Bydureon BCise Drug Interactions

Sulphonylureas: The dose of a sulphonylurea may require adjustment due to the increased risk of hypoglycaemia associated with sulphonylurea therapy (see Dosage & Administration and Precautions).
Gastric emptying: The results of a study using paracetamol as a marker of gastric emptying suggest that the effect of prolonged-release exenatide to slow gastric emptying is minor and not expected to cause clinically significant reductions in the rate and extent of absorption of concomitantly administered oral medicinal products. Therefore, no dose adjustments for medicinal products sensitive to delayed gastric emptying are required.
When 1,000 mg paracetamol tablets were administered, either with or without a meal, following 14 weeks of prolonged-release exenatide therapy, no significant changes in paracetamol AUC were observed compared to the control period. Paracetamol C_max decreased by 16 % (fasting) and 5 % (fed) and t_max was increased from approximately 1 hour in the control period to 1.4 hours (fasting) and 1.3 hours (fed).
The following interaction studies have been conducted using 10 mcg immediate-release exenatide but not prolonged-release exenatide formulations: Warfarin: A delay in t_max of about 2 h was observed when warfarin was administered 35 min after immediate-release exenatide. No clinically relevant effects on C_max or AUC were observed. Increased INR has been spontaneously reported during concomitant use of warfarin and prolonged-release exenatide. INR should be monitored during initiation of prolonged-release exenatide therapy in patients on warfarin and/or cumarol derivatives (see Precautions and Adverse Reactions).
Hydroxy methyl glutaryl coenzyme A reductase inhibitors: Lovastatin AUC and C_max were decreased approximately 40 % and 28 %, respectively, and t_max was delayed about 4 h when immediate-release exenatide was administered concomitantly with a single dose of lovastatin (40 mg) compared with lovastatin administered alone. In 30-week placebo-controlled clinical studies with immediate-release exenatide, concomitant use of exenatide and HMG CoA reductase inhibitors was not associated with consistent changes in lipid profiles (see Pharmacology: Pharmacodynamics under Actions). No predetermined dose adjustment is required; however, lipid profiles should be monitored as appropriate.
Digoxin and lisinopril: In interaction studies of the effect of immediate-release exenatide on digoxin and lisinopril there were no clinical relevant effects on C_max or AUC, however, a delay in t_max of about 2 h was observed.
Ethinyl estradiol and levonorgestrel: Administration of a combination oral contraceptive (30 mcg ethinyl estradiol plus 150 mcg levonorgestrel) one hour before immediate-release exenatide did not alter the AUC, C_max or C_min of either ethinyl estradiol or levonorgestrel. Administration of the oral contraceptive 35 minutes after exenatide did not affect AUC but resulted in a reduction of the C_max of ethinyl estradiol by 45 %, and C_max of levonorgestrel by 27-41 %, and a delay in t_max by 2-4 h due to delayed gastric emptying. The reduction in C_max is of limited clinical relevance and no adjustment of dosing of oral contraceptives is required.
Paediatric population: Interaction studies with exenatide have only been performed in adults.