c-Met inhibitors are a class of drugs that include nonselective and selective molecules. These drugs can differ in terms of pharmacodynamic and pharmacokinetic properties that may be clinically relevant. c-Met inhibitors with high potency and selectivity may allow achieving optimal c-Met inhibition in c-Met-driven tumors while reducing unwanted off-target toxicities due to activation of multiple kinases. Nonselective drugs can instead be considered in tumors that also recognize other drivers (e.g., ALK, ROS, VEGF). Improved understanding of the clinical pharmacokinetics of c-Met inhibitors can help avoid drug-drug interactions and optimize schedules for continuous in vivo inhibition of c-Met phosphorylation. The current review article provides a detailed overview of the clinical pharmacology of molecules used in c-Met-driven tumors.
The expanding family of c-Met inhibitors in solid tumors: a comparative analysis of their pharmacologic and clinical differences / S. Fogli, F. Tabbò, A. Capuano, M.D. Re, F. Passiglia, F. Cucchiara, C. Scavone, V. Gori, S. Novello, M. Schmidinger, R. Danesi. - In: CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY. - ISSN 1040-8428. - 172:(2022 Apr), pp. 103602.1-103602.12. [10.1016/j.critrevonc.2022.103602]
The expanding family of c-Met inhibitors in solid tumors: a comparative analysis of their pharmacologic and clinical differences
R. DanesiUltimo
Writing – Review & Editing
2022
Abstract
c-Met inhibitors are a class of drugs that include nonselective and selective molecules. These drugs can differ in terms of pharmacodynamic and pharmacokinetic properties that may be clinically relevant. c-Met inhibitors with high potency and selectivity may allow achieving optimal c-Met inhibition in c-Met-driven tumors while reducing unwanted off-target toxicities due to activation of multiple kinases. Nonselective drugs can instead be considered in tumors that also recognize other drivers (e.g., ALK, ROS, VEGF). Improved understanding of the clinical pharmacokinetics of c-Met inhibitors can help avoid drug-drug interactions and optimize schedules for continuous in vivo inhibition of c-Met phosphorylation. The current review article provides a detailed overview of the clinical pharmacology of molecules used in c-Met-driven tumors.| File | Dimensione | Formato | |
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