PHA-665752

Catalog No.S1070

PHA-665752 is a potent, selective and ATP-competitive c-Met inhibitor with IC50 of 9 nM in cell-free assays, >50-fold selectivity for c-Met than RTKs or STKs.

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PHA-665752 Chemical Structure

PHA-665752 Chemical Structure
Molecular Weight: 641.61

Validation & Quality Control

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Quality Control & MSDS

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Product Information

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  • Research Area
  • Inhibition Profile
  • PHA-665752 Mechanism

Product Description

Biological Activity

Description PHA-665752 is a potent, selective and ATP-competitive c-Met inhibitor with IC50 of 9 nM in cell-free assays, >50-fold selectivity for c-Met than RTKs or STKs.
Targets c-Met [1]
(Cell-free assay)
RON [1]
(Cell-free assay)
Flk1 [1]
(Cell-free assay)
c-Abl [1]
(Cell-free assay)

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IC50 9 nM 68 nM 200 nM 1.4 μM
In vitro PHA-665752 significantly inhibits c-Met kinase activity with Ki of 4 nM, and exhibits >50-fold selectivity for c-Met compared with various tyrosine and serine-threonine kinases. PHA-665752 potently inhibits the HGF-stimulated c-Met autophosphorylation with IC50 of 25-50 nM. PHA-665752 also significantly blocks HGF- and c-Met-dependent functions such as cell motility and cell proliferation with IC50 of 40-50 nM and 18-42 nM, respectively. In addition, PHA-665752 potently inhibits HGF-stimulated or constitutive phosphorylation of mediators of downstream of c-Met such as Gab-1, ERK, Akt, STAT3, PLC-γ, and FAK in multiple tumor cell lines. [1] PHA-665752 inhibits cell growth in TPR-MET-transformed BaF3 cells with IC50 of <60 nM, and inhibits constitutive cell motility and migration by 92.5% at 0.2 μM. Inhibition of c-Met by PHA665752 (0.2 μM) also induces cell apoptosis of 33.1% and G1 cell cycle arrest with cells in G1 phase increasing from 42.4% to 77.0%. PHA665752 can cooperate with rapamycin to inhibit cell growth of TPR-MET-transformed BaF3 cells and non-small cell lung cancer H441 cells. [2]
Cell Data
Cell LinesAssay TypeConcentrationIncubation TimeFormulationActivity DescriptionPMID
NCI-SNU-5MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?NH3obXVKSzVyPUCuNVI{PzVizszNMWPTRW5ITVJ?
LB2241-RCCM1XEXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7NETjVXJKSzVyPUCuNVU4ODJizszNNUj2VnlZW0GQR1XS
KINGS-1M13BPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7NIK3bmpKSzVyPUCuN|U6OTFizszNMkCxV2FPT0WU
ALL-POM1vneGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7M2HOVmlEPTB;MD64NVI4PyEQvF2=NWfKUVNQW0GQR1XS
SK-LMS-1M4n3dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7NHXnV2tKSzVyPUCuPFk5PDZizszNNFfLUYdUSU6JRWK=
MV-4-11Mk\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?NHrjVYxKSzVyPUGuNlk1PyEQvF2=NXGyRmNJW0GQR1XS
SUP-T1MnPaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?M3HtUmlEPTB;Mj6xN|k3PCEQvF2=M2e3WnNCVkeHUh?=
MRK-nu-1MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?MVTJR|UxRTJwNECwOVYh|ryPMUDTRW5ITVJ?
ES1NWHKUohXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=NX\BWnZOUUN3ME2zMlM1QDZ4IN88US=>MXfTRW5ITVJ?
NOS-1M{PEUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7NULmU4R4UUN3ME20MlM6QDZ5IN88US=>NYTkdVd4W0GQR1XS
KM12MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?NYPqd2lMUUN3ME20MlQyQCEQvF2=MnzXV2FPT0WU
BeckerNGjQO3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=MX;JR|UxRTVwMkS2OkDPxE1?NWjhdXpmW0GQR1XS
NCI-SNU-1MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?MUjJR|UxRTVwNkO3N|Mh|ryPNVTNO5dqW0GQR1XS
EW-22MnnQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?NYDiN2dWUUN3ME23Mlc{PjF2IN88US=>M3zpbnNCVkeHUh?=
ES6MlH3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?MnzpTWM2OD15LkixPVUh|ryPNXTNfJEzW0GQR1XS
A498MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?NVvUdWVpUUN3ME24MlI5PDR4IN88US=>MUjTRW5ITVJ?
EW-16MoWwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?M{LD[GlEPTB;OT62OVQ{KM7:TR?=Mn3vV2FPT0WU
CTV-1MkX6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?MnLhTWM2OD17Lki1NFI1KM7:TR?=NXz3bnlxW0GQR1XS
ETK-1M2DUZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7NYTsXIhZUUN3ME2xNE4zQTNzIN88US=>NULlcmhOW0GQR1XS
NCI-H1395NWT1SYtIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=MmC1TWM2OD1zMD64NFI1KM7:TR?=M{jmR3NCVkeHUh?=
DOHH-2M3zXOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7NF\jSFFKSzVyPUGwMlkzPjRizszNNUO0cmNqW0GQR1XS
GI-1NXzXPI9IT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=Mk\ZTWM2OD1zMT64OVk3KM7:TR?=NWfVUZY2W0GQR1XS
HT-144MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?M3X6S2lEPTB;MUSuNlE3OyEQvF2=M{LG[XNCVkeHUh?=
ES5MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?MlfNTWM2OD1zND60Olch|ryPMk\1V2FPT0WU
NALM-6NWnlNmJsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=Mn;oTWM2OD1zNT6yNVk3KM7:TR?=MVnTRW5ITVJ?
KNS-81-FDMlPJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?M{ThVWlEPTB;MUWuOVg1QSEQvF2=M4LGTXNCVkeHUh?=
TE-15MlPaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?MYHJR|UxRTF4LkW3O|Eh|ryPMWjTRW5ITVJ?
SCC-15MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?MkP2TWM2OD1zOD6zOFk5KM7:TR?=MkLnV2FPT0WU
EoL-1-cellNVL4XWVMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=MVrJR|UxRTF6LkS1OFUh|ryPNFfGOVdUSU6JRWK=
NCI-H720NF3UcHlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=M3;mNmlEPTB;MUiuO|cyKM7:TR?=NX;vd2IxW0GQR1XS
NB14MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?MXrJR|UxRTF7LkW0NlUh|ryPNF33XplUSU6JRWK=
KE-37M1jpe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7NEW0bnJKSzVyPUG5MlgzOzNizszNNYP1WnBLW0GQR1XS
LXF-289M{HI[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7Mn\TTWM2OD1zOT64OlI6KM7:TR?=NVjHdJJoW0GQR1XS
RPMI-8402NIHPb49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=NHnTWYVKSzVyPUKwMlMzPjlizszNNIrTTGlUSU6JRWK=
SK-N-DZNVr2SIN5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=NIXZe4tKSzVyPUKxMlIyOzFizszNNHHMZY1USU6JRWK=
ACNMlvGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?M{\GR2lEPTB;MkKuNlQ6PyEQvF2=MnfUV2FPT0WU
TE-11M4HUbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7M1OxSGlEPTB;Mk[uNFY6KM7:TR?=M3PyPXNCVkeHUh?=
COLO-800NF;oPJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=NYfEW2RwUUN3ME2yO{4yPyEQvF2=M4j0c3NCVkeHUh?=
MOLT-13NIThS3ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=NFv6VWFKSzVyPUK3MlE5PDdizszNNF3HWlBUSU6JRWK=
697NGDJdIlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=NYPT[XFmUUN3ME2yPE44PjN|IN88US=>NHu3TGtUSU6JRWK=
VA-ES-BJNV\COoVMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=MW\JR|UxRTJ7LkO3Nlkh|ryPMUfTRW5ITVJ?
EW-13M1P2S2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7NHTWeItKSzVyPUK5MlUxPDVizszNMmrCV2FPT0WU
NB7MojJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?NG\tb3JKSzVyPUOyMlI3PjVizszNNVTud4k6W0GQR1XS
MONO-MAC-6NWnHe2J2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=M3XmWmlEPTB;M{KuPFc6PSEQvF2=MWHTRW5ITVJ?
SW962MmP0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?NW\2fmxlUUN3ME2zN{41PTF|IN88US=>NHXRelVUSU6JRWK=
KS-1NULGVZJQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=NH;BVGNKSzVyPUOzMlk1QDFizszNNWLNd4Y3W0GQR1XS
KU812MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?MUXJR|UxRTN2LkW3NFIh|ryPM{TX[nNCVkeHUh?=
IMR-5MnTWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?NEjJOo9KSzVyPUO3MlQ{OThizszNMorlV2FPT0WU
BC-1NFztUmJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=MmX0TWM2OD1|OD6wN|Mh|ryPM{myfHNCVkeHUh?=
NCI-H510ANF3LUGhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=NYfBfI1VUUN3ME2zPE4zODN{IN88US=>NEXkXnlUSU6JRWK=
EW-18MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?MnfpTWM2OD12MD64N|A{KM7:TR?=NHO4RpZUSU6JRWK=
CCRF-CEMNHnwfVZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=M{PjOWlEPTB;NEKuNlc6PyEQvF2=NYPkcFVrW0GQR1XS
HHMlOzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?NFPmNnVKSzVyPUSzMlUxPjlizszNNHrrVnFUSU6JRWK=
NCI-H2171NWjsRYRqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm=MUTJR|UxRTR4LkCyO|Ih|ryPMl7kV2FPT0WU
LC-2-adNI[xSmFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=NX31WnJvUUN3ME20PU4yPDF|IN88US=>NUi2bldEW0GQR1XS

... Click to View More Cell Line Experimental Data

In vivo Administration of PHA-665752 induces a dose-dependent tumor growth inhibition of S114 xenografts by 20 %, 39% and 68%, at dose of 7.5, 15, and 30 mg/kg/day, respectively. [1] PHA665752 treatment significantly reduces the tumor growth of NCI-H69, NCI-H441 and A549 in mouse xenografts by 99%, 75%, and 59%, respectively. PHA665752 also significantly inhibits angiogenesis by >85%, due to decreasing the production of vascular endothelial growth factor and increasing the production of the angiogenesis inhibitor thrombospondin-1. [3]
Features

Protocol(Only for Reference)

Kinase Assay: [1]

In vitro enzyme assay The c-Met kinase domain GST-fusion protein is used for the c-Met assay. The IC50 value of PHA-665752 for the inhibition of c-Met is based on phosphorylation of kinase peptide substrates or poly-glu-tyr in the presence of ATP and divalent cation (MgCl2 or MnCl2 10-20 mM). The linear range (i.e., the time period over which the rate remains equivalent to the initial rate) is determined for c-Met, and the kinetic measurement and IC50 determination are performed within this range.

Cell Assay: [1]

Cell lines S114, GTL-16, NCI-H441, and BxPC-3
Concentrations Dissolved in DMSO, final concentrations ~10 μM
Incubation Time 18, or 72 hours
Method For proliferation assays, cells are grown in medium with 0.1% FBS for 48 hours after which they are treated with various concentrations of PHA-665752 in HGF (50 ng/mL) in a medium containing 2% FBS. After 18 hours, cells are incubated with BrdUrd for 1 hour, fixed, and stained with anti-BrdUrd peroxidase-conjugated antibody, and plates are read at 630 nm. For apoptosis assays, cells are grown in medium with 2% FBS in presence and absence of HGF (50 ng/mL) and various concentrations of PHA-665752 for 72 hours. After 72 hours, a mixture containing ethidium bromide and acridine orange is added, and apoptotic cells (bright orange cells or cell fragments) are counted by fluorescence microscopy.

Animal Study: [1]

Animal Models Female athymic mice (nu/nu) bearing S114 or GTL-16 tumor xenografts
Formulation Formulated in vehicle (L-lactate (pH 4.8) and 10% polyethylene glycol)
Dosages ~30 mg/kg/day
Administration Injection via bolus i.v.

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)0.020.151.80.40.0810
Body Surface Area (m2)0.0070.0250.150.050.020.5
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)
1

References

[1] Christensen JG, et al. Cancer Res, 2003, 63(21), 7345-7355.

[2] Ma PC, et al. Clin Cancer Res, 2005, 11(6), 2312-2319.

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Chemical Information

Download PHA-665752 SDF
Molecular Weight (MW) 641.61
Formula

C32H34Cl2N4O4S

CAS No. 477575-56-7
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms N/A
Solubility (25°C) * In vitro DMSO 128 mg/mL (199.49 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 2% DMSO+castor oil 5mg/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 Name (R,Z)-5-(2,6-dichlorobenzylsulfonyl)-3-((3,5-dimethyl-4-(2-(pyrrolidin-1-ylmethyl)pyrrolidine-1-carbonyl)-1H-pyrrol-2-yl)methylene)indolin-2-one

Customer Product Validation(5)


Click to enlarge
Rating
Source Cancer Res 2014 74, 253-62. PHA-665752 purchased from Selleck
Method Immunohistochemical staining
Cell Lines
Concentrations 12.5 mg/kg
Incubation Time 22 days
Results Although a single treatment with PHA-665752, produced a slight decrease in tumor growth, combined treatment resulted in substantial growth inhibition (A). The inhibition of tumor growth persisted in the combination groups for 10 days after the discontinuation of the drugs. Consistent with the observations about tumor size, the combination resume (gefitinib plus PHA-665752 and gefitinib plus NPS-1034) led to the inhibition of tumor proliferation and the induction of apoptosis. Moreover, gefitinib plus PHA-665752 also induced increased apoptosis of tumor growth (B).

Click to enlarge
Rating
Source Clin Cancer Res 2014 20, 4806-15. PHA-665752 purchased from Selleck
Method Western blot analyses
Cell Lines NSCLC cells
Concentrations 1 uM
Incubation Time 6 h
Results All cell lines treated with PHA-665,752 showed a dramatic decrease of phospho-MET as compared with the corresponding untreated cells but only H1993 cells showed a concomitant decrease of phospho-HER3, phospho-AKT, phospho-ERK, and cyclin D1. Also, a strong inhibition of the EGFR pathway was observed in HCC827 cells when treated with erlotinib and not with MET inhibitor (A and B).

Click to enlarge
Rating
Source Biochem Biophys Res Commun 2014 449(1), 49-54. PHA-665752 purchased from Selleck
Method Immunofluorescence
Cell Lines CNE-1, HONE-1 cells
Concentrations 1 uM
Incubation Time 24 h
Results CNE-1 and HONE-1 cells treated with PHA-665752 in combination with IR led to a dramatic persistence of the c-H2AX foci at 24 h post-IR administration compared with exposure to IR alone. Cells treated with HGF and IR led to a less persistence of c-H2AX foci compared with exposure to IR alone, whereas the administration of PHA-665752 reversed the effect induced by HGF.

Click to enlarge
Rating
Source Biochem Biophys Res Commun 2014 449, 49-54. PHA-665752 purchased from Selleck
Method Immunofluorescence
Cell Lines CNE-1/HONE-1 cells
Concentrations 1 uM
Incubation Time 24 h
Results CNE-1 and HONE-1 cells treated with PHA-665752 in combination with IR led to a dramatic persistence of the γ-H2AX foci at 24 h post-IR administration compared with exposure to IR alone. Cells treated with HGF and IR led to a less persistence of γ-H2AX foci compared with exposure to IR alone, whereas the administration of PHA-665752 reversed the effect induced by HGF.

Click to enlarge
Rating
Source Dr. Zhang of Tianjin Medical University. PHA-665752 purchased from Selleck
Method Western blot
Cell Lines
Concentrations 0-100 μM
Incubation Time
Results PHA-665752 treatment resulted in a reduction of c-Met phosphorylation in a concentration-dependent manner.

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.

Tel: +1-832-582-8158 Ext:3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
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