RTKinhibiittorit

RTKinhibiittorit, in Finnish often referred to as RTK-inhibiittorit, are a class of targeted cancer therapies that block receptor tyrosine kinases (RTKs), a family of cell-surface enzymes that relay signals for cell growth, survival, and differentiation. By inhibiting RTK signaling, these drugs can slow or halt the growth of tumors driven by these pathways.

RTK inhibitors include small-molecule tyrosine kinase inhibitors (TKIs) that bind the intracellular kinase domain and monoclonal antibodies that bind extracellular receptor regions or ligands. TKIs typically act by competing with ATP at the catalytic site, while antibodies can block ligand binding, prevent receptor dimerization, or promote receptor downregulation.

Target receptors cover a broad range, including EGFR, VEGFR, ALK, ROS1, MET, HER2, RET, FGFR, and TRK receptors. Clinically used examples encompass gefitinib and erlotinib (EGFR TKIs), imatinib (BCR-ABL and others), crizotinib (ALK/ROS1/MET), and multi-target agents like sunitinib and sorafenib. Antibody therapies such as cetuximab and panitumumab target EGFR, while TRK inhibitors like larotrectinib and entrectinib address NTRK gene fusions. Newer agents provide selective inhibition for RET, MET, FGFR, and other RTKs.

Resistance and safety considerations are central to RTK inhibitor use. Tumors may acquire secondary mutations or activate alternative signaling pathways, reducing efficacy. Common adverse effects include skin rash, diarrhea, hypertension, hepatotoxicity, and fatigue. RTK inhibitors remain a core element of precision oncology, with ongoing development to broaden indications and overcome resistance.