Repaglinide
Repaglinide. Meglitinide — closes pancreatic β-cell K-ATP channels (same target as sulfonylureas, distinct binding site) → insulin release.… Oral half-life 1.7 h.
Meglitinide — closes pancreatic β-cell K-ATP channels (same target as sulfonylureas, distinct binding site) → insulin release. Short half-life supports pre-prandial dosing for post-prandial glucose control. Hepatic CYP2C8 + CYP3A4 substrate.
PK: zero-content on all four — its citation is a mass-balance study with no intravenous arm, reporting no half-life, volume, bioavailability or rate. F 0.6 is replaced by a measured 62.5% against an intravenous infusion. A SCALAR BIOAVAILABILITY IS THE LEAST DEFENSIBLE IN THIS BATCH: exposure varies 16.9-FOLD between individual healthy subjects, with transporter genotype alone accounting for 107 to 188% and a metabolising-enzyme variant for a further 48% reduction. Critically, "The elimination half-life of repaglinide was not associated with any SNP" — so the entire spread lives in bioavailability and first-pass, not in disposition, which is why the fix is a variability flag rather than a different scalar. The half-life is re-sourced to the only published point estimate, which is in ELDERLY type 2 diabetic subjects and is labelled as such. V 30 L is dropped: the only numeric candidate reports its volume in units of litres per hour and is an oral apparent value. The cited study also dosed an oral SOLUTION while the product is a tablet, whose absorption is slower. UNIQUELY IN ITS GROUP THE EFFECT IS COUPLED to plasma, so having no effect compartment is correct.
Pharmacokinetics
- Oral — t½ 1.7 h · F 63%
Sources: PMID:10501822, PMID:9877000, PMID:15961978, PMID:10199798