Results Inhibition of CYP3a4 by ketoconazole increased midostaurin exposure more than tenfold, and induction of CYP3a4 by rifampicin decreased midostaurin exposure by more than tenfold. Midostaurin did not appreciably affect the concentrations of midazolam or its metabolite, 1′-hydroxymidazolam, at single or multiple doses. Conclusion the pharmacokinetics of midostaurin and its metabolites was affected substantially by ketoconazole and rifampicin, suggesting that midostaurin is a sensitive CYP3a4 substrate. Midostaurin did not appear to inhibit or induce CYP3a4 in vivo.
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