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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2 Customer Reviews

  • 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  MkW1SpVv[3Srb36gRZN{[Xl? Mo\qNE42NzFxMj61JO69VQ>? NIG4bnozPCCq MmnBSG1UVw>? NGHjTlBqdmirYnn0d{B1cGViSFfGMYlv\HWlZXSgZ21GXCCyYYToe4F6KGGldHn2ZZRqd25? NWG5U5hUOjV|OUGyOFE>
ONS76 NVj5T49XTnWwY4Tpc44hSXO|YYm= NGrGSIExNjVxMT:yMlUh|ryP NYq3S|RPOjRiaB?= NVX1TFBKTE2VTx?= MXzpcohq[mm2czD0bIUhUEeILXnu[JVk\WRiY13FWEBx[XSqd3H5JIFkfGm4YYTpc44> MX[yOVM6OTJ2MR?=
Daoy  MknVSpVv[3Srb36gRZN{[Xl? M2LOfVAvPS9zL{KuOUDPxE1? MWWyOEBp NUHxT2J2TE2VTx?= NX3hSHI6cW6qaXLpeJMhUEeILX3l[IlifGWmIH3p[5JifGmxbjDhcoQhcW64YYPpc44> NFPBVVEzPTN7MUK0NS=>
ONS76 NF3Zc4VHfW6ldHnvckBCe3OjeR?= NWLWW|dlOC53L{GvNk42KM7:TR?= MkH6NlQhcA>? NIXGWpdFVVOR NF\4cJdqdmirYnn0d{BJT0ZvbXXkbYF1\WRibXnndoF1cW:wIHHu[EBqdn[jc3nvci=> M4nQflI2OzlzMkSx
Daoy  M3PDPGFxd3C2b4Ppd{BCe3OjeR?= Ml63NUDPxE1? MX[yOEBp M4DyZ2ROW09? NF;SUZdqdmS3Y3XzJIFxd3C2b4Ppdy=> MmTSNlU{QTF{NEG=
Daoy  MmWzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUCwMlUwOS9{LkWg{txO NYCwUVBiOjRvOU[gbC=> M1XVbmROW09? MVfpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NFzMU4QzPTN7MUK0NS=>
U251 NHKxR5JHfW6ldHnvckBCe3OjeR?= NEji[GMyODBxM{CwM|kxOCCwTR?= NInmW5IyKGh? MnTPSG1UVw>? M3fFZ4lvcGmkaYTzJJRp\SCyaH;zdIhwenmuYYTpc44hd2ZiTXXyWGvDqA>? M2P1OlI1PjV6M{K2
A172 NHPlcmxHfW6ldHnvckBCe3OjeR?= MVKxNFAwOzByL{mwNEBvVQ>? NUTpUYlbOSCq NFjRZY9FVVOR M2fh[YlvcGmkaYTzJJRp\SCyaH;zdIhwenmuYYTpc44hd2ZiTXXyWGvDqA>? M3\tblI1PjV6M{K2
SF188 M3K0WWZ2dmO2aX;uJGF{e2G7 NGLSc4UyODBxM{CwM|kxOCCwTR?= M{f0RVEhcA>? MnHNSG1UVw>? M3e3Z4lvcGmkaYTzJJRp\SCyaH;zdIhwenmuYYTpc44hd2ZiTXXyWGvDqA>? NXzXb29VOjR4NUizNlY>
U251 MmKxSpVv[3Srb36gRZN{[Xl? M4fGUlExOC9|MECvPVAxKG6P NX3BR3l3OSCq NX;6O4tpTE2VTx?= MnLkbY5pcWKrdIOgeIhmKGGldHn2bZR6KG:oIFH4cEwhXHm{b{O= NVfWXJJCOjR4NUizNlY>
A172 M{XkNWZ2dmO2aX;uJGF{e2G7 MVixNFAwOzByL{mwNEBvVQ>? NXPydHJ7OSCq MmO5SG1UVw>? M1Lr[olvcGmkaYTzJJRp\SCjY4Tpeol1gSCxZjDBfIwtKFS7cn:z NWfpZ4F3OjR4NUizNlY>
SF188 MX\GeY5kfGmxbjDBd5NigQ>? MVSxNFAwOzByL{mwNEBvVQ>? NFLYclkyKGh? MoexSG1UVw>? NUTxXIk2cW6qaXLpeJMhfGinIHHjeIl3cXS7IH;mJGF5dCxiVInyc|M> NFHzeYkzPDZ3OEOyOi=>
U251 M4HTe2Z2dmO2aX;uJGF{e2G7 MmXhNVAxNzNyMD:5NFAhdk1? M4fxfFEhcA>? NF7QdYtFVVOR M3HaU4Rm[3KnYYPld{BCc3RicHjvd5Bpd3K7bHH0bY9vKGmwIHGgZ49v[2WwdILheIlwdiCmZYDlcoRmdnRibXHucoVz M3\TUVI1PjV6M{K2
A172 Ml7JSpVv[3Srb36gRZN{[Xl? MonCNVAxNzNyMD:5NFAhdk1? MmLWNUBp MoThSG1UVw>? MV\k[YNz\WG|ZYOgRYt1KHCqb4PwbI9zgWyjdHnvckBqdiCjIHPvcoNmdnS{YYTpc44h\GWyZX7k[Y51KG2jbn7ldi=> MlXhNlQ3PTh|Mk[=
SF188 MlnSSpVv[3Srb36gRZN{[Xl? NGPqS3QyODBxM{CwM|kxOCCwTR?= M3viclEhcA>? Mn;JSG1UVw>? MlrO[IVkemWjc3XzJGFsfCCyaH;zdIhwenmuYYTpc44hcW5iYTDjc45k\W62cnH0bY9vKGSncHXu[IVvfCCvYX7u[ZI> M1f5WlI1PjV6M{K2
U251 NHzrT4lHfW6ldHnvckBCe3OjeR?= MXuxNFAwOzByL{mwNEBvVQ>? NUfzdYZtOjhiaB?= NVy3SGt4TE2VTx?= NV\zXIZvcW6mdXPld{BRSVKSIHPs[YF3[Wen NIXW[|AzPDZ3OEOyOi=>
SF188 MmjPSpVv[3Srb36gRZN{[Xl? NGTrWXEyODBxM{CwM|kxOCCwTR?= M3vlR|I5KGh? NUjX[XdtTE2VTx?= MXLpcoR2[2W|IGDBVnAh[2ynYY\h[4U> NIXCbJgzPDZ3OEOyOi=>
SF188 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1HublExOC9|MECvPVAxKG6P NH;YT4M1QCCq MVzEUXNQ M4PrVZJm\HWlZYOgZ4VtdCC|dYL2bZZidCCjdDC5NFAhdk1ic3nncolncWOjboTsfS=> NG[x[lkzPDZ3OEOyOi=>
U251 M1\zW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn60NVAxNzNyMD:5NFAhdk1? MWO0PEBp NWjH[2RZTE2VTx?= MlzvdoVlfWOnczDj[YxtKHO3co\peoFtKGG2IEmwNEBvVSC|aXfubYZq[2GwdHz5 MoDyNlQ3PTh|Mk[=
A172 MnnjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MY[xNFAwOzByL{mwNEBvVQ>? MkDuOFghcA>? Mm\5SG1UVw>? MlG1doVlfWOnczDj[YxtKHO3co\peoFtKGG2IEmwNEBvVSC|aXfubYZq[2GwdHz5 MVGyOFY2QDN{Nh?=
SF188 MYLGeY5kfGmxbjDBd5NigQ>? MYSxNFAwOzByL{mwNEBvVQ>? NFPBVYozPCCq M4nZU2ROW09? M1HkSIFjem:pYYTld{BucWe{YYTpc44h[W6mIHnueoF{cW:wIH;mJIdtcW:vYTDj[YxteyCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MnnoNlQ3PTh|Mk[=
U251 M3:3bWZ2dmO2aX;uJGF{e2G7 NYLEcmRQOTByL{OwNE86ODBibl2= MY[yOEBp Ml\VSG1UVw>? MVPhZpJw\2G2ZYOgcYloemG2aX;uJIFv\CCrbo\hd4lwdiCxZjDncIlwdWFiY3XscJMhcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MV2yOFY2QDN{Nh?=
A172 MY\GeY5kfGmxbjDBd5NigQ>? MWSxNFAwOzByL{mwNEBvVQ>? MWGyOEBp NXG4XG5VTE2VTx?= MXrhZpJw\2G2ZYOgcYloemG2aX;uJIFv\CCrbo\hd4lwdiCxZjDncIlwdWFiY3XscJMhcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MX2yOFY2QDN{Nh?=
Ba/F3 MYDD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NUDZVFJ3OC5yMECxMVExKM7:TR?= M1zNTFczKGh? MoexbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NFzXTGgzPDJzOEW4PS=>
HCC78 MXzD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NVS4UpU3OC5yMT2xNEDPxE1? Moi5O|IhcA>? Mk\tbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NV6xNoRXOjR{MUi1PFk>
SK-HEP1 Mn7PR4VtdCCYaXHibYxqfHliQYPzZZk> Ml\4NE4zPS1zLkWg{txO MYKyOOKhcA>? NYnINWt2cW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NF7DU4IzOjF6N{G3NS=>
SK-HEP2 MVfGeY5kfGmxbjDBd5NigQ>? NFewW3YyKM7:TR?= M1XTWlI1KGh? MYPicI9kc3NiSFfGMYlv\HWlZXSgZ4VtdCCvb4TpcIl1gQ>? MXyyNlE5PzF5MR?=
SK-HEP2 NUnqR5BVTnWwY4Tpc44hSXO|YYm= MoHxNUDPxE1? NYDjZpdyOjRiaB?= MkHKZ4F2e2W|IFeyM20heGijc3WgZZJz\XO2IIfpeIghemWmdXP0bY9vKGmwIITo[UBIOC:JMdMgZY5lKFNicHjhd4V{ NYf6PFMyOjJzOEexO|E>
MKN-45  M1fUZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHK5WmcxNjBzLUGwJO69VQ>? MX21JIQ> MljETWM2OD16IH7N M1nJXFIyPjV3OUG4
KATO-III M1flVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPINE4xOS1zMDFOwG0> M1fRXlUh\A>? NF7EdIpKSzVyPUOwJI5O M2PVWVIyPjV3OUG4
MKN-45  MoTTSpVv[3Srb36gRZN{[Xl? MXuxJO69VQ>? NEfV[5AzPCCq Mom5bY5pcWKrdIOgdIhwe3Cqb4L5cIF1cW:wIH;mJG1GXCxiQXv0MEBidmRiRWLLNU8zKGmwIF3LUk01PQ>? Mlj6NlE3PTV7MUi=
KATO-III M2ThU2Z2dmO2aX;uJGF{e2G7 MX:xJO69VQ>? MXSyOEBp NXvFSoxzcW6qaXLpeJMheGixc4Doc5J6dGG2aX;uJI9nKE2HVDygRYt1NCCjbnSgSXJMOS9{IHnuJG1MVi12NR?= MWKyNVY2PTlzOB?=
H1648 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MojxTWM2OD1zLkK4JOKyOC5zMjFOwG0> MViyNVI2OjJ6NB?=
H1573 M2ro[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHTvb3FKSzVyPUGuOlIhyrFiMD6wOUDPxE1? NF;TWmQzOTJ3MkK4OC=>
H596 NWDPOZJjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEfzTGVKSzVyPUGuNlEhyrFiMD6xO{DPxE1? NHjjblgzOTJ3MkK4OC=>
HOP92 NYLveYd[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\WTWM2OD1yLkixJOKyKDBwMkmg{txO MX2yNVI2OjJ6NB?=
H69 NX3VcYlPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoTYTWM2OD1zLkG4JOKyKDBwMEig{txO MoPlNlEzPTJ{OES=
H1975 NXq2WodmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnLqTWM2OD1zLkO5JOKyKDBwM{Og{txO NWrWRlZpOjF{NUKyPFQ>
SCC15 NHezcpBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2\abGlEPTB;MD62N{DDuSByLkC0JO69VQ>? MXSyNVI2OjJ6NB?=
HN5 Moq3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWqzPHVNUUN3ME2wMlY2KMLzIECuNlYh|ryP MYiyNVI2OjJ6NB?=

... 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 127 mg/mL (200.74 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 30% propylene glycol, 5% Tween 80, 65% D5W 30 mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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 2009 Phase 1
NCT00742261 Completed Solid Tumours GlaxoSmithKline August 2008 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID