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CCT241736

  Cat. No.:  DC10911   Featured
Chemical Structure
1402709-93-6
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More than 5000 active chemicals with high quality for research!
Field of application
CCT241736 is a novel, orally bioavailable Dual FLT3-Aurora Kinase Inhibitor.
Cas No.: 1402709-93-6
Chemical Name: CCT241736
Synonyms: CCT241736;3H-IMidazo[4,5-b]pyridine, 6-chloro-7-[4-[(4-chlorophenyl)Methyl]-1-piperazinyl]-2-(1,3-diMethyl-1H-pyrazol-4-yl)-;6-chloro-7-[4-[(4-chlorophenyl)methyl]piperazin-1-yl]-2-(1,3-dimethylpyrazol-4-yl)-1H-imidazo[4,5-b]pyridine;CCT-241736;CCT 241736;CS-2683;6-Chloro-7-(4-(4-chlorobenzyl)piperazin-1-yl)-2-(1,3-dimethyl-1H-pyrazol-4-yl)-1H-imidazo[4,5-b]pyridine;CCT 241736,Fms like tyrosine kinase 3,CCT241736,CD135,Inhibitor,FLT3,CCT-241736,Aurora Kinase,Cluster of differentiation antigen 135,inhibit
SMILES: C12NC(C3=CN(C)N=C3C)=NC1=C(N1CCN(CC3=CC=C(Cl)C=C3)CC1)C(Cl)=CN=2
Formula: C22H23Cl2N7
M.Wt: 456.370921373367
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: CCT241736 is a novel, orally bioavailable Dual FLT3-Aurora Kinase Inhibitor. CCT241736 has IC50 values against FLT3, Aurora A and Aurora B of 0.035, 0.015 and 0.1 uM respectively. Furthermore, CCT241736 inhibits a wide range of FLT3 mutants, including FLT3-ITD, -D835Y, -D835H, -K663Q and –N841I. In cellular assays, CCT241736 inhibits viability of the human FLT3-ITD positive AML cell lines MOLM-13 and MV-4-11 with EC50 values of 0.1 and 0.27 uM respectively. Unlike the selective FLT3 inhibitors MLN518 and AC220, the in vitro cellular efficacy of CCT241736 is not affected by high levels of FL. In vivo, mouse tumor xenograft models of MOLM-13, MV-4-11, and the doubly-mutated cell line MOLM-13-RES are also sensitive to CCT241736 at well tolerated oral doses, with biomarker modulation consistent with dual inhibition of FLT3 and Aurora kinases. Based on allometric scaling from mouse and rat data, CCT241736 has favorable predicted human pharmacokinetics and phase I clinical trials are planned. In summary, dual inhibition of FLT3 and the critical mitotic kinase Aurora by CCT241736 may represent a novel treatment strategy for FLT3-mutated AML by overcoming the effects of high FL levels and limiting resistance caused by secondary mutations of the FLT3 gene.
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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