Uncontrolled cell proliferation and dysregulated signaling pathways are hallmarks of the diverse group of disorders known as cancer. Tyrosine kinase-mediated signal transduction, which controls angiogenesis, metastasis, cell survival, and proliferation, is a key factor in oncogenesis. Despite its effectiveness in quickly proliferating cells, conventional chemotherapy is frequently constrained by systemic toxicity, non-specific targeting, and the emergence of drug resistance. As a result, targeted treatments that specifically block carcinogenic signaling molecules have been developed, providing increased effectiveness and fewer side effects. Tyrosine kinase inhibitors (TKIs), which are particularly made to stop aberrant kinase activity that propels tumor growth, have become a key component of precision oncology. TKIs have shown notable clinical advantages in a number of cancers, such as lung cancer, breast cancer, and chronic myeloid leukemia, by enhancing quality of life and survival rates. Targeting both receptor and non-receptor tyrosine kinases, TKIs have a variety of pharmacological modes of action. Genetic mutations, drug metabolism, and resistance mechanisms all affect how effective they are. There are still issues with them despite their therapeutic potential, such as primary and acquired resistance, high treatment costs, side effects, and inconsistent patient adherence. Future directions for TKI research include combination treatments, next-generation inhibitors, patient selection based on biomarkers, and methods for overcoming resistance. Optimizing patient outcomes, directing treatment selection, and developing precision medicine techniques in oncology all depend on an understanding of the pharmacology and clinical use of TKIs.
Mary et al. (2026) studied this question.