Imatinib Analogs in Chronic Myeloid Leukemia: a Systematic Qualitative Review

Purpose of ReviewThe development of the Philadelphia chromosome characterizes chronic myeloid leukemia (CML) and the subsequent oncogenesis of fusion protein BCR-ABL activation. Our improved awareness of the molecular underpinnings of CML has enabled the creation of exceptionally potent targeted medications that prevent the action of BCR-ABL tyrosine kinase. Imatinib (1st TKIs) was developed with the intention of treating chronic myeloid leukemia (CML) at the molecular level. It continues to be the most prevalent frequently used for CML therapy and is currently also approved for a number of additional malignancies caused by BCR-ABL, c-KIT, and PDGFR. Imatinib is 95% bound to plasma proteins, is taken orally, is primarily hepatically removed with an inadequate liver clearance proportion, and acts intracellularly. Patients, however, may experience imatinib resistance, which is frequently brought on by BCR-ABL mutations. Adverse reactions in imatinib-treated patients have shown to be manageable across a spectrum of severity with timely and adequate care and very seldom necessitate a permanent cessation of medication. A number of small agents, notably dasatinib, imatinib, nilotinib, bosutinib, and ponatinib, asciminib, and olverembatinib, are employed to treat CML. Some novel strategies adopted for CML made this manuscript valuable for readers.Recent FindingsEvidence suggests the purpose of imatinib analogs (TKIs) in treatment for chronic myeloid leukemia. Still, there is recent development in chronic myeloid leukemia therapy due to emergence of resistance.SummaryThis review paper emphasizes 1st-generation, 2nd-generation, 3rd-generation, 4th-generation TKIs, their limitations, success, and some future possible strategies to eradicate future Ph + CML cells from a biological perspective.