ABSTRACT Bosutinib is an orally available Src/Abl tyrosine kinase inhibitor and has been approved for the treatment of patients with Ph + chronic myelogenous leukemia. Bosutinib is a substrate of P‐glycoprotein (P‐gp) in vitro and is predominantly metabolized by CYP3A4 in humans with minimal urinary excretion. We present our perspective on using physiologically based pharmacokinetic modeling to understand the atypical changes in oral exposure of bosutinib, a CYP3A and P‐gp substrate, in hepatic impairment patients.
Muto et al. (Thu,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: