Summary of Tyrosine Kinase STI-571 in the Treatment of Chronic Myeloid Leukemia

Abstract

Chronic Myeloid Leukemia (CML) is a hematological malignancy characterized by the presence of the Philadelphia chromosome, which results in the formation of the BCR-ABL fusion protein with constitutive tyrosine kinase activity. The discovery and development of targeted therapies, such as the tyrosine kinase inhibitor STI-571 (Imatinib), revolutionized the treatment of CML by specifically inhibiting the BCR-ABL kinase activity. This abstract provides a summary of the therapeutic efficacy and clinical impact of STI-571 in the management of CML.Sti-571, a specific tyrosine kinase inhibitor, is a novel antitumor drug that has entered clinical trials and can effectively treat chronic myeloid leukemia caused by abnormal proliferation of hematopoietic stem cells. In this paper, the mechanism of action and regulation of cell cycle of this drug were summarized, and the problems of drug resistance were explored in depth and the development prospects of this drug were briefly introduced. The introduction of STI-571 has dramatically changed the management of CML, leading to a paradigm shift from conventional chemotherapy and allogeneic stem cell transplantation as the primary treatment options. The drug has shown superior efficacy compared to interferon-alpha therapy, the standard treatment before its introduction. STI-571 is generally well-tolerated, with fewer severe adverse effects, making it an attractive option for long-term therapy. Resistance to STI-571 has been observed in a subset of patients, primarily due to the emergence of BCR-ABL kinase domain mutations. However, the development of second-generation tyrosine kinase inhibitors, such as dasatinib and nilotinib, has provided alternative treatment options for patients who fail to respond to or develop resistance to STI-571.