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  M3nzTmZ2dmO2aX;uJGF{e2G7 MlL1NE42NzFxMj61JO69VQ>? MUCyOEBp NVTxVod5TE2VTx?= M360[YlvcGmkaYTzJJRp\SCKR1[tbY5lfWOnZDDjUWVVKHCjdHj3ZZkh[WO2aY\heIlwdg>? M3zDZlI2OzlzMkSx
ONS76 Ml:0SpVv[3Srb36gRZN{[Xl? MYewMlUwOS9{LkWg{txO MYGyOEBp NF;TflVFVVOR NUe3UWt[cW6qaXLpeJMhfGinIFjHSk1qdmS3Y3XkJINOTVRicHH0bJdigSCjY4TpeoF1cW:w MXeyOVM6OTJ2MR?=
Daoy  MUjGeY5kfGmxbjDBd5NigQ>? MUOwMlUwOS9{LkWg{txO Mn\kNlQhcA>? M3z4VmROW09? MlvHbY5pcWKrdIOgTGdHNW2nZHnheIVlKG2rZ4LheIlwdiCjbnSgbY53[XOrb36= MVqyOVM6OTJ2MR?=
ONS76 NHHWRVFHfW6ldHnvckBCe3OjeR?= Mlv2NE42NzFxMj61JO69VQ>? Mm[xNlQhcA>? MnzPSG1UVw>? NEHUfGJqdmirYnn0d{BJT0ZvbXXkbYF1\WRibXnndoF1cW:wIHHu[EBqdn[jc3nvci=> Ml\4NlU{QTF{NEG=
Daoy  Mlm5RZBweHSxc3nzJGF{e2G7 NHTFRoMyKM7:TR?= NGP3dIYzPCCq MYTEUXNQ MnfIbY5lfWOnczDhdI9xfG:|aYO= M2fmTVI2OzlzMkSx
Daoy  M2Pwd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFrJRowxNjVxMT:yMlUh|ryP NH24T3czPC17NjDo NV;s[WtXTE2VTx?= NVTJdXhLcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MWqyOVM6OTJ2MR?=
U251 NGHEe5RHfW6ldHnvckBCe3OjeR?= M3f5XlExOC9|MECvPVAxKG6P NXXiOo9[OSCq MkTDSG1UVw>? NITE[mlqdmirYnn0d{B1cGVicHjvd5Bpd3K7bHH0bY9vKG:oIF3ldnRMyqB? M1Tse|I1PjV6M{K2
A172 NGHqT5NHfW6ldHnvckBCe3OjeR?= NGDwfnIyODBxM{CwM|kxOCCwTR?= M2nBUVEhcA>? MkHrSG1UVw>? NViyOWt4cW6qaXLpeJMhfGinIIDoc5NxcG:{eXzheIlwdiCxZjDN[ZJVU8Li MXSyOFY2QDN{Nh?=
SF188 M4XpfWZ2dmO2aX;uJGF{e2G7 MVWxNFAwOzByL{mwNEBvVQ>? MUKxJIg> MnK0SG1UVw>? NV;aZZptcW6qaXLpeJMhfGinIIDoc5NxcG:{eXzheIlwdiCxZjDN[ZJVU8Li NXn4NXNIOjR4NUizNlY>
U251 NYLkb|U1TnWwY4Tpc44hSXO|YYm= MU[xNFAwOzByL{mwNEBvVQ>? M{[0[|EhcA>? MXvEUXNQ MV\pcohq[mm2czD0bIUh[WO2aY\peJkhd2ZiQYjsMEBVgXKxMx?= M3r3Z|I1PjV6M{K2
A172 NVvWO4VETnWwY4Tpc44hSXO|YYm= M4TucVExOC9|MECvPVAxKG6P M4nEb|EhcA>? MnXvSG1UVw>? NInVXZJqdmirYnn0d{B1cGViYXP0bZZqfHlib3[gRZhtNCCWeYLvNy=> NWfsRmNWOjR4NUizNlY>
SF188 NXn6WXpXTnWwY4Tpc44hSXO|YYm= NHuyeIIyODBxM{CwM|kxOCCwTR?= MnvENUBp M1rySWROW09? NVLrUWVLcW6qaXLpeJMhfGinIHHjeIl3cXS7IH;mJGF5dCxiVInyc|M> NIjad5MzPDZ3OEOyOi=>
U251 NHHhS4pHfW6ldHnvckBCe3OjeR?= MnXWNVAxNzNyMD:5NFAhdk1? MmL3NUBp NV3mO|hPTE2VTx?= NWnndmt1\GWlcnXhd4V{KEGtdDDwbI9{eGixconsZZRqd25iaX6gZUBkd26lZX70doF1cW:wIHTldIVv\GWwdDDtZY5v\XJ? M4rLSFI1PjV6M{K2
A172 MXrGeY5kfGmxbjDBd5NigQ>? M{nBNlExOC9|MECvPVAxKG6P MkLkNUBp NWnqWWM4TE2VTx?= Mlfs[IVkemWjc3XzJGFsfCCyaH;zdIhwenmuYYTpc44hcW5iYTDjc45k\W62cnH0bY9vKGSncHXu[IVvfCCvYX7u[ZI> M3PuNFI1PjV6M{K2
SF188 MljGSpVv[3Srb36gRZN{[Xl? M2LldVExOC9|MECvPVAxKG6P NWKxWpNDOSCq NYfteWI4TE2VTx?= NVr4eXJH\GWlcnXhd4V{KEGtdDDwbI9{eGixconsZZRqd25iaX6gZUBkd26lZX70doF1cW:wIHTldIVv\GWwdDDtZY5v\XJ? M{e2flI1PjV6M{K2
U251 NXnqblJETnWwY4Tpc44hSXO|YYm= MlvXNVAxNzNyMD:5NFAhdk1? NI\GO20zQCCq M17Qc2ROW09? MYLpcoR2[2W|IGDBVnAh[2ynYY\h[4U> NELBbIIzPDZ3OEOyOi=>
SF188 M2HTSWZ2dmO2aX;uJGF{e2G7 M3TWcVExOC9|MECvPVAxKG6P NXnkWmJyOjhiaB?= M{D2PGROW09? NITOelNqdmS3Y3XzJHBCWlBiY3zlZZZi\2V? MmHyNlQ3PTh|Mk[=
SF188 NEfZVpVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlTMNVAxNzNyMD:5NFAhdk1? NGHST3E1QCCq Mn\6SG1UVw>? NYLnWY44emWmdXPld{Bk\WyuIIP1dpZqfmGuIHH0JFkxOCCwTTDzbYdvcW[rY3HueIx6 NVTDWFdSOjR4NUizNlY>
U251 NX;oe3NlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NG\vfosyODBxM{CwM|kxOCCwTR?= NEHJUpg1QCCq NEDkV2FFVVOR M3Hze5Jm\HWlZYOgZ4VtdCC|dYL2bZZidCCjdDC5NFAhdk1ic3nncolncWOjboTsfS=> NHHpT3AzPDZ3OEOyOi=>
A172 M1zFcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEjhOlAyODBxM{CwM|kxOCCwTR?= NWf2RXhZPDhiaB?= MYjEUXNQ M1HEXJJm\HWlZYOgZ4VtdCC|dYL2bZZidCCjdDC5NFAhdk1ic3nncolncWOjboTsfS=> NWLiTXV6OjR4NUizNlY>
SF188 MWTGeY5kfGmxbjDBd5NigQ>? MXSxNFAwOzByL{mwNEBvVQ>? M1XFUFI1KGh? NEnoNIxFVVOR MnHsZYJzd2ejdHXzJI1q\3KjdHnvckBidmRiaX72ZZNqd25ib3[g[4xqd22jIHPlcIx{KGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MXeyOFY2QDN{Nh?=
U251 M13DdGZ2dmO2aX;uJGF{e2G7 NHTESW8yODBxM{CwM|kxOCCwTR?= MX6yOEBp MVvEUXNQ NWWzO2k5[WK{b3fheIV{KG2rZ4LheIlwdiCjbnSgbY53[XOrb36gc4Yh\2yrb33hJINmdGy|IHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MoC0NlQ3PTh|Mk[=
A172 M{DwXmZ2dmO2aX;uJGF{e2G7 MlXHNVAxNzNyMD:5NFAhdk1? MlK5NlQhcA>? MnLLSG1UVw>? MnexZYJzd2ejdHXzJI1q\3KjdHnvckBidmRiaX72ZZNqd25ib3[g[4xqd22jIHPlcIx{KGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MoHCNlQ3PTh|Mk[=
Ba/F3 NHfOcnFE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MWGwMlAxODFvMUCg{txO MonGO|IhcA>? NW\O[ZdbcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MXiyOFIyQDV6OR?=
HCC78 MVPD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MkfSNE4xOS1zMDFOwG0> MnvaO|IhcA>? M4C5OIlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz M3LuPVI1OjF6NUi5
SK-HEP1 NEW2e5NE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M364cVAvOjVvMT61JO69VQ>? MV:yOOKhcA>? NVf0dJdEcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MVSyNlE5PzF5MR?=
SK-HEP2 MWrGeY5kfGmxbjDBd5NigQ>? MUexJO69VQ>? NWjybXYxOjRiaB?= M{PLNIJtd2OtczDIS2YucW6mdXPl[EBk\WyuIH3veIltcXS7 NXvJSoJ4OjJzOEexO|E>
SK-HEP2 NEWzbWlHfW6ldHnvckBCe3OjeR?= NUTH[lFpOSEQvF2= NYLnbpBGOjRiaB?= MVXjZZV{\XNiR{KvUUBxcGG|ZTDhdpJme3Rid3n0bEBz\WS3Y4Tpc44hcW5idHjlJGcxN0dzwrDhcoQhWyCyaHHz[ZM> NI\nd2YzOjF6N{G3NS=>
MKN-45  MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkDINE4xOS1zMDFOwG0> MUK1JIQ> MkTwTWM2OD16IH7N NY[xPHd3OjF4NUW5NVg>
KATO-III MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml3ZNE4xOS1zMDFOwG0> MVm1JIQ> MV3JR|UxRTNyIH7N NISyZm8zOTZ3NUmxPC=>
MKN-45  NXe0SGpZTnWwY4Tpc44hSXO|YYm= NXPLW2I5OSEQvF2= MnzFNlQhcA>? Mn24bY5pcWKrdIOgdIhwe3Cqb4L5cIF1cW:wIH;mJG1GXCxiQXv0MEBidmRiRWLLNU8zKGmwIF3LUk01PQ>? MlPWNlE3PTV7MUi=
KATO-III MX7GeY5kfGmxbjDBd5NigQ>? M{\td|Eh|ryP NEjIeJozPCCq NVjVfFlqcW6qaXLpeJMheGixc4Doc5J6dGG2aX;uJI9nKE2HVDygRYt1NCCjbnSgSXJMOS9{IHnuJG1MVi12NR?= M3:3ZVIyPjV3OUG4
H1648 NI\hUWxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWrJbmk1UUN3ME2xMlI5KMLzMD6xNkDPxE1? NH;tOG4zOTJ3MkK4OC=>
H1573 NHTYcJdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NW\6cJp[UUN3ME2xMlYzKMLzIECuNFUh|ryP NH;LPZQzOTJ3MkK4OC=>
H596 MmLDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXvJR|UxRTFwMkGgxtEhOC5zNzFOwG0> M1rxelIyOjV{Mki0
HOP92 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlzmTWM2OD1yLkixJOKyKDBwMkmg{txO Mm[3NlEzPTJ{OES=
H69 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3myPGlEPTB;MT6xPEDDuSByLkC4JO69VQ>? MXKyNVI2OjJ6NB?=
H1975 M3zoTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYnKW3NbUUN3ME2xMlM6KMLzIECuN|Mh|ryP M2i4[lIyOjV{Mki0
SCC15 M3n0dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXzJR|UxRTBwNkOgxtEhOC5yNDFOwG0> MmrrNlEzPTJ{OES=
HN5 NFHSVIVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnrVTWM2OD1yLk[1JOKyKDBwMk[g{txO MVqyNVI2OjJ6NB?=

... 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
NCT00743067 Completed Solid Tumours GlaxoSmithKline August 9 2006 Phase 1
NCT00725712 Completed Neoplasms Gastrointestinal Tract GlaxoSmithKline March 31 2007 Phase 2
NCT00726323 Completed Carcinoma Renal Cell GlaxoSmithKline June 30 2006 Phase 2
NCT00725764 Completed Neoplasms Head and Neck GlaxoSmithKline August 27 2007 Phase 2
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

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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