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Clinically significant interactions mediated by umeclidinium bromide at clinical doses are considered unlikely due to the low plasma concentrations achieved after inhaled dosing.
Other antimuscarinics: Co-administration of umeclidinium bromide with other long-acting muscarinic antagonists or medicinal products containing this active substance has not been studied and is not recommended as it may potentiate known inhaled muscarinic antagonist adverse reactions.
Metabolic and transporter based interactions: Umeclidinium bromide is a substrate of cytochrome P450 2D6 (CYP2D6). The steady-state pharmacokinetics of INCRUSE were assessed in healthy volunteers lacking CYP2D6 (poor metabolisers). No effect on umeclidinium AUC or Cmax was observed at a dose 4-fold higher than the therapeutic dose. An approximately 1.3-fold increase in umeclidinium bromide AUC was observed at an 8-fold higher dose with no effect on umeclidinium bromide Cmax. Based on the magnitude of these changes, no clinically relevant drug interaction is expected when umeclidinium is co-administered with CYP2D6 inhibitors or when administered to subjects genetically deficient in CYP2D6 activity (poor metabolisers).
Umeclidinium bromide is a substrate of P-glycoprotein (P-gp) transporter. The effect of the moderate P-gp inhibitor verapamil (240 mg once daily) on the steady-state pharmacokinetics of umeclidinium bromide was assessed in healthy volunteers. No effect of verapamil was observed on umeclidinium bromide Cmax. An approximately 1.4-fold increase in umeclidinium bromide AUC was observed. Based on the magnitude of these changes, no clinically relevant interaction is expected when INCRUSE is co-administered with P-gp inhibitors.
Other medicinal products for COPD: Although no formal in vivo interaction studies have been performed, inhaled INCRUSE has been used concomitantly with other COPD medicinal products including short and long acting sympathomimetic bronchodilators and inhaled corticosteroids without clinical evidence of interactions.
