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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4 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.

    Oncotarget, 2018, 9(32):22769-22784. 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  MWrGeY5kfGmxbjDBd5NigQ>? NUL2UYlWOC53L{GvNk42KM7:TR?= MnPhNlQhcA>? MYXEUXNQ NETPcWRqdmirYnn0d{B1cGViSFfGMYlv\HWlZXSgZ21GXCCyYYToe4F6KGGldHn2ZZRqd25? MYWyOVM6OTJ2MR?=
ONS76 Ml3oSpVv[3Srb36gRZN{[Xl? MViwMlUwOS9{LkWg{txO NF3UN|MzPCCq NHHiTlJFVVOR NUXXUohUcW6qaXLpeJMhfGinIFjHSk1qdmS3Y3XkJINOTVRicHH0bJdigSCjY4TpeoF1cW:w NHjoUHQzPTN7MUK0NS=>
Daoy  NWLTN2VTTnWwY4Tpc44hSXO|YYm= MUWwMlUwOS9{LkWg{txO M3r6UFI1KGh? NGLhSlVFVVOR MV;pcohq[mm2czDIS2YudWWmaXH0[YQhdWmpcnH0bY9vKGGwZDDpcpZie2mxbh?= NXjCc5ZOOjV|OUGyOFE>
ONS76 MorUSpVv[3Srb36gRZN{[Xl? MUiwMlUwOS9{LkWg{txO Mn;uNlQhcA>? MVPEUXNQ M2W5XIlvcGmkaYTzJGhITi2vZXTpZZRm\CCvaXfyZZRqd25iYX7kJIlvfmG|aX;u NIfteokzPTN7MUK0NS=>
Daoy  NX\nWFRGSXCxcITvd4l{KEG|c3H5 NV;UWIdOOSEQvF2= NIjkTFgzPCCq MmPTSG1UVw>? NFPHZ|ZqdmS3Y3XzJIFxd3C2b4Ppdy=> M{LVOVI2OzlzMkSx
Daoy  MmLTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2[z[FAvPS9zL{KuOUDPxE1? MoXrNlQuQTZiaB?= M1jRXGROW09? NWPoRmFScW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NVzsXWtFOjV|OUGyOFE>
U251 M1zCSWZ2dmO2aX;uJGF{e2G7 MlLhNVAxNzNyMD:5NFAhdk1? NVfyempJOSCq Mk[3SG1UVw>? NX:ySFBDcW6qaXLpeJMhfGinIIDoc5NxcG:{eXzheIlwdiCxZjDN[ZJVU8Li MViyOFY2QDN{Nh?=
A172 Ml;qSpVv[3Srb36gRZN{[Xl? NIHrb4MyODBxM{CwM|kxOCCwTR?= MXGxJIg> NInodYpFVVOR NVH3em9ncW6qaXLpeJMhfGinIIDoc5NxcG:{eXzheIlwdiCxZjDN[ZJVU8Li Mn7YNlQ3PTh|Mk[=
SF188 MmPjSpVv[3Srb36gRZN{[Xl? MXSxNFAwOzByL{mwNEBvVQ>? NHizOmkyKGh? NWfV[mVGTE2VTx?= MlPabY5pcWKrdIOgeIhmKHCqb4PwbI9zgWyjdHnvckBw\iCPZYLUT:Kh MoO5NlQ3PTh|Mk[=
U251 MofnSpVv[3Srb36gRZN{[Xl? M3;4XVExOC9|MECvPVAxKG6P MmPZNUBp M3jUNWROW09? M{L4[IlvcGmkaYTzJJRp\SCjY4Tpeol1gSCxZjDBfIwtKFS7cn:z NYr5UI5SOjR4NUizNlY>
A172 M3HhXmZ2dmO2aX;uJGF{e2G7 M{nRdlExOC9|MECvPVAxKG6P NWDqcHdiOSCq M2nrVWROW09? M1TOUolvcGmkaYTzJJRp\SCjY4Tpeol1gSCxZjDBfIwtKFS7cn:z MnnDNlQ3PTh|Mk[=
SF188 MX7GeY5kfGmxbjDBd5NigQ>? MUSxNFAwOzByL{mwNEBvVQ>? NHjlOWMyKGh? MoTDSG1UVw>? NXXIVnpScW6qaXLpeJMhfGinIHHjeIl3cXS7IH;mJGF5dCxiVInyc|M> MWmyOFY2QDN{Nh?=
U251 NH32[VFHfW6ldHnvckBCe3OjeR?= M3rudVExOC9|MECvPVAxKG6P MlziNUBp NWrwO5hZTE2VTx?= Mle2[IVkemWjc3XzJGFsfCCyaH;zdIhwenmuYYTpc44hcW5iYTDjc45k\W62cnH0bY9vKGSncHXu[IVvfCCvYX7u[ZI> Mmm0NlQ3PTh|Mk[=
A172 MoDUSpVv[3Srb36gRZN{[Xl? MmrzNVAxNzNyMD:5NFAhdk1? NXHmPHBvOSCq MoLmSG1UVw>? MljM[IVkemWjc3XzJGFsfCCyaH;zdIhwenmuYYTpc44hcW5iYTDjc45k\W62cnH0bY9vKGSncHXu[IVvfCCvYX7u[ZI> NYjBfGhkOjR4NUizNlY>
SF188 MYPGeY5kfGmxbjDBd5NigQ>? NUDubHpDOTByL{OwNE86ODBibl2= NVjwPJdvOSCq M3PENGROW09? MX7k[YNz\WG|ZYOgRYt1KHCqb4PwbI9zgWyjdHnvckBqdiCjIHPvcoNmdnS{YYTpc44h\GWyZX7k[Y51KG2jbn7ldi=> M2\VfVI1PjV6M{K2
U251 MWXGeY5kfGmxbjDBd5NigQ>? NHv6fVgyODBxM{CwM|kxOCCwTR?= Mlf5NlghcA>? NYLvd5VlTE2VTx?= MV\pcoR2[2W|IGDBVnAh[2ynYY\h[4U> NXLVe5FnOjR4NUizNlY>
SF188 M3XLTmZ2dmO2aX;uJGF{e2G7 NVqzdIJHOTByL{OwNE86ODBibl2= NYO1RYxlOjhiaB?= MW\EUXNQ M4LsWIlv\HWlZYOgVGFTWCClbHXheoFo\Q>? MXKyOFY2QDN{Nh?=
SF188 MnfqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF7VZ4IyODBxM{CwM|kxOCCwTR?= Ml61OFghcA>? NXj0[VBjTE2VTx?= M3e5b5Jm\HWlZYOgZ4VtdCC|dYL2bZZidCCjdDC5NFAhdk1ic3nncolncWOjboTsfS=> MUGyOFY2QDN{Nh?=
U251 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3XUVVExOC9|MECvPVAxKG6P MV60PEBp NWi0UIFYTE2VTx?= NH;NPWRz\WS3Y3XzJINmdGxic4Xyeol3[WxiYYSgPVAxKG6PIIPp[45q\mmlYX70cJk> MWSyOFY2QDN{Nh?=
A172 NUnMWYw1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF7tUoYyODBxM{CwM|kxOCCwTR?= M4fCZ|Q5KGh? M3n4emROW09? M1\jWJJm\HWlZYOgZ4VtdCC|dYL2bZZidCCjdDC5NFAhdk1ic3nncolncWOjboTsfS=> NGfFW2wzPDZ3OEOyOi=>
SF188 MWfGeY5kfGmxbjDBd5NigQ>? NVLBcoU5OTByL{OwNE86ODBibl2= M1XHelI1KGh? MVTEUXNQ NWXvSZZo[WK{b3fheIV{KG2rZ4LheIlwdiCjbnSgbY53[XOrb36gc4Yh\2yrb33hJINmdGy|IHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ M3rPcFI1PjV6M{K2
U251 NV\zTVhUTnWwY4Tpc44hSXO|YYm= NUT4d|A3OTByL{OwNE86ODBibl2= M4DBVVI1KGh? M4ryXWROW09? MW\hZpJw\2G2ZYOgcYloemG2aX;uJIFv\CCrbo\hd4lwdiCxZjDncIlwdWFiY3XscJMhcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M3rIPFI1PjV6M{K2
A172 M1H6S2Z2dmO2aX;uJGF{e2G7 NILQSpEyODBxM{CwM|kxOCCwTR?= NEHwRmQzPCCq M4HPSWROW09? NF74TYFi[nKxZ3H0[ZMhdWmpcnH0bY9vKGGwZDDpcpZie2mxbjDv[kBodGmxbXGgZ4VtdHNiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MVqyOFY2QDN{Nh?=
Ba/F3 M2[1bmNmdGxiVnnhZoltcXS7IFHzd4F6 NWTRUZltOC5yMECxMVExKM7:TR?= MXq3NkBp MXzpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MVKyOFIyQDV6OR?=
HCC78 NFv0dmtE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MnvUNE4xOS1zMDFOwG0> MUS3NkBp MlG4bY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NVLCSnpuOjR{MUi1PFk>
SK-HEP1 M1LLdWNmdGxiVnnhZoltcXS7IFHzd4F6 M{XBTFAvOjVvMT61JO69VQ>? M{fBPVI1yqCq MlXIbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NGn1UGUzOjF6N{G3NS=>
SK-HEP2 MWDGeY5kfGmxbjDBd5NigQ>? MXixJO69VQ>? MYOyOEBp MkP6Zoxw[2u|IFjHSk1qdmS3Y3XkJINmdGxibX;0bYxqfHl? Mof0NlIyQDdzN{G=
SK-HEP2 NXfLVVhNTnWwY4Tpc44hSXO|YYm= MWixJO69VQ>? MmS0NlQhcA>? M2frR4NifXOnczDHNk9OKHCqYYPlJIFzemW|dDD3bZRpKHKnZIXjeIlwdiCrbjD0bIUhTzBxR{JCpIFv\CCVIIDoZZNmew>? MU[yNlE5PzF5MR?=
MKN-45  NX7Md4twT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M17HVlAvODFvMUCg{txO NFO4Z3I2KGR? MlnwTWM2OD16IH7N NXL0VVNNOjF4NUW5NVg>
KATO-III MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3LublAvODFvMUCg{txO NWrMc4I4PSCm NILxPVBKSzVyPUOwJI5O MUiyNVY2PTlzOB?=
MKN-45  MmPtSpVv[3Srb36gRZN{[Xl? M2nYNlEh|ryP NUjBc3NSOjRiaB?= NHz6eZBqdmirYnn0d{BxcG:|cHjvdplt[XSrb36gc4YhVUWWLDDBb5QtKGGwZDDFVmsyNzJiaX6gUWtPNTR3 NV3kRYpSOjF4NUW5NVg>
KATO-III M1f2OWZ2dmO2aX;uJGF{e2G7 NYO5OWZWOSEQvF2= M4rZO|I1KGh? NW[5RpRkcW6qaXLpeJMheGixc4Doc5J6dGG2aX;uJI9nKE2HVDygRYt1NCCjbnSgSXJMOS9{IHnuJG1MVi12NR?= NYP3N5hjOjF4NUW5NVg>
H1648 Ml:zS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUXJR|UxRTFwMkigxtExNjF{IN88US=> MYKyNVI2OjJ6NB?=
H1573 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYfJR|UxRTFwNkKgxtEhOC5yNTFOwG0> NVnNZ2M4OjF{NUKyPFQ>
H596 NUW4XIFnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYPJR|UxRTFwMkGgxtEhOC5zNzFOwG0> MVWyNVI2OjJ6NB?=
HOP92 M{PPO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPLTWM2OD1yLkixJOKyKDBwMkmg{txO NV;RSo5FOjF{NUKyPFQ>
H69 NGLyfJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MY\JR|UxRTFwMUigxtEhOC5yODFOwG0> M{LTXFIyOjV{Mki0
H1975 MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnzSTWM2OD1zLkO5JOKyKDBwM{Og{txO NV31NYtZOjF{NUKyPFQ>
SCC15 NYqzW|NXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2XQNWlEPTB;MD62N{DDuSByLkC0JO69VQ>? M3LPSVIyOjV{Mki0
HN5 NUHQbZNTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1;KPWlEPTB;MD62OUDDuSByLkK2JO69VQ>? Mly2NlEzPTJ{OES=

... 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(Data is from Selleck tests instead of citations):
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
in solvent
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 12 2009 Phase 1
NCT00742261 Completed Solid Tumours GlaxoSmithKline August 11 2008 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID