Table 2.
Proton pump inhibitor | Characteristic |
---|---|
Dexlansoprazole | R-enantiomer of lansoprazole |
Dual delayed release formulation | |
Dual-peaked pharmacokinetic profile | |
24-hour symptom control | |
Administration without regard to food | |
Hepatic metabolism: CYP2C19, CYP3A4 | |
Weak inhibition of CYP2C19 | |
No clinically important effect on exposure to the active metabolite of clopidogrel or clopidogrel-induced platelet inhibition | |
Esomeprazole | S-isomer of omeprazole |
Low initial oral bioavailability increasing over time | |
Hepatic metabolism: CYP2C19, CYP3A4 | |
Potent inhibition of CYP2C19 | |
Possible interaction with clopidogrel via CYP2C19 | |
Delayed absorption with food | |
Lansoprazole | Constant high bioavailability at therapeutic doses |
Rapid onset of maximal acid suppression | |
Delayed absorption with food | |
Concurrent antacid therapy reduces bioavailability | |
Increased theophylline metabolism | |
Hepatic metabolism: CYP2C19, CYP3A4 | |
Weak inhibition of CYP2C19 | |
No clinically important effect on exposure to the active metabolite of clopidogrel or clopidogrel-induced platelet inhibition | |
Omeprazole | Low initial oral bioavailability (35–40%) increasing to ~65% over time |
Dose-dependent kinetics | |
Delayed absorption with food | |
Hepatic metabolism: CYP2C19 | |
Potent inhibition of CYP2C19 | |
Interaction with clopidogrel via CYP2C19 | |
Pantoprazole | Constant bioavailability (~77%) |
Delayed absorption with food | |
Hepatic metabolism: CYP2C19, CYP3A4 | |
Weak inhibition of CYP2C19 | |
No clinically important effect on exposure to the active metabolite of clopidogrel or clopidogrel-induced platelet inhibition |
Rabeprazole has a non-enzymatic pathway so it is not considered here.
CYP, cytochrome P450.