ATP-based oncogenic protein kinase inhibitor: implications for CML Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent
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W. Deininger and Brian J. Druker Sundaramoorthi, William C. Shakespeare, David Dalgarno, Tim Clackson, Tomi K. Sawyer, Michael Moseson, Victor M. Rivera, Hao Tang, Chester A. Metcalf III, Regine S. Bohacek, Yihan Wang, Raji Thomas O'Hare, Roy Pollock, Eric P. Stoffregen, Jeffrey A. Keats, Omar M. Abdullah, Erika M. ATP-based oncogenic protein kinase inhibitor: implications for CML Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent
منابع مشابه
Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML.
The deregulated, oncogenic tyrosine kinase Bcr-Abl causes chronic myeloid leukemia (CML). Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectively inhibits proliferation and promotes apoptosis of CML cells. Despite the success of imatinib mesylate in the treatment of CML, resistance is observed, particularly in advanced disease. The most common imatinib mesylate resistance m...
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Kinase inhibitors that target Bcr-Abl are highly effective in the treatment of chronic myeloid leukemia (CML). However, these inhibitors are often invalidated due to the drug resistance. Therefore, the discovery and development of novel Bcr-Abl inhibitors is required to overwhelm the drug resistance in the treatment of CML resistant to the currently used first-line Bcr-Abl inhibitors. Herein we...
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Chronic myeloid leukemia (CML) is caused by the constitutively activated tyrosine kinase breakpoint cluster (BCR)-ABL. Current frontline therapy for CML is imatinib, an inhibitor of BCR-ABL. Although imatinib has a high rate of clinical success in early phase CML, treatment resistance is problematic, particularly in later stages of the disease, and is frequently mediated by mutations in BCR-ABL...
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Chronic myeloid leukemia (CML) is characterized by constitutively active fusion protein tyrosine kinase BCR-ABL. Although the tyrosine kinase inhibitor (TKI) against BCR-ABL, imatinib, is the first-line therapy for CML, acquired resistance almost inevitably emerges. The underlying mechanism are point mutations within the BCR-ABL gene, among which T315I is notorious because it resists to almost ...
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تاریخ انتشار 2004