A powerful family of pharmaceuticals known as protein kinase inhibitors has completely changed the field of targeted cancer treatment. The mechanism of action of these inhibitors is to block the activity of protein kinases, which are essential enzymes in cellular signaling pathways that control a variety of physiological functions. Since protein kinases are frequently involved in the development, spread, and metastasis of cancer, they are desirable targets for therapeutic intervention.The discovery of imatinib, the first tyrosine kinase inhibitor to receive FDA approval and usher in a new age in precision medicine, was one of the seminal developments in protein kinase inhibition. With its ability to induce sustained responses and dramatically improve patient outcomes, imatinib, a medication that targets the BCR-ABL fusion protein in chronic myeloid leukemia (CML), demonstrated the promise of targeted therapy. Subsequently, an abundance of protein kinase inhibitors targeting distinct kinases linked to distinct malignancies have been created. These inhibitors, which have different benefits and drawbacks, can be categorized according to how they work, such as covalent, allosteric, and ATP-competitive inhibitors.Inhibiting kinase activity, ATP-competitive inhibitors like sunitinib and sorafenib compete with ATP for binding to the kinase domain. Similar to allosteric AKT inhibitors, allosteric inhibitors bind to locations other than the ATP-binding pocket to modify kinase activity, providing an alternative to ATP-competitive inhibitor resistance. Covalent inhibitors, such as those that target EGFR mutations in non-small cell lung cancer, bind to cysteine residues inside the kinase domain in an irreversible manner. Even with protein kinase inhibitors' amazing success, problems still exist, such as acquired resistance, off-target effects, and limited effectiveness in some cancers. Research is currently being done to produce next-generation inhibitors with better pharmacokinetic, potent, and selectivity characteristics in order to solve these issues. Additionally, combination therapies show promise in overcoming resistance and improving therapeutic efficacy by utilizing the synergistic effects of protein kinase inhibitors with immunotherapy, conventional chemotherapy, or other targeted medicines. In BRAF-mutant melanoma, for example, the combination of BRAF and MEK inhibitors has shown better results than monotherapy. To sum up, protein kinase inhibitors are an essential component of contemporary cancer treatment, providing individualized regimens depending on the molecular makeup of individual cancers. The development of new targets, combinatorial approach investigation, and inhibitor design optimization will all contribute to the improvement and expansion of the cancer treatment toolbox.
