Because BCR-ABL is a key cause of Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) and remains the driver of the disease throughout the chronic phase, BCR-ABL inhibition is the focus of CML treatment. Nilotinib was rationally designed to antagonize the aberrant tyrosine kinase activity of Bcr-Abl-positive cells.
Nilotinib binds to and stabilizes the inactive conformation of the kinase domain of the Abl protein of the Bcr-Abl fusion protein, resulting in the inhibition of the Bcr-Abl-mediated proliferation of Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) cells. This drug also inhibits the receptor tyrosine kinases platelet-derived growth factor receptor (PDGF-R) and c-kit, a receptor tyrosine kinase mutated and constitutively activated in most gastrointestinal stromal tumors (GISTs). With a binding mode that is energetically more favorable than that of imatinib, Nilotinib has been shown to have an approximately 30-fold increased potency in kinase and proliferation assays compared to imatinib.
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