BMS-777607

For research use only.

Catalog No.S1561

31 publications

BMS-777607 Chemical Structure

CAS No. 1025720-94-8

BMS-777607 is a Met-related inhibitor for c-Met, Axl, Ron and Tyro3 with IC50 of 3.9 nM, 1.1 nM, 1.8 nM and 4.3 nM in cell-free assays, 40-fold more selective for Met-related targets versus Lck, VEGFR-2, and TrkA/B, and more than 500-fold greater selectivity versus all other receptor and non receptor kinases. Phase 1/2.

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Selleck's BMS-777607 has been cited by 31 publications

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Biological Activity

Description BMS-777607 is a Met-related inhibitor for c-Met, Axl, Ron and Tyro3 with IC50 of 3.9 nM, 1.1 nM, 1.8 nM and 4.3 nM in cell-free assays, 40-fold more selective for Met-related targets versus Lck, VEGFR-2, and TrkA/B, and more than 500-fold greater selectivity versus all other receptor and non receptor kinases. Phase 1/2.
Features A potent inhibitor of the Met family, and >40-fold selectivity vs. Lck, VEGFR2, and TrkA/B and >500-fold selective vs. other receptor and non-receptor kinases.
Targets
Axl [1]
(Cell-free assay)		 RON [1]
(Cell-free assay)		 Met [1]
(Cell-free assay)		 Tyro3 [1]
(Cell-free assay)		 Mer [1]
(Cell-free assay)
1.1 nM 1.8 nM 3.9 nM 4.3 nM 14 nM
In vitro

BMS-777607 is a selective ATP-competitive Met kinase inhibitor which potently blocks the autophosphorylation of c-Met with IC50 of 20 nM in GTL-16 cell lysates, and demonstrates selective inhibition of proliferation in Met-driven tumor cell lines, such as GTL-16 cell line, H1993 and U87. [1] BMS-777607 inhibits hepatocyte growth factor (HGF)-triggered c-Met autophosphorylation with IC50 of <1 nM in PC-3 and DU145 prostate cancer cells. BMS 777607 has little effect on tumor cell growth, but exhibits inhibitory effect on HGF-induced cell scattering in PC-3 and DU145 cells, with almost complete inhibition at 0.5 μM. BMS 777607 also suppresses stimulated cell migration and invasion in a dose-dependent fashion (IC50 < 0.1 μM) in both cell lines. [2] Application of BMS 777607 (~10 μM) to the highly metastatic murine KHT cells for 2 hours potently eliminates basal levels of autophosphorylated c-Met with IC50 of 10 nM without affecting the total c-Met, leading to dose-dependent inhibition of phosphorylation of downstream signaling molecules including ERK, Akt, p70S6K and S6. Treatment with BMS-777607 (~1 μM) for 24 hours potently inhibits the KHT cell scatter, motility and invasion at doses in the nanomolar range which consists with MET gene knockdown, and modestly affects cell proliferation and colony formation. [3]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
GTL-16 NUnu[WJ6U2mwYYPlJIF{e2G7 MVPEUXNQ M{WxNIlvcGmkaYTzJG1mfCCtaX7hd4Uhf2m2aDDJR|UxKG:oIEGwNEBvVQ>? NFzUW5QyQTJ4MEexNS=>
H1993 NGPHNY9Iem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NHy3V|B,OTBizszN NHzLUnZFVVOR NUXWdXlEUUN3ME2xOVAhdk1? M4PyfFE6OjZyN{Gx
U87 NGixNoRIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= M{\kRp4yOCEQvF2= M4K5TGROW09? NIjVTYtKSzVyPUG2NEBvVQ>? M4LaXFE6OjZyN{Gx
PC-3 NFPleVJHfW6ldHnvckBie3OjeR?= MXOwMlEh|ryP MmnkSG1UVw>? MkX0[ZhpcWKrdIOgbY5pcWKrdH;yfUBm\m[nY4Sgc44hUEeILXnu[JVk\WRiY3XscEB{[2G2dHXybY5o MoHuNlA2OTV7NEO=
DU145 MUPGeY5kfGmxbjDhd5NigQ>? Ml34NE4yKM7:TR?= M2Pn[WROW09? NUfnOG5J\XiqaXLpeJMhcW6qaXLpeI9zgSCnZn\lZ5Qhd25iSFfGMYlv\HWlZXSgZ4VtdCC|Y3H0eIVzcW6p M1PublIxPTF3OUSz
PC-3 M16xNWZ2dmO2aX;uJIF{e2G7 MmH2NE4xOSEQvF2= NF\VdYJFVVOR NWjsWmh4e3WycILld5NmeyCKR1[tbY5lfWOnZDDj[YxtKG2rZ4LheIlwdg>? M173eFIxPTF3OUSz
DU145 MWLGeY5kfGmxbjDhd5NigQ>? MUKwMlAyKM7:TR?= MV3EUXNQ NVm2NYdZe3WycILld5NmeyCKR1[tbY5lfWOnZDDj[YxtKG2rZ4LheIlwdg>? NWDSW5dyOjB3MUW5OFM>
PC-3 MV3GeY5kfGmxbjDhd5NigQ>? MnHENE4yKM7:TR?= M4nkd2ROW09? MkWybY1x[Wm{czDIS2YudWWmaXH0[YQh[2WubDDpcpZie2mxbh?= MV[yNFUyPTl2Mx?=
DU145 MljPSpVv[3Srb36gZZN{[Xl? NFXzSGIxNjFizszN NYWzW5RZTE2VTx?= M1\5OolueGGrcoOgTGdHNW2nZHnheIVlKGOnbHygbY53[XOrb36= NIe1TWwzODVzNUm0Ny=>
PC-3 NXHrUm43T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MVL+NVAh|ryP NH;VVI1FVVOR MUHy[YR2[2W|IHPlcIwheHKxbHnm[ZJifGmxbh?= M3H2eVIxPTF3OUSz
KHT NVu2Om1zU2mwYYPlJIF{e2G7 NH3RZ4JFVVOR NV;GflhV[myxY3vzJJRp\SClLV3leEB{cWewYXzpcocheGG2aIfhfUB4cXSqIFnDOVAhd2ZiMUCgcm0> MV2yNlI5PjV{Mx?=
KHT MoK0SpVv[3Srb36gZZN{[Xl? MX3+NUDPxE1? MX3EUXNQ NEDCcpJxemW4ZX70d{B{eG:wdHHu[Y92eyCNSGSgZ4VtdCC|Y3H0eIVzcW6pIIfpeIghUUN3MDDv[kAxNjFvMD61JO69VQ>? NUTEUZNROjJ{OE[1NlM>
KHT NFzyOWlHfW6ldHnvckBie3OjeR?= MoGzglAvPSEQvF2= MYnEUXNQ NGmxcGhqdmirYnn0d{Bk\WyuIH3p[5JifGmxbh?= NVv5VHNGOjJ{OE[1NlM>
KHT M2\w[WZ2dmO2aX;uJIF{e2G7 NYC2XVVNhjBwNTFOwG0> NWG2T2pUTE2VTx?= NFvCXY1qdmirYnn0d{Bk\WyuIHnueoF{cW:w Mlq5NlIzQDZ3MkO=
KHT NH3xUHRIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NF;0O29,OTBizszN NUnMVIdZTE2VTx?= NUjVfJRYcW6qaXLpeJMhU0iWIHPlcIwheHKxbHnm[ZJifGmxbh?= M1\JWVIzOjh4NUKz
T-47D M1jNVGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MXr+OUDPxE1? NYLqbpFRTE2VTx?= Mo[4bY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;u MoLnNlM1Pjh3Mkm=
ZR-75-1 NF3z[YJIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= M4C5TZ42KM7:TR?= M4S0c2ROW09? MUnpcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36= MlnzNlM1Pjh3Mkm=
T-47D NYrIS5FoTnWwY4Tpc44h[XO|YYm= M2PQ[lExKM7:TR?= NYXsb3FETE2VTx?= NVfIRZZCUW6mdXPld{Bxd2y7cHzvbYR6KGK7IEi2JEU> M3nHR|I{PDZ6NUK5
ZR-75-1 MY\GeY5kfGmxbjDhd5NigQ>? NIDodWYyOCEQvF2= MVPEUXNQ MYDJcoR2[2W|IIDvcJlxdG:rZImgZpkhQDhn NIfXcYIzOzR4OEWyPS=>
T-47D NHHq[|lHfW6ldHnvckBie3OjeR?= NGnaVHkyOCEQvF2= NHjkZ4FFVVOR NIHDe4pqdmirYnn0d{BCXVKNLVKg[pVv[3Srb36gZY5lKGmwZIXj[ZMhcXS|IIDyc5RmcW5iZHXndoFl[XSrb36= NF3uZWczOzR4OEWyPS=>
CHRF NXzyZW9vTnWwY4Tpc44h[XO|YYm= MXOxNEDPxE1? NG\hNFNFVVOR MYHpcohq[mm2czDj[YxtKGSrdnnzbY9v NGr5c4EzPTNyNEmwNC=>
HPDE NESxO5dHfW6ldHnvckBie3OjeR?= NE\aT3UyOCEQvF2= NWnqO5R7TE2VTx?= MlnlZoxw[2u|IHPvcpN1cXS3dHn2[UBi[3SrdnH0bY9vKGGwZDDk[YNz\WG|ZXSgRWtVKHOrZ37hcIlv\w>? MoDhNlY1Pzd|MUS=
U118MG Ml7YT4lv[XOnIHHzd4F6 NH;xepJ,OyEQvF2= MWnEUXNQ Mk\OZoxw[2u|IFHYUEBxcG:|cHjvdplt[XSrb36= NIT4VG0zPjh2OEWyOC=>
SF126 MoDiT4lv[XOnIHHzd4F6 MWD+N{DPxE1? MoTSSG1UVw>? MWjicI9kc3NiQWjMJJBpd3OyaH;yfYxifGmxbh?= NXXXeVZkOjZ6NEi1NlQ>
U118MG MmHUR5l1d3irY3n0fUBie3OjeR?= MnviNVIvPSEQvF2= NEX0bmJFVVOR M2\iboRm[3KnYYPld{BodGmxbXGgZ4VtdCC4aXHibYxqfHl? MVGyOlg1QDV{NB?=
SF126 M3u0bmN6fG:6aXPpeJkh[XO|YYm= M1S4ZVEzNjVizszN NF\PT|FFVVOR MlfK[IVkemWjc3XzJIdtcW:vYTDj[YxtKH[rYXLpcIl1gQ>? Mo\UNlY5PDh3MkS=
U118MG NWPPO|JKSXCxcITvd4l{KGG|c3H5 NFnFd5MyOi53IN88US=> NIHseolFVVOR MoPObY5lfWOnczDncIlwdWFiY3XscEBieG:ydH;zbZM> MmLPNlY5PDh3MkS=
SF126 M4fJfmFxd3C2b4Ppd{Bie3OjeR?= M1\aeFEzNjVizszN Ml7aSG1UVw>? NELCeIdqdmS3Y3XzJIdtcW:vYTDj[YxtKGGyb4D0c5Nqew>? MlT3NlY5PDh3MkS=
U118MG NHTabW5HfW6ldHnvckBie3OjeR?= NF3RZYUyOi53IN88US=> NYnxNng6TE2VTx?= NIXnXHdjdG:la4Og[4xqd22jIHPlcIwhdWmpcnH0bY9vKGGwZDDpcpZie2m4ZTDndo94fGhicHH0eIVzdg>? MoXlNlY5PDh3MkS=
SF126 M{HhfmZ2dmO2aX;uJIF{e2G7 MlvtNVIvPSEQvF2= MlXOSG1UVw>? MUHicI9kc3NiZ3zpc41iKGOnbHygcYloemG2aX;uJIFv\CCrbo\hd4l3\SCpcn;3eIgheGG2dHXyci=> MYKyOlg1QDV{NB?=

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
p-c-Met / c-Met / p-FAK / p-c-Src / p-Akt / p-S6K / p-S6; 

PubMed: 22639908     


Effect of BMS-777607 on c-Met signaling in PC-3 cells PC-3 cells were treated with indicated doses of BMS-777607 for 1 h (A) or with BMS-777607 (1 μM) for indicated times (B). Whole cell lysates were harvested and analyzed by Western blot, with actin as a loading control. Data represent 1 of 2 independent experiments.

p53 / p21 / Survivin / p-Rb / Rb ; 

PubMed: 24444656     


BMS-777607 increases p21/WAF1 and survivin expression but down-regulates Rb expression. T-47D and ZR-75-1 cells were treated with 5 μM BMS-777607 for different time intervals. Cellular proteins (50 μg per sample) from cell lysates were subjected to Western blot analysis using individual antibodies specific to p53, p21/WAF1, survivin, regular and phospho-Rb. B-actin was used as the loading control.

22639908 24444656
Immunofluorescence
α-tubulin / survivin; 

PubMed: 24444656     


Abnormal accumulation of survivin and its disassociation with condensed DNA and mitotic spindle. Both T-47D and ZR-75-1 cells were treated with 5 μM BMS-777607 for 72 h followed by immunofluorescent analysis using antibodies specific to survivin and α-tubulin. Cells were also stained with DAPI for nuclear DNA. Images shown here are from one of two experiments with similar results.

24444656
In vivo Oral administration of BMS 777607 (6.25-50 mg/kg) significantly reduces tumor volumes of the GTL-16 human tumor xenografts in athymic mice with no observed toxicity. [1] Administration of BMS 777607 (25 mg/kg/day) decreases the number of KHT lung tumor nodules (28.3%), improves the morphological hemorrhage, and significantly impairs the metastatic phenotype in the 6-8 week-old female C3H/HeJ mice injected with rodent fibrosarcoma KHT cells without apparent systemic toxicity compared to the control treatment. A low dose of BMS 777607 (10 mg/kg) also offers a mild but not significant inhibition of lung nodule formation compared to the vehicle control. [3]

Protocol

Kinase Assay:[4]
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Met Kinase Assay:

The kinase reaction consists of baculovirus expressed GST-Met, 3 μg of poly(Glu/Tyr), 0.12 μCi 33P γ-ATP, 1 μM ATP in 30 μL of kinase buffer (20 mM Tris-Cl, 5 mM MnCl2, 0.1 mg/mL BSA, 0.5 mM DTT). Reactions are incubated for 1 hour at 30 °C and stopped by the addition of cold trichloroacetic acid (TCA) to a final concentration of 8%. TCA precipitates are collected onto GF/C unifilter plates using a Filtermate universal harvester, and the filters are quantitated using a TopCount 96-well liquid scintillation counter. Dose response curves are generated to determine the concentration required to inhibit 50% of substrate phosphorylation (IC50). BMS 777607 is dissolved at 10 mM in dimethylsulfoxide (DMSO) and evaluated at 10 concentrations, in duplicate.
Cell Research:[3]
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  • Cell lines: Rodent fibrosarcoma KHT cells
  • Concentrations: Dissolved in DMSO as a stock solution (10 mM), final concentration ~10 μM.
  • Incubation Time: 2, 24 and 96 hours
  • Method: KHT cells are exposed to serial dilution of BMS 777607 for 96 hours, then the MTT assay and trypan blue exclusion are used for the determination of cell proliferation and cell death, respectively. KHT cell colonies are incubated with BMS 777607 for 24 hours and then stained with crystal violet (0.1%) and photographed for the assessment of cell scattering. 2 mm scratch on the confluent KHT cell monolayer is made using a sterilized 1 ml pipette tip followed by treated with BMS-777607 for 24 hours, then the number of cells that have migrated into the denuded area is counted on 4 random fields for the evaluation of cell migration. For the examination of cell invasion, the commercial transwell inserts (8 μm pore membrane) pre-loaded with Matrigel are incubated with serum-free medium in the presence or absence of BMS 777607 at 37 °C for 2 hours to allow rehydration of Matrigel. Then cells suspended in serum-free medium are loaded onto the top chamber (5 × 103/insert) and complete medium (containing 10% FBS) is used in the lower chamber as a chemoattractant. After incubation for 24 hours, the Matrigel is removed and the inserts are stained with crystal violet. Invaded cells on the underside of the filter are photographed and counted.
    (Only for Reference)
Animal Research:[3]
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  • Animal Models: Rodent fibrosarcoma KHT cells are established in female C3H/HeJ mice.
  • Dosages: 10-25 mg/kg.
  • Administration: Oral gavage once daily.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 47 mg/mL (91.63 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
4% DMSO+45% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing. 		5mg/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 512.89
Formula

C25H19ClF2N4O4
CAS No. 1025720-94-8
Storage powder
in solvent
Synonyms N/A
Smiles CCOC1=C(C(=O)N(C=C1)C2=CC=C(C=C2)F)C(=O)NC3=CC(=C(C=C3)OC4=C(C(=NC=C4)N)Cl)F

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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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Frequently Asked Questions

  • Question 1:

    What formulation can we use to dissolve S1561 for mice in vivo study?

  • Answer:

    S1561 BMS-777607 in 1% DMSO+30% polyethylene glycol+1% Tween 80 at 30 mg/ml is a suspension. It is fine for oral gavage. If you are going to use it for injection, please try the following vehicle: 4% DMSO+30% PEG 300+ddH2O. BMS-777607 can be dissolved in it at 5 mg/ml as a clear solution.

selleck catalog

c-Met Signaling Pathway Map

c-Met Inhibitors with Unique Features

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    Crizotinib (PF-02341066) : Approved by FDA for non-small cell lung carcinoma (NSCLC).

  • Newest c-Met Inhibitor

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  • Bemcentinib (R428) New

    Bemcentinib (R428, BGB324) is an inhibitor of Axl with IC50 of 14 nM, >100-fold selective for Axl versus Abl. Selectivty for Axl is also greater than Mer and Tyro3 (50-to-100- fold more selective) and InsR, EGFR, HER2, and PDGFRβ (100- fold more selective).

  • Crizotinib (PF-02341066)

    Crizotinib (PF-02341066) is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nM in cell-based assays, respectively. It is also a potent ROS1 inhibitor with Ki value less than 0.025 nM. Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.

  • Foretinib (GSK1363089)

    Foretinib (GSK1363089, EXEL-2880, XL-880) 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.

  • Capmatinib (INCB28060)

    Capmatinib (INCB28060, INC280, NVP-INC280) is a novel, ATP-competitive inhibitor of c-MET with IC50 of 0.13 nM in a cell-free assay, inactive against RONβ, as well as EGFR and HER-3. Capmatinib (INCB28060) inhibits Wnt/β-catenin and EMT signaling pathways and induces apoptosis in diffuse gastric cancer positive for c-MET amplification. Phase 1.

    Features:Inactive against RONβ, another member of the c-MET RTK family, as well as EGFR and HER-3 (members of the EGFR RTK family).

  • Tivantinib (ARQ 197)

    Tivantinib (ARQ 197) is the first non-ATP-competitive c-Met inhibitor with Ki of 0.355 μM in a cell-free assay, little activity to Ron, and no inhibition to EGFR, InsR, PDGFRα or FGFR1/4. Tivantinib (ARQ 197) induces a G2/M arrest and apoptosis. Phase 3.

    Features:The first selective c-Met inhibitor to be advanced into human clinical trials.

  • PHA-665752

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID