U> M3L4eVI1PjV6M{K2
SF188 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY[xNFAwOzByL{mwNEBvVQ>? NVrUcodmPDhiaB?= NIDPVmxFVVOR NGK3dlhz\WS3Y3XzJINmdGxic4Xyeol3[WxiYYSgPVAxKG6PIIPp[45q\mmlYX70cJk> NH;6SmEzPDZ3OEOyOi=>
U251 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGrJS20yODBxM{CwM|kxOCCwTR?= NGm4Z4o1QCCq NWGwVnoyTE2VTx?= NFHDbYFz\WS3Y3XzJINmdGxic4Xyeol3[WxiYYSgPVAxKG6PIIPp[45q\mmlYX70cJk> NEPFRmYzPDZ3OEOyOi=>
A172 MmC1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH2zZVUyODBxM{CwM|kxOCCwTR?= MojWOFghcA>? M1vFT2ROW09? NVHDcYF6emWmdXPld{Bk\WyuIIP1dpZqfmGuIHH0JFkxOCCwTTDzbYdvcW[rY3HueIx6 NGTOcXczPDZ3OEOyOi=>
SF188 NYnXbW5OTnWwY4Tpc44hSXO|YYm= MkCzNVAxNzNyMD:5NFAhdk1? M1TkWVI1KGh? Mo\HSG1UVw>? MX7hZpJw\2G2ZYOgcYloemG2aX;uJIFv\CCrbo\hd4lwdiCxZjDncIlwdWFiY3XscJMhcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MVqyOFY2QDN{Nh?=
U251 Mlf4SpVv[3Srb36gRZN{[Xl? M4rUfVExOC9|MECvPVAxKG6P MYmyOEBp NHK4[WlFVVOR MV7hZpJw\2G2ZYOgcYloemG2aX;uJIFv\CCrbo\hd4lwdiCxZjDncIlwdWFiY3XscJMhcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MmfhNlQ3PTh|Mk[=
A172 MmfoSpVv[3Srb36gRZN{[Xl? NYfQZ5pyOTByL{OwNE86ODBibl2= M3fq[VI1KGh? MXXEUXNQ NEfBTY1i[nKxZ3H0[ZMhdWmpcnH0bY9vKGGwZDDpcpZie2mxbjDv[kBodGmxbXGgZ4VtdHNiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MlHTNlQ3PTh|Mk[=
Ba/F3 NUT0fVc5S2WubDDWbYFjcWyrdImgRZN{[Xl? M4m2SFAvODByMT2xNEDPxE1? NHS0TI04OiCq NInXPGVqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? Mnu0NlQzOTh3OEm=
HCC78 NGP2blFE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NYHac5pZOC5yMT2xNEDPxE1? NFqyUpY4OiCq NIPMcoNqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? M3HZXVI1OjF6NUi5
SK-HEP1 MUHD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M33PPFAvOjVvMT61JO69VQ>? MXKyOOKhcA>? M{nwOIlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MY[yNlE5PzF5MR?=
SK-HEP2 M1TNVGZ2dmO2aX;uJGF{e2G7 MV:xJO69VQ>? NVnG[I5QOjRiaB?= M4excIJtd2OtczDIS2YucW6mdXPl[EBk\WyuIH3veIltcXS7 MkjQNlIyQDdzN{G=
SK-HEP2 MWjGeY5kfGmxbjDBd5NigQ>? NWnvSGcxOSEQvF2= MkiyNlQhcA>? NEewZXlk[XW|ZYOgS|IwVSCyaHHz[UBienKnc4Sge4l1cCC{ZXT1Z5Rqd25iaX6geIhmKEdyL1exxsBidmRiUzDwbIF{\XN? NHXlb5kzOjF6N{G3NS=>
MKN-45  M2qyRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV:wMlAyNTFyIN88US=> NH30eWg2KGR? MXzJR|UxRThibl2= NXXhV5NbOjF4NUW5NVg>
KATO-III NWLmdZFjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2DTS|AvODFvMUCg{txO Mn[zOUBl NVvXc5l5UUN3ME2zNEBvVQ>? M4f4OVIyPjV3OUG4
MKN-45  MkHrSpVv[3Srb36gRZN{[Xl? MWixJO69VQ>? NED4[mszPCCq M3HGWolvcGmkaYTzJJBpd3OyaH;yfYxifGmxbjDv[kBOTVRuIFHreEwh[W6mIFXST|EwOiCrbjDNT24uPDV? NUThZ|U1OjF4NUW5NVg>
KATO-III MnLMSpVv[3Srb36gRZN{[Xl? MnmyNUDPxE1? MXeyOEBp MmnZbY5pcWKrdIOgdIhwe3Cqb4L5cIF1cW:wIH;mJG1GXCxiQXv0MEBidmRiRWLLNU8zKGmwIF3LUk01PQ>? MV[yNVY2PTlzOB?=
H1648 NYjPSm1xT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH35SG5KSzVyPUGuNlghyrFyLkGyJO69VQ>? NH;YOo4zOTJ3MkK4OC=>
H1573 M1HKTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX3JR|UxRTFwNkKgxtEhOC5yNTFOwG0> M124TVIyOjV{Mki0
H596 MlfBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHm3d4JKSzVyPUGuNlEhyrFiMD6xO{DPxE1? MXKyNVI2OjJ6NB?=
HOP92 M1zTcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml\2TWM2OD1yLkixJOKyKDBwMkmg{txO NWfhVmdmOjF{NUKyPFQ>
H69 M1HMcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1zZe2lEPTB;MT6xPEDDuSByLkC4JO69VQ>? NH7XN5czOTJ3MkK4OC=>
H1975 NIHldWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M37uTGlEPTB;MT6zPUDDuSByLkOzJO69VQ>? NHTDcmIzOTJ3MkK4OC=>
SCC15 MkexS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVPJR|UxRTBwNkOgxtEhOC5yNDFOwG0> MViyNVI2OjJ6NB?=
HN5 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXzzRYlEUUN3ME2wMlY2KMLzIECuNlYh|ryP M{XINFIyOjV{Mki0

... Click to View More Cell Line Experimental Data

In vivo A single 100 mg/kg oral gavage dose of XL880 results in substantial inhibition of phosphorylation of B16F10 tumor Met and ligand (e.g., HGFor VEGF)-induced receptor phosphorylation of Met in liver and Flk-1/KDR in lung, which both persisted through 24 hours. Treatment with XL880 (30-100 mg/kg, once daily, oral gavage) results in reduction in tumor burden. The lung surface tumor burden is reduced by 50% and 58% following treatment with 30 and 100 mg/kg XL880, respectively. XL880 treatment of mice bearing B16F10 solid tumors also results in dose-dependent tumor growth inhibition of 64% and 87% at 30 and 100 mg/kg, respectively. For both studies, administration of XL880 is well tolerated with no significant body weight loss. [1] XL880 is developed to target abnormal signaling of HGF through Met and simultaneously target several receptors tyrosine kinase involved in tumor angiogenesis. XL880 caused tumor hemorrhage and necrosis in human xenografts within 2 to 4 hours, and maximal tumornecrosis is observed at 96 hours (after five daily doses), resulting in complete regression. [3]

Protocol

Kinase Assay:

[1]

+ Expand

Kinase Inhibition Assay:

Kinase inhibition is investigated using one of three assay formats: [33P]phosphoryl transfer, luciferase-coupled chemiluminescence, or AlphaScreen tyrosine kinase technology. IC50s are calculated by nonlinear regression analysis using XLFit.33P -Phosphoryl Transfer Kinase Assay Reactions are performed in 384-well white, clear bottom, high-binding microtiter plates (Greiner, Monroe, NC). Plates are coated with 2 μg/well of protein or peptide substrate in a 50 μL volume of coating buffer contained 40 μg/mL substrate (poly(Glu, Tyr) 4:1, 22.5 mM Na2CO3, 27.5 mM NaHCO3, 50 mM NaCl and 3 mM NaN 3. Coated plates are washed once with 50 μL of assay buffer following overnight incubation at room temperature (RT). Test compounds and enzymes are combined with 33P-γ-ATP (3.3 μCi/nmol) in a total volume of 20 μL. The reaction mixture is incubated at RT for 2 hours and terminated by aspiration. The microtiter plates are subsequently washed 6 times with 0.05% Tween-PBS buffer (PBST). Scintillation fluid (50 μL/well) is added and incorporated 33P is measured by liquid scintillation spectrometry using a MicroBeta scintillation counter.Luciferase-Coupled Chemiluminescence Assay Reactions are conducted in 384-well white, medium binding microtiter plates (Greiner). In a first step enzyme and compound are combined and incubated for 60 minutes; reactions are initiated by addition of ATP and peptide substrate (poly(Glu, Tyr) 4:1) in a final voume of 20 μL, and incubated at RT for 2-4 hours. Following the kinase reaction, a 20 μL aliquot of Kinase Glo (Promega, Madison, WI) is added and luminescence signal is measured using a Victor plate reader. Total ATP consumption is limited to 50%. AlphaScreenTM Tyrosine Kinase Assay Donor beads coated with streptavidin and acceptor beads coated with PY100 anti-phosphotyrosine antibody are used. Biotinylated poly(Glu,Tyr) 4:1 is used as the substrate. Substrate phosphorylation is measured by addition of donor/acceptor beads by luminescence following donor-acceptor bead complex formation. Kinase and test compounds are combined and preincubated for 60 minutes, followed by addition of ATP, and biotinylated poly(Glu, Tyr) in a total volume of 20 μL in 384-well white, medium binding microtiter plates (Greiner). Reaction mixtures are incubated for 1 hour at room temperature. Reactions are quenched by addition of 10 μL of 15-30 μg/mL AlphaScreen bead suspension containing 75 mM Hepes, pH 7.4, 300 mM NaCl, 120 mM EDTA, 0.3% BSA and 0.03% Tween-20. After 2-16 hours incubation at room temperature plates are read using an AlphaQuest reader.
Cell Research:

[1]

+ Expand
  • Cell lines: B16F10, A549, and HT29 cells
  • Concentrations: 40 nM
  • Incubation Time: 12 to 14 days
  • Method:

    B16F10, A549, and HT29 cells (1.2× 103 per well) are mixed with soft agar and seeded in a 96-well plate containing 10% FBS and EXEL-2880 over a base agar layer. For normoxic conditions, the plates are incubated (37°C) for 12 to 14 days in 21% oxygen, 5% CO2, and 74% nitrogen, whereas incubation (37 °C) under hypoxic conditions is done in a hypoxia chamber in 1% oxygen, 5% CO2, and 94% nitrogen. The number of colonies is evaluated under each condition following addition of 50% Alamar Blue and fluorescence detection.


    (Only for Reference)
Animal Research:

[1]

+ Expand
  • Animal Models: B16F10 tumor cells (2 × 10 5) are implanted via i.v. tail vein injection into athymic nude mice (NCr or BALB/c) 5 to 8 weeks old
  • Formulation: 0.9% normal saline
  • Dosages: 100 mg/kg
  • Administration: Administered via oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 100 mg/mL (158.06 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order:
30% propylene glycol, 5% Tween 80, 65% D5W
For best results, use promptly after mixing.
30 mg/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 632.65
Formula

C34H34F2N4O6

CAS No. 849217-64-7
Storage powder
Synonyms EXEL-2880,XL-880

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02034097 Withdrawn Cancer GlaxoSmithKline April 2014 Phase 2
NCT01138384 Completed Breast Cancer NCIC Clinical Trials Group|Canadian Cancer Trials Group June 2010 Phase 1|Phase 2
NCT01147484 Completed Recurrent Breast Cancer NCIC Clinical Trials Group|Canadian Cancer Trials Group May 2010 Phase 2
NCT01068587 Completed Lung Cancer NCIC Clinical Trials Group|Canadian Cancer Trials Group December 2009 Phase 1|Phase 2
NCT00920192 Completed Carcinoma, Hepatocellular GlaxoSmithKline August 2009 Phase 1
NCT00742261 Completed Solid Tumours GlaxoSmithKline August 2008 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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID