Lisinopril
Lisinopril. ACE inhibitor — blocks angiotensin I → II conversion in vascular endothelium. Lowers blood pressure, reduces afterload in heart… Oral half-life 13 h.
ACE inhibitor — blocks angiotensin I → II conversion in vascular endothelium. Lowers blood pressure, reduces afterload in heart failure, slows diabetic nephropathy. Renally cleared unchanged; no CYP metabolism. Cough (~10%) from bradykinin accumulation.
PK: F 0.25 is right but was cited to the WRONG PMID — it is verbatim in this record own other reference, "has an oral bioavailability of 25 percent +/- 4 percent, which is unaffected by food", and independently corroborated at 26-27%. THE HALF-LIFE IS NEITHER DISPOSITION NOR SIMPLY WRONG: the primary states "The half-life for the terminal phase (approximately 40 h) was NOT PREDICTIVE of steady-state parameters ... The mean effective half-life for accumulation was 12.6 h", and attributes that terminal phase to binding to the target enzyme. So 12.6 h is the dosing-relevant value and the 40 h is a SATURABLE ACE-BINDING artefact rather than elimination — a distinction that matters because storing the binding phase would make a model predict accumulation that does not occur. ka 0.5 is quantitatively impossible: absorption is carrier-mediated with a time to peak of 6-8 h, and the only published rate is 0.075 /h, nearly sevenfold smaller. V 30 L is dropped; the only candidate is an apparent volume from a paediatric oral-only fit and would double-divide by F.
Pharmacokinetics
- Oral — t½ 12.6 h · F 25%
Sources: PMID:2844083, PMID:2547465, PMID:3014110