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.

Size Price Stock Quantity  
In DMSO USD 286 In stock
USD 170 In stock
USD 870 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  MV;GeY5kfGmxbjDBd5NigQ>? MVuwMlUwOS9{LkWg{txO MlzDNlQhcA>? NYfFWHhtTE2VTx?= MXPpcohq[mm2czD0bIUhUEeILXnu[JVk\WRiY13FWEBx[XSqd3H5JIFkfGm4YYTpc44> NIG0cnEzPTN7MUK0NS=>
ONS76 NF60coNHfW6ldHnvckBCe3OjeR?= MoP3NE42NzFxMj61JO69VQ>? M3zvcFI1KGh? NEWxVG1FVVOR MV;pcohq[mm2czD0bIUhUEeILXnu[JVk\WRiY13FWEBx[XSqd3H5JIFkfGm4YYTpc44> MXyyOVM6OTJ2MR?=
Daoy  NFfvRXdHfW6ldHnvckBCe3OjeR?= M3\k[VAvPS9zL{KuOUDPxE1? NETHOIMzPCCq NGj0ZmlFVVOR NWPMcXl4cW6qaXLpeJMhUEeILX3l[IlifGWmIH3p[5JifGmxbjDhcoQhcW64YYPpc44> MViyOVM6OTJ2MR?=
ONS76 M2\nRWZ2dmO2aX;uJGF{e2G7 MmDPNE42NzFxMj61JO69VQ>? MYOyOEBp NXfOPHozTE2VTx?= NF;rUJhqdmirYnn0d{BJT0ZvbXXkbYF1\WRibXnndoF1cW:wIHHu[EBqdn[jc3nvci=> NVXae3VHOjV|OUGyOFE>
Daoy  MknSRZBweHSxc3nzJGF{e2G7 MkH5NUDPxE1? NVjLR5h{OjRiaB?= M3zZdGROW09? MVvpcoR2[2W|IHHwc5B1d3Orcx?= M4T3b|I2OzlzMkSx
Daoy  MnjDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUGwMlUwOS9{LkWg{txO NVewPG83OjRvOU[gbC=> MnLmSG1UVw>? NVvGOZNCcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MVGyOVM6OTJ2MR?=
U251 NFfRWodHfW6ldHnvckBCe3OjeR?= M1nmO|ExOC9|MECvPVAxKG6P MUexJIg> Mn:zSG1UVw>? Mn;4bY5pcWKrdIOgeIhmKHCqb4PwbI9zgWyjdHnvckBw\iCPZYLUT:Kh MVqyOFY2QDN{Nh?=
A172 NVXkRW84TnWwY4Tpc44hSXO|YYm= M4XSNVExOC9|MECvPVAxKG6P NVPkbWg2OSCq MmX6SG1UVw>? MkHjbY5pcWKrdIOgeIhmKHCqb4PwbI9zgWyjdHnvckBw\iCPZYLUT:Kh NXL3UmFMOjR4NUizNlY>
SF188 MUfGeY5kfGmxbjDBd5NigQ>? NIj1fYoyODBxM{CwM|kxOCCwTR?= NUXLVppDOSCq MV3EUXNQ MlS5bY5pcWKrdIOgeIhmKHCqb4PwbI9zgWyjdHnvckBw\iCPZYLUT:Kh NYHBbIdHOjR4NUizNlY>
U251 Mo\4SpVv[3Srb36gRZN{[Xl? M1Pq[FExOC9|MECvPVAxKG6P MV6xJIg> M2XxVmROW09? NYXEXnhScW6qaXLpeJMhfGinIHHjeIl3cXS7IH;mJGF5dCxiVInyc|M> NEj1SVIzPDZ3OEOyOi=>
A172 MXjGeY5kfGmxbjDBd5NigQ>? MVOxNFAwOzByL{mwNEBvVQ>? NF\MXFcyKGh? NXfzW21{TE2VTx?= NFXMW5dqdmirYnn0d{B1cGViYXP0bZZqfHlib3[gRZhtNCCWeYLvNy=> NHL3NHozPDZ3OEOyOi=>
SF188 MXTGeY5kfGmxbjDBd5NigQ>? Mkm3NVAxNzNyMD:5NFAhdk1? NI\WRWwyKGh? NWjrRlFiTE2VTx?= MVvpcohq[mm2czD0bIUh[WO2aY\peJkhd2ZiQYjsMEBVgXKxMx?= NYX4VJc5OjR4NUizNlY>
U251 Mkj4SpVv[3Srb36gRZN{[Xl? M1fQclExOC9|MECvPVAxKG6P Mn\mNUBp MVHEUXNQ MWXk[YNz\WG|ZYOgRYt1KHCqb4PwbI9zgWyjdHnvckBqdiCjIHPvcoNmdnS{YYTpc44h\GWyZX7k[Y51KG2jbn7ldi=> NH3yeWwzPDZ3OEOyOi=>
A172 MUHGeY5kfGmxbjDBd5NigQ>? M{\lVFExOC9|MECvPVAxKG6P M3\PVVEhcA>? NVjjVmpPTE2VTx?= NV:3WpJV\GWlcnXhd4V{KEGtdDDwbI9{eGixconsZZRqd25iaX6gZUBkd26lZX70doF1cW:wIHTldIVv\GWwdDDtZY5v\XJ? MV:yOFY2QDN{Nh?=
SF188 MULGeY5kfGmxbjDBd5NigQ>? M4P0dlExOC9|MECvPVAxKG6P NWHMSXJVOSCq NUnDO2FHTE2VTx?= NYr2[IN{\GWlcnXhd4V{KEGtdDDwbI9{eGixconsZZRqd25iaX6gZUBkd26lZX70doF1cW:wIHTldIVv\GWwdDDtZY5v\XJ? NYHZUYZ[OjR4NUizNlY>
U251 MXjGeY5kfGmxbjDBd5NigQ>? MUKxNFAwOzByL{mwNEBvVQ>? NXi4OpFpOjhiaB?= M4fje2ROW09? MmTBbY5lfWOnczDQRXJRKGOuZXH2ZYdm M4jVdFI1PjV6M{K2
SF188 MWDGeY5kfGmxbjDBd5NigQ>? M3OwRlExOC9|MECvPVAxKG6P NEnNUmozQCCq M4Pk[mROW09? MUjpcoR2[2W|IGDBVnAh[2ynYY\h[4U> M3TlUlI1PjV6M{K2
SF188 M3\LbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUexNFAwOzByL{mwNEBvVQ>? NVKxdWZvPDhiaB?= MYPEUXNQ NUn4cIs2emWmdXPld{Bk\WyuIIP1dpZqfmGuIHH0JFkxOCCwTTDzbYdvcW[rY3HueIx6 MmnQNlQ3PTh|Mk[=
U251 NIrTTVZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2G0PFExOC9|MECvPVAxKG6P NGrLU401QCCq M1n1VGROW09? NEX1OlBz\WS3Y3XzJINmdGxic4Xyeol3[WxiYYSgPVAxKG6PIIPp[45q\mmlYX70cJk> M33Mc|I1PjV6M{K2
A172 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEjUW3AyODBxM{CwM|kxOCCwTR?= NHvFUpk1QCCq NF\sPG9FVVOR M1\Le5Jm\HWlZYOgZ4VtdCC|dYL2bZZidCCjdDC5NFAhdk1ic3nncolncWOjboTsfS=> NGDJO|AzPDZ3OEOyOi=>
SF188 MX7GeY5kfGmxbjDBd5NigQ>? MmGwNVAxNzNyMD:5NFAhdk1? MlO5NlQhcA>? NGK4d4tFVVOR MYnhZpJw\2G2ZYOgcYloemG2aX;uJIFv\CCrbo\hd4lwdiCxZjDncIlwdWFiY3XscJMhcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NVu2TndMOjR4NUizNlY>
U251 MVfGeY5kfGmxbjDBd5NigQ>? NIHoS4MyODBxM{CwM|kxOCCwTR?= NVHkc5c2OjRiaB?= NVi4T4FkTE2VTx?= MW\hZpJw\2G2ZYOgcYloemG2aX;uJIFv\CCrbo\hd4lwdiCxZjDncIlwdWFiY3XscJMhcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M1nXfFI1PjV6M{K2
A172 MVLGeY5kfGmxbjDBd5NigQ>? M4DPT|ExOC9|MECvPVAxKG6P MX2yOEBp Mn24SG1UVw>? M2H3TYFjem:pYYTld{BucWe{YYTpc44h[W6mIHnueoF{cW:wIH;mJIdtcW:vYTDj[YxteyCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MViyOFY2QDN{Nh?=
Ba/F3 MYDD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NYDhZ4RpOC5yMECxMVExKM7:TR?= M3fsclczKGh? MlXCbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> Ml:xNlQzOTh3OEm=
HCC78 NEnZe29E\WyuIG\pZYJqdGm2eTDBd5NigQ>? NGnMN3oxNjBzLUGwJO69VQ>? NYLGeZVNPzJiaB?= NYHIeXFXcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MonoNlQzOTh3OEm=
SK-HEP1 MVHD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M3r6UlAvOjVvMT61JO69VQ>? MXqyOOKhcA>? Mn3obY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MmjsNlIyQDdzN{G=
SK-HEP2 M3nYZ2Z2dmO2aX;uJGF{e2G7 NGTvflQyKM7:TR?= NEnDZ5UzPCCq NYO4W4I{[myxY3vzJGhITi2rbnT1Z4VlKGOnbHygcY91cWyrdIm= MYeyNlE5PzF5MR?=
SK-HEP2 MXjGeY5kfGmxbjDBd5NigQ>? NX:x[m1MOSEQvF2= MUWyOEBp MkXIZ4F2e2W|IFeyM20heGijc3WgZZJz\XO2IIfpeIghemWmdXP0bY9vKGmwIITo[UBIOC:JMdMgZY5lKFNicHjhd4V{ NUfrT2lUOjJzOEexO|E>
MKN-45  M2j5ZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn\lNE4xOS1zMDFOwG0> NFjtSWE2KGR? MVnJR|UxRThibl2= M{TPfFIyPjV3OUG4
KATO-III NIPKdnVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH7wNo4xNjBzLUGwJO69VQ>? MXu1JIQ> MW\JR|UxRTNyIH7N NHfFdnMzOTZ3NUmxPC=>
MKN-45  Mn;TSpVv[3Srb36gRZN{[Xl? MlntNUDPxE1? MmXtNlQhcA>? MlrQbY5pcWKrdIOgdIhwe3Cqb4L5cIF1cW:wIH;mJG1GXCxiQXv0MEBidmRiRWLLNU8zKGmwIF3LUk01PQ>? NGHBW4MzOTZ3NUmxPC=>
KATO-III MoW1SpVv[3Srb36gRZN{[Xl? MkfRNUDPxE1? Moe2NlQhcA>? NEi4RYFqdmirYnn0d{BxcG:|cHjvdplt[XSrb36gc4YhVUWWLDDBb5QtKGGwZDDFVmsyNzJiaX6gUWtPNTR3 MoPCNlE3PTV7MUi=
H1648 NX7SbpZJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{fRTGlEPTB;MT6yPEDDuTBwMUKg{txO MVGyNVI2OjJ6NB?=
H1573 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{DWRmlEPTB;MT62NkDDuSByLkC1JO69VQ>? MlnJNlEzPTJ{OES=
H596 M{\MXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2riV2lEPTB;MT6yNUDDuSByLkG3JO69VQ>? NIHqfWwzOTJ3MkK4OC=>
HOP92 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHH4W25KSzVyPUCuPFEhyrFiMD6yPUDPxE1? NGDLdngzOTJ3MkK4OC=>
H69 NVTWXZhPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV7JR|UxRTFwMUigxtEhOC5yODFOwG0> NFHrXWUzOTJ3MkK4OC=>
H1975 NXzsS4xIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4DUWWlEPTB;MT6zPUDDuSByLkOzJO69VQ>? M{XrXlIyOjV{Mki0
SCC15 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlXsTWM2OD1yLk[zJOKyKDBwMESg{txO NI\sO5YzOTJ3MkK4OC=>
HN5 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmfMTWM2OD1yLk[1JOKyKDBwMk[g{txO MWOyNVI2OjJ6NB?=

... 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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID