Authors Baska, F; Sipos, A; Orfi, Z; Nemes, Z; Dobos, J; Szantai-Kis, C; Szabo, E; Szenasi, G; Dezsi, L; Hamar, P; Cserepes, MT; Tovari, J; Garamvolgyi, R; Kreko, M; Orfi, L in ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER published article about ACUTE MYELOID-LEUKEMIA; RISK MYELODYSPLASTIC SYNDROME; ACUTE MYELOGENOUS LEUKEMIA; TYROSINE KINASE; ACTIVATING MUTATION; TANDEM DUPLICATION; WILD-TYPE; IN-VITRO; PHASE-I; RECEPTOR in [Baska, Ferenc; Sipos, Anna; Nemes, Zoltan; Dobos, Judit; Szantai-Kis, Csaba; Garamvolgyi, Rita; Orfi, Laszlo] Vichem Chem Res Ltd, H-1022 Budapest, Hungary; [Orfi, Zoltan] Max Planck Inst Biochem, Dept Mol Biol, D-82152 Martinsried, Germany; [Szabo, Eszter] Semmelweis Univ, Dept Paediat 1, H-1083 Budapest, Hungary; [Szenasi, Gabor; Dezsi, Laszlo; Hamar, Peter] Semmelweis Univ, Inst Pathophysiol, H-1089 Budapest, Hungary; [Dezsi, Laszlo] Semmelweis Univ, Nanomed Res & Educ Ctr, H-1089 Budapest, Hungary; [Cserepes, Mihaly T.; Tovari, Jozsef] Natl Inst Oncol, Dept Expt Pharmacol, H-1122 Budapest, Hungary; [Kreko, Marcell; Orfi, Laszlo] Semmelweis Univ, Dept Pharmaceut Chem, Hogyes Endre U 9, H-1085 Budapest, Hungary; [Orfi, Laszlo] Drug Res Co, Batthyany U 92, H-1161 Budapest, Hungary in 2019, Cited 62. Application In Synthesis of 1,4-Dioxa-8-azaspiro[4.5]decane. The Name is 1,4-Dioxa-8-azaspiro[4.5]decane. Through research, I have a further understanding and discovery of 177-11-7
Aberrant activation of FMS-like tyrosine receptor kinase 3 (FLT3) is implicated in the pathogenesis of acute myeloid leukemia (AML) in 20-30% of patients. In this study we identified a highly selective (phenylethenyl)quinazoline compound family as novel potent inhibitors of the FLT3-ITD and FLT3-D835Y kinases. Their prominent effects were confirmed by biochemical and cellular proliferation assays followed by mice xenograft studies. Our modelling experiments and the chemical structures of the compounds predict the possibility of covalent inhibition. The most effective compounds triggered apoptosis in FLT3-ITD AML cells but had either weak or no effect in FLT3-independent leukemic and non-leukemic cell lines. Our results strongly suggest that our compounds may become therapeutics in relapsing and refractory AML disease harboring various ITD and tyrosine kinase domain mutations, by their ability to overcome drug resistance. (C) 2019 Elsevier Masson SAS. All rights reserved.
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