448104
c-Met/RON Dual Kinase Inhibitor
The c-Met/RON Dual Kinase Inhibitor, also referenced under CAS 913376-84-8, controls the biological activity of c-Met/RON.
Synonym(s):
c-Met/RON Dual Kinase Inhibitor, Met Kinase Inhbitor IV, Ron Inhibitor I, N-(3-Fluoro-4-(7-methoxy-4-quinolinyl)phenyl)-1-(2-hydroxy-2-methylpropyl)-5-methyl-3-oxo-phenyl-2,3-dihydro-1H-pyrazole carboxamide, Compound I
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About This Item
Empirical Formula (Hill Notation):
C31H29FN4O5
CAS Number:
Molecular Weight:
556.58
UNSPSC Code:
12352200
Quality Level
Assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
light tan
solubility
DMSO: 40 mg/mL
shipped in
ambient
storage temp.
2-8°C
General description
A cell-permeable quinoline compound that acts as a potent inhibitor against the kinase activities of HGF (Cat. No. 375228) receptor c-Met and MSP (Macrophage Stimulating Protein) receptor RON (IC50 = 4 and 9 nM, respectively), while exhibiting much weaker potency toward Lck, Tie2, Src, BTK, IGFR, or VEGFR2 (IC50 = 160, 400, 410, 710, 1000, and 1900 nM, respectively), and little or no activity against B-Raf and more than 20 other kinases IC50 >1 µM). Shown to effectively supress (IC50<100 nM) the ligand-induced autophosphorylations of wild-type c-Met (in HT-29 and BxPC3 cultures) and RON (in NIH3T3 RON and BxPC3 cultures) as well as the ligand-independent autophosphorylations of the constitutively active mutants TPR-Met and RONΔ160 (in NIH3T3 TRP-Met and HT-29 cultures, respectively). Reported to inhibit NIH3T3 TRP-Met and U-87 tumor growth in mice in vivo in a dose-dependent manner (complete inhibition via daily p.o. dose of 100 mg/kg), but is less efficacious against HT-29, whose in vivo tumor growth is also dependent on V600E B-raf.
A cell-permeable quinoline compound that acts as a potent inhibitor against the kinase activities of HGF receptor c-Met and MSP (Macrophage Stimulating Protein) receptor RON (IC50 = 4 and 9 nM, respectively), while exhibiting much weaker potency toward Lck, Tie2, Src, BTK, IGFR, or VEGFR2 (IC50 = 160, 400, 410, 710, 1000, and 1900 nM, respectively), and little or no activity against B-Raf and more than 20 other kinases IC50 >1 M). Shown to effectively supress (IC50<100 nM) the ligand-induced autophosphorylations of wild-type c-Met (in HT-29 and BxPC3 cultures) and RON (in NIH3T3 RON and BxPC3 cultures) as well as the ligand-independent autophosphorylations of the constitutively active mutants TPR-Met and RONΔ160 (in NIH3T3 TRP-Met and HT-29 cultures, respectively). Reported to inhibit NIH3T3 TRP-Met and U-87 tumor growth in mice in vivo in a dose-dependent manner (complete inhibition via daily p.o. dose of 100 mg/kg), but is less efficacious against HT-29, whose in vivo tumor growth is also dependent on V600E B-raf.
Packaging
Packaged under inert gas
Warning
Toxicity: Standard Handling (A)
Reconstitution
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Other Notes
Zhang, Y., et al. 2008. Cancer Res.68, 6680.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Yihong Zhang et al.
Cancer research, 68(16), 6680-6687 (2008-08-15)
Recepteur d'origine nantais (RON) is a receptor tyrosine kinase closely related to c-Met. Both receptors are involved in cell proliferation, migration, and invasion, and there is evidence that both are deregulated in cancer. Receptor overexpression has been most frequently described
Kentaro Kajiwara et al.
Life science alliance, 4(4) (2021-02-13)
Compensatory growth of organs after loss of their mass and/or function is controlled by hepatocyte growth factor (HGF), but the underlying regulatory mechanisms remain elusive. Here, we show that CUB domain-containing protein 1 (CDCP1) promotes HGF-induced compensatory renal growth. Using
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