BMS-777607

Catalog No.S1561

BMS-777607 Chemical Structure

Molecular Weight(MW): 512.89

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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In DMSO USD 250 In stock
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Cited by 14 Publications

7 Customer Reviews

  • Numbers of clonogenic cells from L3.6pl cells and CSCs+24/44/ESAin duplicate were counted. Clonogenic growth from the cell control was set as 100%.

    Mol Cancer Ther 2014 13(1), 37-48. BMS-777607 purchased from Selleck.

  • The inhibitory effect of BMS-777607 on survival and proliferation of L3.6pl and CSCs+24/44/ESA was determined by the clonogenic assay. Briefly, L3.6pl cells (6,000 cells/well) in minimum essential media (MEM) with 5% FBS were cultured in duplicate in a 24-well plate and then treated with different amounts of BMS-777607 for 12 days. CSCs+24/44/ESA in stem cell culture media were incubated for 18 days in the ultra-low attachment culture plate coated with a thin layer of 0.2% of agarose to facilitate cell anchored growth. Clonogenic cells were stained with Hema-3 staining solution (Fisher Scientific), photographed using an Olympus BK71 microscope equipped with CCD camera, and counted. The number of clonogenic growth from individual groups is presented.

    Mol Cancer Ther 2014 13(1), 37-48. BMS-777607 purchased from Selleck.

  • Effect of MEK inhibitor BMS-777607 in A549 cells. A549 cells were incubated with increasing concentrations of BMS-777607 for 2 h. The cell lysates were harvested and phosphorylation of indicated proteins was determined by Western blotting.

    2014 Dr.Wang from Southern Medical Hospital. BMS-777607 purchased from Selleck.

  • Mol Oncol 2013 10.1016/j.molonc.2013.12.014. BMS-777607 purchased from Selleck.

  • BMS-777607 increases p21/WAF1 and survivin expression but down-regulates Rb expression. T-47D and ZR-75-1 cells (2×106 cells in 60 mm diameter culture dish) were treated with 5 mM BMS-777607 for different time intervals. Cellular proteins (50 mg 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.

    Mol Oncol 2013 8, 469-82. BMS-777607 purchased from Selleck.

  • Effect of BMS-777607 on growth and survival of breast cancer cells. A, the effect of BMS-777607 on survival and proliferation of MCF-7, ZR-75-1, and T-47D cells was determined by clonogenic assay. Briefly, cells (8,000 cells per well) in RPMI-1640 with 5% FBS were cultured in duplicate in a 24-well plate and then treated with different amounts of BMS-777607 for 10 days. Clonogenic cells were stained with Hema-3 staining solution (Fisher Scientific) and photographed using an Olympus BK71 microscope equipped with CCD camera. B, numbers of clonogenic cells in duplicate from 3 cell lines were counted.

    Acta Pharmacol Sin 2013 34, 1545-53. BMS-777607 purchased from Selleck.

  • IHC for phospho-Neu Y1248 in tumors, 1 hour after lapatinib treatment (day 1, d1), and day 7 (d7), 1 hour after final treatment with BMS-777607. Representative images are shown.

    Cancer Res, 2018, 149:63-76. BMS-777607 purchased from Selleck.

Purity & Quality Control

Choose Selective c-Met Inhibitors

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 M4TpfWtqdmG|ZTDhd5NigQ>? M4XYVGROW09? M{\pNYlvcGmkaYTzJG1mfCCtaX7hd4Uhf2m2aDDJR|UxKG:oIEGwNEBvVQ>? M2LNcVE6OjZyN{Gx
H1993 M{W2Omdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NYXZbJFwhjFyIN88US=> NYf4T5h5TE2VTx?= MoXaTWM2OD1zNUCgcm0> MVexPVI3ODdzMR?=
U87 NVfpfHN5T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= Ml\hglExKM7:TR?= NVS5SFFkTE2VTx?= M1fvb2lEPTB;MU[wJI5O M{i1[|E6OjZyN{Gx
PC-3 NYfD[mQzTnWwY4Tpc44h[XO|YYm= NVzweoxLOC5zIN88US=> MV7EUXNQ NIjTUZdmgGirYnn0d{BqdmirYnn0c5J6KGWoZnXjeEBwdiCKR1[tbY5lfWOnZDDj[YxtKHOlYYT0[ZJqdmd? NX;TbmRsOjB3MUW5OFM>
DU145 NIXEWXFHfW6ldHnvckBie3OjeR?= M3nHVVAvOSEQvF2= NH;KbWJFVVOR NI\QXI1mgGirYnn0d{BqdmirYnn0c5J6KGWoZnXjeEBwdiCKR1[tbY5lfWOnZDDj[YxtKHOlYYT0[ZJqdmd? NYDRVWpEOjB3MUW5OFM>
PC-3 NHWzTW9HfW6ldHnvckBie3OjeR?= MmT1NE4xOSEQvF2= NWfa[ItVTE2VTx?= Mo\nd5VxeHKnc4Pld{BJT0ZvaX7keYNm\CClZXzsJI1q\3KjdHnvci=> NH;lfIEzODVzNUm0Ny=>
DU145 NEnp[XNHfW6ldHnvckBie3OjeR?= NWD2VppwOC5yMTFOwG0> M{X3NWROW09? NGLSfnV{fXCycnXzd4V{KEiJRj3pcoR2[2WmIHPlcIwhdWmpcnH0bY9v MkP3NlA2OTV7NEO=
PC-3 M165TmZ2dmO2aX;uJIF{e2G7 NYS5UYpKOC5zIN88US=> MXfEUXNQ MlnUbY1x[Wm{czDIS2YudWWmaXH0[YQh[2WubDDpcpZie2mxbh?= NXfHTZJ2OjB3MUW5OFM>
DU145 Mk\mSpVv[3Srb36gZZN{[Xl? MYKwMlEh|ryP NXHZd4tYTE2VTx?= NWnJPHV4cW2yYXnyd{BJT0ZvbXXkbYF1\WRiY3XscEBqdn[jc3nvci=> M3PpelIxPTF3OUSz
PC-3 MX3Hdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MnfrglExKM7:TR?= M4K3WmROW09? M16xb5Jm\HWlZYOgZ4VtdCCycn;sbYZmemG2aX;u NIqzR44zODVzNUm0Ny=>
KHT MlXYT4lv[XOnIHHzd4F6 MmjDSG1UVw>? NVf0fGlE[myxY3vzJJRp\SClLV3leEB{cWewYXzpcocheGG2aIfhfUB4cXSqIFnDOVAhd2ZiMUCgcm0> MVOyNlI5PjV{Mx?=
KHT MojOSpVv[3Srb36gZZN{[Xl? NWjpbJRuhjFizszN M2C2SmROW09? NVvHPIlWeHKndnXueJMhe3CxboThcoVwfXNiS1jUJINmdGxic3PheJRmemmwZzD3bZRpKEmFNUCgc4YhOC5zLUCuOUDPxE1? MkTXNlIzQDZ3MkO=
KHT NF\CfGpHfW6ldHnvckBie3OjeR?= M4rJeJ4xNjVizszN NUPLSpVUTE2VTx?= M{L6UolvcGmkaYTzJINmdGxibXnndoF1cW:w M1HGdFIzOjh4NUKz
KHT M4\3VmZ2dmO2aX;uJIF{e2G7 NU\qXFBChjBwNTFOwG0> MYPEUXNQ MXjpcohq[mm2czDj[YxtKGmwdnHzbY9v NYXie21{OjJ{OE[1NlM>
KHT M3yyPWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MoWxglExKM7:TR?= M1zKUGROW09? M{G1eolvcGmkaYTzJGtJXCClZXzsJJBzd2yrZnXyZZRqd25? NEHNZlQzOjJ6NkWyNy=>
T-47D M1G0T2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M2rETZ42KM7:TR?= MWrEUXNQ NXziNYx4cW6qaXLpeJMh[2WubDDwdo9tcW[ncnH0bY9v MWmyN|Q3QDV{OR?=
ZR-75-1 MVXHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? Mm[1glUh|ryP MYrEUXNQ NW\BfYY{cW6qaXLpeJMh[2WubDDwdo9tcW[ncnH0bY9v MW[yN|Q3QDV{OR?=
T-47D MUHGeY5kfGmxbjDhd5NigQ>? MUexNEDPxE1? M2XaWmROW09? NFvVdZNKdmS3Y3XzJJBwdHmybH;p[Jkh[nliOE[gKS=> M2PlNVI{PDZ6NUK5
ZR-75-1 MonvSpVv[3Srb36gZZN{[Xl? NX74W49ROTBizszN M3zyT2ROW09? MUnJcoR2[2W|IIDvcJlxdG:rZImgZpkhQDhn NV7EO4V{OjN2Nki1Nlk>
T-47D M2DxcGZ2dmO2aX;uJIF{e2G7 MVWxNEDPxE1? MlLmSG1UVw>? MXfpcohq[mm2czDBWXJMNUJiZoXuZ5Rqd25iYX7kJIlv\HWlZYOgbZR{KHC{b4TlbY4h\GWpcnHkZZRqd25? NWrpR41tOjN2Nki1Nlk>
CHRF MWrGeY5kfGmxbjDhd5NigQ>? M{TZVVExKM7:TR?= NWDtW5B[TE2VTx?= MWXpcohq[mm2czDj[YxtKGSrdnnzbY9v MoO2NlU{ODR7MEC=
HPDE NUe3eZdQTnWwY4Tpc44h[XO|YYm= MUCxNEDPxE1? NVjZZnpCTE2VTx?= MnLHZoxw[2u|IHPvcpN1cXS3dHn2[UBi[3SrdnH0bY9vKGGwZDDk[YNz\WG|ZXSgRWtVKHOrZ37hcIlv\w>? NFT0c|kzPjR5N{OxOC=>
U118MG NIS2O|RMcW6jc3WgZZN{[Xl? MUL+N{DPxE1? MlrxSG1UVw>? NH;nZYVjdG:la4OgRXhNKHCqb4PwbI9zgWyjdHnvci=> NYrqN4UxOjZ6NEi1NlQ>
SF126 NHPiOYZMcW6jc3WgZZN{[Xl? M2[4XJ4{KM7:TR?= NWLhRY1DTE2VTx?= M4nVZYJtd2OtczDBXGwheGixc4Doc5J6dGG2aX;u MYSyOlg1QDV{NB?=
U118MG NHfDSmxEgXSxeHnjbZR6KGG|c3H5 M320elEzNjVizszN MmWySG1UVw>? NEHBVpZl\WO{ZXHz[ZMh\2yrb33hJINmdGxidnnhZoltcXS7 M2XwSlI3QDR6NUK0
SF126 MnfTR5l1d3irY3n0fUBie3OjeR?= MljzNVIvPSEQvF2= NVG4UoxjTE2VTx?= NVv2cndy\GWlcnXhd4V{KGeuaX;tZUBk\WyuII\pZYJqdGm2eR?= MXuyOlg1QDV{NB?=
U118MG NHXPTGFCeG:ydH;zbZMh[XO|YYm= MUexNk42KM7:TR?= NHXPRpVFVVOR NFTEfI9qdmS3Y3XzJIdtcW:vYTDj[YxtKGGyb4D0c5Nqew>? NYLk[o5ROjZ6NEi1NlQ>
SF126 NVOySmhiSXCxcITvd4l{KGG|c3H5 NGLUUJgyOi53IN88US=> MkTHSG1UVw>? MYLpcoR2[2W|IHfsbY9u[SClZXzsJIFxd3C2b4Ppdy=> MUOyOlg1QDV{NB?=
U118MG M2POWWZ2dmO2aX;uJIF{e2G7 NWnCRYszOTJwNTFOwG0> M2fmOmROW09? M{jYc4Jtd2OtczDncIlwdWFiY3XscEBucWe{YYTpc44h[W6mIHnueoF{cX[nIHfyc5d1cCCyYYT0[ZJv NIG3d5UzPjh2OEWyOC=>
SF126 M2rVcWZ2dmO2aX;uJIF{e2G7 NF;IflQyOi53IN88US=> NUDI[Vd[TE2VTx?= M2jjdYJtd2OtczDncIlwdWFiY3XscEBucWe{YYTpc44h[W6mIHnueoF{cX[nIHfyc5d1cCCyYYT0[ZJv NY\DWG53OjZ6NEi1NlQ>

... 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]
+ Expand

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]
+ Expand
  • 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]
+ Expand
  • Animal Models: Rodent fibrosarcoma KHT cells are established in female C3H/HeJ mice.
  • Formulation: Dissolved in DMSO as a stock solution (10 mM).
  • 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

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01721148 Completed Malignant Solid Tumour Aslan Pharmaceuticals October 2012 Phase 1
NCT01721148 Completed Malignant Solid Tumour Aslan Pharmaceuticals October 2012 Phase 1
NCT00605618 Completed Advanced Solid Tumors Bristol-Myers Squibb March 2008 Phase 1|Phase 2
NCT00605618 Completed Advanced Solid Tumors Bristol-Myers Squibb March 2008 Phase 1|Phase 2

Tech Support

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.

Handling Instructions

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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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID