Tivantinib

Synonyms: ARQ 197

Tivantinib 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.

Tivantinib Chemical Structure

Tivantinib Chemical Structure

CAS No. 905854-02-6

Purity & Quality Control

Tivantinib Related Products

Signaling Pathway

Cell Data

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MNK-45 Kinase assay ~10 μM inhibits c-Met phosphorylation and downstream c-Met signaling pathways
HT29 Kinase assay ~10 μM inhibits c-Met phosphorylation and downstream c-Met signaling pathways
MDA-MB-231 Kinase assay ~10 μM inhibits c-Met phosphorylation and downstream c-Met signaling pathways
NCI-H441 Kinase assay ~10 μM inhibits c-Met phosphorylation and downstream c-Met signaling pathways
SK-MEL-28 Growth inhibitory assay 33 μM IC50>33 μM
NCI-H661 Growth inhibitory assay 33 μM IC50>33 μM
NCI-H446 Growth inhibitory assay 33 μM IC50=7 μM
MDA-MB-231 Growth inhibitory assay 33 μM IC50=0.55 μM
DLD-1 Growth inhibitory assay 33 μM IC50=0.53 μM
A549 Growth inhibitory assay 33 μM IC50=0.59 μM
SK-OV-3 Growth inhibitory assay 33 μM IC50=0.66 μM
NCI-H460 Growth inhibitory assay 33 μM IC50=0.6 μM
A375 Growth inhibitory assay 33 μM IC50=0.42 μM
NCI-H441 Growth inhibitory assay 33 μM IC50=0.3 μM
HT29 Growth inhibitory assay 33 μM IC50=0.49 μM
MKN-45 Growth inhibitory assay 33 μM IC50=0.58 μM
HT29 Apoptosis assay ~10 μM significantly induces apoptosis by 80-90%.
MKN-45 Apoptosis assay ~10 μM significantly induces apoptosis by 80-90%.
MDA-MB-231 Apoptosis assay ~10 μM modestly induces apoptosis by 35%.
MDA-MB-231/TGL Growth inhibitory assay ~100 μM GI50=1.2 μM
1833/TGL Growth inhibitory assay ~100 μM GI50=3.7 μM
EBC1 Cytotoxic assay ~10 μM inhibits the cell growth.
SNU638 Cytotoxic assay ~10 μM inhibits the cell growth.
A549 Cytotoxic assay ~10 μM not affect
H460 Cytotoxic assay ~10 μM not affect
HCC827 Cytotoxic assay ~10 μM not affect
A549 Function assay 10 μM disrupts microtubule
EBC1 Function assay 10 μM disrupts microtubule
H460 Function assay 10 μM inhibits tubulin polymerization
K562/VCR Cytotoxic assay ~10 μM shows cytotoxic activity
CEM/VBL Cytotoxic assay ~10 μM shows cytotoxic activity
U266 Cytotoxic assay ~3 μM  IC50=1.1 μM
OPM-2 Cytotoxic assay ~3 μM  IC50=1.8 μM
MM.1S Cytotoxic assay ~3 μM  IC50=1.6 μM
MM.1R Growth inhibitory assay 3 μM  inhibits cell growth by 49%
RPMI-8226 Cytotoxic assay ~3 μM  IC50=0.9 μM
ANBL-6 Cytotoxic assay 1 μM  induces cell death by more than 50%
ANLB-6/V10R Cytotoxic assay 1 μM  induces cell death by more than 50%
KAS-6/1 Cytotoxic assay 1 μM  induces cell death by more than 50%
KAS-6/V10R Cytotoxic assay 1 μM  induces cell death by more than 50%
KAS-6/R10R Cytotoxic assay 1 μM  induces cell death by more than 50%
8226/S Growth inhibitory assay 3 μM  inhibits cell growth by 54%
8226/LR-5 Growth inhibitory assay 3 μM  inhibits cell growth by 54%
Huh7 Cytotoxic assay ~4.8 μM  DMSO IC50=9.9 nM
Hep3B Cytotoxic assay ~4.8 μM  DMSO IC50=448.7 nM
HepG2 Cytotoxic assay ~4.8 μM  DMSO IC50=139.77 nM
Chang Cytotoxic assay ~4.8 μM  DMSO IC50=448.7 nM
Huh7 Function assay 1.6 μM  DMSO causes a G2/M cell cycle arrest
Hep3B Function assay 1.6 μM  DMSO causes a G2/M cell cycle arrest
HepG2 Function assay 1.6 μM  DMSO causes a G2/M cell cycle arrest
Chang Function assay 1.6 μM  DMSO causes a G2/M cell cycle arrest
MHCC97L Growth inhibitory assay ~10 μM DMSO IC50=315 nM
MHCC97H Growth inhibitory assay ~10 μM DMSO IC50=368  nM
Huh7 Growth inhibitory assay ~10 μM DMSO IC50=265 nM
HepG2 Growth inhibitory assay ~10 μM DMSO IC50=392 nM
MHCC97L Function assay 1 μM  DMSO induces microtubules depolymerization
Huh7 Function assay 1 μM  DMSO induces microtubules depolymerization
MHCC97L Apoptosis assay 1 μM  DMSO induces apoptosis
Huh7 Apoptosis assay 1 μM  DMSO induces apoptosis
C3H 10T1/2 mouse fibroblasts Kinase assay 25 μM DMSO reduces Histone H3 and H4 acetylation levels 
H23 Growth inhibitory assay 25 μM DMSO significantly inhibits cell growth.
WM35 Growth inhibitory assay 10 μM DMSO significantly inhibits cell growth.
NIH 3T3 Growth inhibitory assay 10 μM DMSO does not have a significant inhibitory effect
H838 Growth inhibitory assay 10 μM DMSO does not have a significant inhibitory effect
H1395 Growth inhibitory assay 10 μM DMSO does not have a significant inhibitory effect
Quiescent S2 Kinase assay 30 μM DMSO completely abrogates TSA-induced hyperacetylation of H3K4me3 histones
PC3 Apoptosis assay 20 μM DMSO induces apoptosis
Du145 Apoptosis assay 20 μM DMSO induces apoptosis
LNCaP Apoptosis assay 20 μM DMSO induces apoptosis
LAPC-4 Apoptosis assay 20 μM DMSO induces apoptosis
LNCaP Function assay 20 μM DMSO decreases PSA secretion and p65 expression levels
LAPC-4 Function assay 20 μM DMSO decreases PSA secretion and p65 expression levels
Kasumi-1 Growth inhibitory assay ~50 μM DMSO inhibits cell proliferation
SKNO-1 Growth inhibitory assay ~50 μM DMSO inhibits cell proliferation
Kasumi-1 Kinase assay ~10 μM DMSO reduces expression of acetylated histone H3, c-kit and bcl-2
SKNO-1 Kinase assay ~10 μM DMSO reduces expression of acetylated histone H3, c-kit and bcl-2
A549 Function assay 10 μM DMSO enhances mitotic catastrophe
NRK-52E Function assay 10 μM DMSO inhibits Ang II-induced STAT3 nuclear translocation and the expression of TGF-β1, collagen IV and fibronectin
PC12 Growth inhibitory assay ~12.5 μM DMSO prevents TSA-induced neurite formation
HPMCs Function assay reverses epithelial to mesenchymal transition of human peritoneal mesothelial cells
A549 Function assay ~50 μM DMSO affects the viral life cycle and host response
RAW264.7 Function assay ~30 μM DMSO reduces pro-inflammatory gene expression
MEMM Kinase assay 15 µM DMSO decreases acetylation of histone H3
MEMM Growth inhibitory assay ~20 µM DMSO inhibits cell proliferation
MEMM Apoptosis assay 15 µM DMSO induces the presence of the apoptosis protein, cleaved Caspase-3
T47D Growth inhibitory assay 10 μM DMSO IC50=72 nM
ZR-75-1 Growth inhibitory assay 10 μM DMSO IC50=79 nM
BT474 Growth inhibitory assay 10 μM DMSO IC50=86 nM
HCC1954 Growth inhibitory assay 10 μM DMSO IC50=119 nM
MDA-MB-453 Growth inhibitory assay 10 μM DMSO IC50=975 nM
MDA-MB-468 Growth inhibitory assay 10 μM DMSO IC50=3208 nM
SkBr3 Growth inhibitory assay 10 μM DMSO IC50>10,000 nM
MDA-MB-231 Growth inhibitory assay 10 μM DMSO IC50>10,000 nM
HCT116 Growth inhibitory assay 10 μM DMSO IC50=5836 nM
HT29 Growth inhibitory assay 10 μM DMSO IC50>10,000 nM
HFF Growth inhibitory assay 10 μM DMSO IC50=7615 nM
HN5 Growth inhibitory assay 10 μM DMSO IC50>10,000 nM
786-0 Growth inhibitory assay 10 μM DMSO IC50=4009 nM
H157 Growth inhibitory assay 10 μM DMSO IC50=2642 nM
NCI-H460 Growth inhibitory assay 10 μM DMSO IC50>2,500 nM
SKOV-3 Growth inhibitory assay 10 μM DMSO IC50=2126 nM
OVCAR-3 Growth inhibitory assay 10 μM DMSO IC50=2918 nM
BXPC3 Growth inhibitory assay 10 μM DMSO IC50=3141 nM
MiaPaCa Growth inhibitory assay 10 μM DMSO IC50=5433 nM
PANC-1 Growth inhibitory assay 10 μM DMSO IC50=8681 nM
LNCaP Growth inhibitory assay 10 μM DMSO IC50=147 nM
DU145 Growth inhibitory assay 10 μM DMSO IC50=3812 nM
PC3 Growth inhibitory assay 10 μM DMSO IC50>10,000 nM
BT474 Kinase assay 10 μM DMSO inhibits pGSK3β with IC50 of 160 nM
786-0 Kinase assay 10 μM DMSO inhibits pGSK3β with IC50 of 150 nM
LNCaP Kinase assay 10 μM DMSO inhibits pGSK3β with IC50 of 43 nM
PC3 Kinase assay 10 μM DMSO inhibits pGSK3β with IC50 of 49 nM
KARPAS-231 Growth inhibitory assay 10 μM DMSO EC50=41 nM
CCRFSB Growth inhibitory assay 10 μM DMSO EC50=155 nM
SUP B15 Growth inhibitory assay 10 μM DMSO EC50=197 nM
SD-1 Growth inhibitory assay 10 μM DMSO EC50=320 nM
RS4;11 Growth inhibitory assay 10 μM DMSO EC50=654 nM
MN-60 Growth inhibitory assay 10 μM DMSO EC50=3602 nM
Tanoue Growth inhibitory assay 10 μM DMSO EC50=4517 nM
RCH-ACV Growth inhibitory assay 10 μM DMSO EC50=152 nM
SEM Growth inhibitory assay 10 μM DMSO EC50=202 nM
KASUMI-2 Growth inhibitory assay 10 μM DMSO EC50=225 nM
REH Growth inhibitory assay 10 μM DMSO EC50=288 nM
697 Growth inhibitory assay 10 μM DMSO EC50=338 nM
NALM-6 Growth inhibitory assay 10 μM DMSO EC50=421 nM
MHH-CALL–3 Growth inhibitory assay 10 μM DMSO EC50=812 nM
MHH-CALL–2 Growth inhibitory assay 10 μM DMSO EC50=2114 nM
J.GAMMA-1 Growth inhibitory assay 10 μM DMSO EC50=65 nM
JR45.01 Growth inhibitory assay 10 μM DMSO EC50=68 nM
A3 Growth inhibitory assay 10 μM DMSO EC50=69 nM
I 2.1 Growth inhibitory assay 10 μM DMSO EC50=73 nM
MOLT-3 Growth inhibitory assay 10 μM DMSO EC50=74 nM
P116 Growth inhibitory assay 10 μM DMSO EC50=78 nM
J.Cam1.6 Growth inhibitory assay 10 μM DMSO EC50=79 nM
I 9.2 Growth inhibitory assay 10 μM DMSO EC50=80 nM
LOUCY Growth inhibitory assay 10 μM DMSO EC50=117 nM
J.RT3-T3.5 Growth inhibitory assay 10 μM DMSO EC50=123 nM
800000 Growth inhibitory assay 10 μM DMSO EC50=163 nM
Jurkat Growth inhibitory assay 10 μM DMSO EC50=225 nM
MOLT-4 Growth inhibitory assay 10 μM DMSO EC50=232 nM
Molt-16 Growth inhibitory assay 10 μM DMSO EC50=241 nM
CEM/C3 Growth inhibitory assay 10 μM DMSO EC50=257 nM
CEM/C2 Growth inhibitory assay 10 μM DMSO EC50=271 nM
CCRFCEM Growth inhibitory assay 10 μM DMSO EC50=327 nM
CEM/C1 Growth inhibitory assay 10 μM DMSO EC50=382 nM
SUPTI[VB] Growth inhibitory assay 10 μM DMSO EC50=619 nM
CCRF–HSB-2 Growth inhibitory assay 10 μM DMSO EC50=2117 nM
I 2.1 Apoptosis assay 10 μM DMSO induces apoptosis
I 9.2 Apoptosis assay 10 μM DMSO induces apoptosis
A3 Apoptosis assay 10 μM DMSO induces apoptosis
RD Growth inhibitory assay 10 μM IC50>10 μM
Rh41 Growth inhibitory assay 10 μM IC50=33.8 nM
Rh18 Growth inhibitory assay 10 μM IC50=303 nM
Rh30 Growth inhibitory assay 10 μM IC50=4.81 μM
BT-12 Growth inhibitory assay 10 μM IC50>10 μM
CHLA-266 Growth inhibitory assay 10 μM IC50=1.22 μM
TC-71 Growth inhibitory assay 10 μM IC50=2.52 μM
CHLA-9 Growth inhibitory assay 10 μM IC50=591 nM
CHLA-10 Growth inhibitory assay 10 μM IC50=102 nM
CHLA-258 Growth inhibitory assay 10 μM IC50=1.05 μM
GBM2 Growth inhibitory assay 10 μM IC50=9.15 μM
NB-1643 Growth inhibitory assay 10 μM IC50=5.4 μM
NB-Ebc1 Growth inhibitory assay 10 μM IC50>10 μM
CHLA-90 Growth inhibitory assay 10 μM IC50>10 μM
CHLA-136 Growth inhibitory assay 10 μM IC50>10 μM
NALM-6 Growth inhibitory assay 10 μM IC50=265 nM
COG-LL-317 Growth inhibitory assay 10 μM IC50=6.49 nM
RS4;11 Growth inhibitory assay 10 μM IC50=147 nM
MOLT-4 Growth inhibitory assay 10 μM IC50=40 nM
CCRF-CEM Growth inhibitory assay 10 μM IC50=268 nM
Kasumi-1 Growth inhibitory assay 10 μM IC50=107 nM
Karpas-299 Growth inhibitory assay 10 μM IC50=2.93 μM
Ramos-RA1 Growth inhibitory assay 10 μM IC50=7.35 μM
H1299 Kinase assay 10 μM inhibits IKBKE-induced Akt Activation
Click to View More Cell Line Experimental Data

Biological Activity

Description Tivantinib 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.
Features The first selective c-Met inhibitor to be advanced into human clinical trials.
Targets
c-Met [1]
(Cell-free assay)
0.355 μM(Ki)
In vitro
In vitro

ARQ-197 has been shown to prevent HGF/c-met induced cellular responses in vitro. ARQ-197 possesses antitumor activity; inhibiting proliferation of A549, DBTRG and NCI-H441 cells with IC50 of 0.38, 0.45, 0.29 μM. Treatment with ARQ-197 results in a decrease in phosphorylation of the MAPK signaling cascade and prevention of invasion and migration. In addition, ectopic expression of c-Met in NCI-H661, a cell line having no endogenous expression of c-Met, causes it to acquire an invasive phenotype that is also suppressed by ARQ-197. Although the addition of increasing concentrations of ARQ-197 does not significantly affect the Km of ATP, exposure of c-Met to 0.5 μM ARQ-197 decreased the Vmax of c-Met by approximately 3-fold. The ability of ARQ-197 to decrease the Vmax without affecting the Km of ATP confirmed that ARQ-197 inhibits c-Met through a non–ATP-competitive mechanism and may therefore account for its high degree of kinase selectivity. ARQ-197 prevents human recombinant c-Met with a calculated inhibitory constant Ki of approximately 355 nM. Although the highest concentration of ATP used is 200 μM, the potency of ARQ-197 against c-Met is not reduced by using concentrations of ATP up to 1 mM. ARQ-197 blocks c-Met phosphorylation and downstream c-Met signaling pathways. ARQ-197 suppresses constitutive and ligand-mediated c-Met autophosphorylation and, by extension, c-Met activity, in turn leading to the inhibition of downstream c-Met effectors. ARQ-197 induction of caspase-dependent apoptosis is increased in c-Met–expressing human cancer cells including HT29, MKN-45, and MDA-MB-231 cells.[1][2]

Kinase Assay c-Met SDS-PAGE in vitro kinase assay
Recombinant c-Met protein (100 ng) is preincubated with increasing concentrations of ARQ-197 for 30 minutes at room temperature. Following preincubation, 100 μM of poly-Glu-Tyr substrate and various concentrations of ATP containing 5 μCi of [γ-32P]ATP are added to the reaction mixture. The reaction is incubated for 5 minutes at room temperature and then stopped by the addition of 5 μL of SDS-polyacrylamide gel, reducing sample buffer. The samples are then loaded onto a 7.5% acrylamide gel and SDS-PAGE is performed. The phosphorylated poly-Glu-Tyr substrates are ultimately visualized by autoradiography. c-Met activity is quantified by densitometry.
Cell Research Cell lines T29, MKN-45 and MDA-MB-231 cells
Concentrations 0.03-10 μM
Incubation Time 24, 32, and 48 hours
Method

HT29, MKN-45, and MDA-MB-231 cells are seeded in black 96-well plates at 5 × 103 cells per well overnight in a medium with 10% FBS. The next day, cells are treated with increasing concentrations of ARQ-197 (0.03-10 μM) for 24, 32, and 48 hours at 37 °C. After ARQ-197 treatment, the drug-containing medium is removed and cells are incubated for at least 10 minutes in a labeling solution (10 mM HEPES, 140 mM NaCl, and 6 mM CaCl2) containing 2 μg/mL Hoescht 33342 (blue channel), 500-times diluted Annexin V-FITC (green channel), and 1 μg/mL propidium iodide (red channel). High-content image acquisition and analysis are carried out. The program is set to take four images per well. The exposure time is set at 16.7 ms/10% gain, 500 ms/35% gain, and 300 ms/30% gain for the 4,6-diamidino-2-phenylindole, FITC, and rhodamine channels, respectively. Images are processed and the numbers of positive cells for each channel and each condition are determined. In addition, HT29 cells are treated with increasing concentrations of ARQ-197 for 32 hours in the absence or the presence of 25, 50, and 100 μM ZvAD-FMK (irreversible general caspase inhibitor), and the same procedures are undertaken. All experiments are done in triplicate. To determine whether the apoptotic effect is due to c-Met inhibition, the effect of ARQ-197 when glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and c-Met are knocked down using siRNA is investigated. HT29, MKN-45, and MDA-MB-231 cells are transfected with a nontargeted control siRNA, a gapgh-targeted control siRNA, or a met-targeted siRNA. After 3 days, c-Met, GAPDH, and β-actin expression levels are determined using specific antibodies. To determine if the effect is caspase dependent, HT29, MKN-45, and MDA-MB-231 cells are transfected with a met-targeted siRNA for 2 days and incubated in the absence or the presence of increasing concentrations of ZvAD-FMK for 1 additional day. A nontargeted siRNA and a gapgh-targeted siRNA (siRNA GAPDH) are also transfected in parallel, as controls. Cells are then stained with Annexin V-FITC and propidium iodide, and the percentage of apoptotic cells is determined.

Experimental Result Images Methods Biomarkers Images PMID
Western blot cMET / p-cMET / p-AKT / p-ERK / p-rpS6 S2753-WB1 23022995
Growth inhibition assay Cell viability S2753-viability1 23598276
In Vivo
In vivo

All three xenograft models treated with ARQ-197 display reductions in tumor growth: 66% in the HT29 model, 45% in the MKN-45 model, and 79% in the MDA-MB-231 model. In these xenograft studies, no significant body weight changes following oral administration of ARQ-197 at 200 mg/kg are observed. Pharmacodynamically, the phosphorylation of c-Met in human colon xenograft tumors (HT29) is strongly inhibited by ARQ-197, as assessed by a dramatic reduction of c-Met autophosphorylation 24 hours after a single oral dose of 200 mg/kg of ARQ-197. This same dosage in mice exhibits that tumor xenografts are exposed to sustained plasma levels of ARQ-197, consistent with the observed pharmacodynamic inhibition of c-Met phosphorylation and inhibition of proliferation of c-Met harboring cancer cell lines. Plasma levels of ARQ-197 10 hours after dosing are determined to be 1.3 μM, more than 3-fold above the biochemical inhibitory constant of ARQ-197 for c-Met. Therefore, ARQ-197 is able to suppress its target in vivo in the xenografted human tumor tissue. In conclusion, ARQ-197 inhibits the growth of c-Met-dependent xenografted human tumors.[1]

Animal Research Animal Models Female athymic nude mice bearing HT29, MKN-45, or MDA-MB-231 tumor xenografts
Dosages 200 mg/kg
Administration Orally administered
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02150733 Completed
Hepatic Impairment|Solid Tumor|Cancer
Daiichi Sankyo|Medpace Inc.
April 2014 Phase 1
NCT01892527 Completed
Colorectal Cancer Metastatic|C-met Overexpression
Armando Santoro MD|Istituto Clinico Humanitas
March 2013 Phase 2
NCT02049060 Completed
Malignant Pleural Mesothelioma|Nonsquamous Nonsmall Cell Neoplasm of Lung
Armando Santoro MD|Istituto Clinico Humanitas
January 2013 Phase 1|Phase 2
NCT01755767 Completed
Hepatocellular Carcinoma
Daiichi Sankyo|ArQule Inc. a subsidiary of Merck Sharp & Dohme LLC a subsidiary of Merck & Co. Inc. (Rahway NJ USA)
December 27 2012 Phase 3
  • https://pubmed.ncbi.nlm.nih.gov/20484018/
  • https://pubmed.ncbi.nlm.nih.gov/18511928/

Chemical Information & Solubility

Molecular Weight 369.42 Formula

C23H19N3O2

CAS No. 905854-02-6 SDF Download Tivantinib SDF
Smiles C1CC2=C3C(=CC=C2)C(=CN3C1)C4C(C(=O)NC4=O)C5=CNC6=CC=CC=C65
Storage (From the date of receipt)

In vitro
Batch:

DMSO : 73 mg/mL ( (197.6 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 35 mg/mL

Water : Insoluble


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In vivo
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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:
Are there any other solutions (apart from DMSO) I can dissolve S2753 for in vivo experiment?

Answer:
S2753 Tivantinib (ARQ 197) can be dissolved in 1% methylcellulose at15 mg/ml as a suspension.

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