DCC-2701 MedChemExpress (MCE)

Product Name	Altiratinib
Synonyms	DP 5164 DCC-2701 ALTIRATINIB Altiratinib Altiratinib(DCC2701) DCC2701 (Altiratinib) Altiratinib(DCC-22701) Synonyms DP 5164 DCC-2701 ALTIRATINIB Altiratinib Altiratinib(DCC2701) DCC2701 (Altiratinib) Altiratinib(DCC-22701) Altiratinib(DCC2701,DP5164) N-(4-(2-(cyclopropanecarboxamido)pyridin-4-yloxy)-2,5-difluorophenyl)-N-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide
CAS	1345847-93-9
EINECS	1592732-453-0
Chemical Formula	C26H21F3N4O4
Molecular Weight	510.46
inchi
Package	10 mM * 1 mL;5 mg;10 mg;50 mg;100 mg
Price	Email to quote
Descriptions	Altiratinib Altiratinib MedChemExpress (MCE) HY-B0791 1345847-93-9 DCC-2701 98.05% Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year Room temperature in continental US Descriptions Altiratinib Altiratinib MedChemExpress (MCE) HY-B0791 1345847-93-9 DCC-2701 98.05% Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year Room temperature in continental US may vary elsewhere. Altiratinib (DCC-2701) is a multi-targeted kinase inhibitor with IC50s of 2.7, 8, 9.2, 9.3, 0.85, 4.6, 0.83 nM for MET, TIE2, VEGFR2, FLT3, Trk1, Trk2, and Trk3 respectively. Altiratinib also inhibits MET isoforms METD1228H, MET D1228N, METY1230C, METY1230D, METY1230H, METM1250T with IC50s of 3.6, 1.3, 1.2, 0.37, 1.5 and 6 nM, respectively. Altiratinib inhibits MET phosphorylation with IC50 values of 0.85 and 2.2 nM, respectively. In the U-87 glioblastoma cell line, MET and HGF are both expressed. Altiratinib blocks autocrine activation of MET phosphorylation in these cells (IC50=6.2 nM). Altiratinib potently inhibits cellular proliferation in MET-amplified EBC-1 and MKN-45 cells, as well as TPM3-TRKA fusion KM-12 cells. Activation of MET is known to increase the motility and invasiveness of cancer cells: Altiratinib inhibits HGF-induced A549 cell migration, with an IC50 of 13 nM. Altiratinib also inhibits FLT3-ITD mutant MV-4-11 cell proliferation with an IC50 of 12 nM[1]. A single oral dose of 30 mg/kg Altiratinib leads to >95% inhibition of MET phosphorylation for the entire 24-hour period. A single 10 mg/kg oral dose of Altiratinib exhibits complete inhibition of MET phosphorylation through 12 hours and 73% inhibition at 24 hours postdose. Altiratinib dosed at 10 mg/kg twice a day leads to a significant 90% decrease in BLI signal. Altiratinib exhibits properties amenable to oral administration and exhibits substantial blood–brain barrier penetration, an attribute of significance for eventual treatment of brain cancers and brain metastases[1]. Mice: Female nude mice are inoculated subcutaneously. On days 9 to 10, when tumor volumes reached 326 mg on average, mice are randomly assigned to groups and dosed once orally with 0.4% HMPC, (n=3) Altiratinib at 30 mg/kg (n=21) or Altiratinib at 10 mg/kg (n=21). At specified time points, whole blood and tumors are collected. Pharmacokinetic analysis is performed. Tumor samples are processed in the Western blot assay methods[1]. Altiratinib is dispensed into assay plates. Cells are added to 96-well (EBC-1, M-NFS-60, and SK-MEL-28: 2,500 cells/well MKN-45: 5,000 cells/well MV-4-11: 10,000 cells/well) or 384-well plates (A375 and HCT-116: 625 cells/well BT-474, KM-12, PC-3, and U-87-MG: 1,250 cells/well). Plates are incubated for 72 hours. Viable cells are quantified using resazurin using a plate reader with excitation at 540 nm and emission at 600 nm[1]. VEGFR2 9.2 nM (IC50) Trk1 0.85 nM (IC50) Trk2 4.6 nM (IC50) Trk3 0.93 nM (IC50) MET 2.7 nM (IC50) TIE2 8 nM (IC50) FLT3 9.3 nM (IC50) \| \| \| \| \| \| \| \| \| \| [1]. Smith BD, et al. Altiratinib Inhibits Tumor Growth, Invasion, Angiogenesis, and Microenvironment-Mediated DrugResistance via Balanced Inhibition of MET, TIE2, and VEGFR2. Mol Cancer Ther. 2015 Sep 14(9):2023-34. [Content Brief]
Last Update	2025-04-01 14:45:47

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