ChemicalBook--->CAS DataBase List--->1345847-93-9

1345847-93-9

1345847-93-9 Structure

1345847-93-9 Structure
IdentificationBack Directory
[Name]

Altiratinib
[CAS]

1345847-93-9
[Synonyms]

DP 5164
CS-1690
DCC-2701
Altiratinib
Altiratinib, >98%
Altiratinib(DCC2701)
DCC2701 (Altiratinib)
Altiratinib(DCC-22701)
Altiratinib(DCC2701,DP5164)
ALTIRATINIB; DCC2701;DCC 2701
ALTIRATINIB; DCC2701;DCC 2701;DCC-2701
N-(4-(2-(cyclopropanecarboxamido)pyridin-4-yloxy)-2,5-difluorophenyl)-N-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide
1,1-Cyclopropanedicarboxamide, N-[4-[[2-[(cyclopropylcarbonyl)amino]-4-pyridinyl]oxy]-2,5-difluorophenyl]-N'-(4-fluorophenyl)-
[EINECS(EC#)]

1592732-453-0
[Molecular Formula]

C26H21F3N4O4
[MDL Number]

MFCD28900672
[MOL File]

1345847-93-9.mol
[Molecular Weight]

510.46
Chemical PropertiesBack Directory
[Boiling point ]

763.5±60.0 °C(Predicted)
[density ]

1.557±0.06 g/cm3(Predicted)
[storage temp. ]

Store at -20°C
[solubility ]

≥21.55 mg/mL in DMSO; insoluble in H2O; insoluble in EtOH
[form ]

solid
[pka]

12.09±0.70(Predicted)
[color ]

Light yellow to khaki
Safety DataBack Directory
[Symbol(GHS) ]


GHS07
[Signal word ]

Warning
[Hazard statements ]

H302-H315-H319-H335
[Precautionary statements ]

P261-P305+P351+P338
Spectrum DetailBack Directory
[Spectrum Detail]

Altiratinib(1345847-93-9)1HNMR
Hazard InformationBack Directory
[Biological Activity]

altiratinib (dcc-2701) is a potent inhibitor of c-met/tie-2/vegfr with ic50 values of 2.7, 8.0 and 9.2 nm, respectively [1].hepatocyte growth factor receptor (c-met) is a tyrosine kinase receptor for hepatocyte growth factor and is essential for wound healing and embryonic development. tek tyrosine kinase (tie-2) is a receptor for angiopoietin-1 (ang-1) and is important for endothelial cell-smooth muscle cell communication. vegfr is a tyrosine kinase receptor for vascular endothelial growth factor that involved in both vasculogenesis and angiogenesis.altiratinib (dcc-2701) is a potent c-met/tie-2/vegfr inhibitor. altiratinib potently inhibited met kinase and activating oncogenic met mutations and also inhibited trka, trkb and trkc kinases with ic50 values of 0.85, 4.6, and 0.83 nm, respectively. in ebc-1 nsclc and mkn-45 gastric cancer cell lines overexpressing met, altiratinib inhibited met phosphorylation with ic50 values of 0.85 and 2.2 nm, respectively. in vegf-stimulated huvecs, altiratinib inhibited vegfr2 phosphorylation with ic50 value of 4.7 nm. in huvecs and ea.hy926 cells, altiratinib inhibited tie2 phosphorylation stimulated by ang-1 with ic50 values of 1.0 and 2.6 nm, respectively [1].in the met-amplified mkn-45 xenograft model, altiratinib (30 mg/kg) inhibited met phosphorylation by >95% for the 24-hour period [1]. in nude mouse xenografted skov3 cells, dcc-2701 (10 or 20 mg/kg for 28 days) significantly reduced tumor burden by 53% and 52%, respectively [2].
[References]

[1]. smith bd, kaufman md, leary cb, et al. altiratinib inhibits tumor growth, invasion, angiogenesis, and microenvironment-mediated drug resistance via balanced inhibition of met, tie2, and vegfr2. mol cancer ther, 2015.
[2]. kwon y, smith bd, zhou y, et al. effective inhibition of c-met-mediated signaling, growth and migration of ovarian cancer cells is influenced by the ovarian tissue microenvironment. oncogene, 2015, 34(2): 144-153.
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