Introduction: Maribavir is a potent and orally bioavailable antiviral with a novel mechanism of action against cytomegalovirus (CMV). The efficacy and safety of maribavir for treatment of CMV infections are being evaluated in ongoing Phase 3 trials. Characterization of drugÀdrug interaction (DDI) properties of maribavir is necessary in informing potential DDIs with co-medications. Objective: To evaluate the potential cytochrome p450 and p-glycoproteinÀmediated drugÀdrug interaction by maribavir. Methods: Cytochrome P450 (CYP) reversible inhibition: Probe substrates of CYPs were incubated with human liver microsomes (HLM) and maribavir. Percent remaining CYP activity was plotted against maribavir concentrations for IC 50 determination. Time-dependent inhibition (TDI) for CYPs: After pre-incubation with maribavir for varying durations, percent remaining CYP activity in HLM was measured. The concentration at half-maximal inactivation (K I ) and maximum inactivation rate constant (k inact ) were calculated. CYP induction: After treating human hepatocytes with maribavir for three days, CYP mRNA expression was plotted against maribavir concentrations to determine half-maximal induction concentration (EC 50 ) and maximal fold induction (E max ). Pglycroprotein (P-gp) inhibition: Bi-directional transport of digoxin in Caco-2 cells with maribavir was measured and IC 50 calculated by plotting percent transporter activity against maribavir concentration. Results: Maribavir is not a reversible inhibitor of CYP2A6, CYP2B6, CYP2C8, CYP2D6, CYP2E1, or CYP3A4 and is a weak inhibitor of CYP1A2, CYP2C9, and CYP2C19 (IC 50 40, 18, and 35 mM). Maribavir is not a TDI of CYP1A2, CYP2C8, CYP2C9, CYP2C19, or CYP2D6 but a weak TDI for CYP3A (K I 41.2 mM, k in-
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