标题
The clinical development of FLT3 inhibitors in acute myeloid leukemia
作者
关键词
-
出版物
EXPERT OPINION ON INVESTIGATIONAL DRUGS
Volume 20, Issue 10, Pages 1377-1395
出版商
Informa Healthcare
发表日期
2011-09-07
DOI
10.1517/13543784.2011.611802
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- FLT3 ligand impedes the efficacy of FLT3 inhibitors in vitro and in vivo
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- Insertion of FLT3 internal tandem duplication in the tyrosine kinase domain-1 is associated with resistance to chemotherapy and inferior outcome
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- AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML)
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- KW-2449, a novel multikinase inhibitor, suppresses the growth of leukemia cells with FLT3 mutations or T315I-mutated BCR/ABL translocation
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- Identification ofN-(5-tert-Butyl-isoxazol-3-yl)-N′-{4-[7-(2-morpholin-4-yl-ethoxy)imidazo[2,1-b][1,3]benzothiazol-2-yl]phenyl}urea Dihydrochloride (AC220), a Uniquely Potent, Selective, and Efficacious FMS-Like Tyrosine Kinase-3 (FLT3) Inhibitor
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- A pharmacodynamic study of the FLT3 inhibitor KW-2449 yields insight into the basis for clinical response
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- Targeting the leukemia microenvironment by CXCR4 inhibition overcomes resistance to kinase inhibitors and chemotherapy in AML
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- MS-275, a novel histone deacetylase inhibitor with selectivity against HDAC1, induces degradation of FLT3 via inhibition of chaperone function of heat shock protein 90 in AML cells
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- Sorafenib (Nexavar®) induces molecular remission and regression of extramedullary disease in a patient with FLT3-ITD+ acute myeloid leukemia
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- Sorafenib in Advanced Hepatocellular Carcinoma
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