Isradipine
Isradipine. Dihydropyridine CCB — vascular smooth muscle preference. Studied for Parkinson disease neuroprotection (STEADY-PD III, neutral).… Oral half-life 2.8 h.
Dihydropyridine CCB — vascular smooth muscle preference. Studied for Parkinson disease neuroprotection (STEADY-PD III, neutral). Less commonly used than amlodipine for routine hypertension.
PK: MY FORMULATION PRIOR WAS REFUTED AND THE UNDERLYING DEFECT WAS REAL ANYWAY. The cited study used oral SOLUTION and CAPSULES only - no sustained-release arm exists in it - so the nifedipine defect is NOT present here. But the stored half-life was absorption-limited by a different route, and the paper that proves it asks the question in its own title, "half-life shorter than expected?": "A terminal half-life of 8-9 hr has been reported, in several pharmacokinetic studies after ORAL administration of isradipine ... Mean terminal half-life after INTRAVENOUS administration was calculated to be 2.8 hr". The stored 8 was precisely the oral artefact. F 0.17 was never measured either - the cited study determined RELATIVE bioavailability only and states no percentage - and becomes 0.28, verbatim and absolute against an intravenous comparator in the same crossover, so the F and the half-life now come from one internally consistent study. ADVERSARIAL CAVEAT RECORDED: that study sampled only 10-12 h, which may truncate a long terminal phase and bias the intravenous half-life short; an AUC ratio is far less sensitive to truncation than a half-life, so the bioavailability is the sturdier of the two. ka 1.5 is removed - it is both the capsule tmax of 1.57 h and a back-derivation to a round 2.02 h peak. V 196 L is in no abstract.
Pharmacokinetics
- Oral — t½ 2.8 h · F 28% · Vd 196 L
Sources: PMID:2965165, PMID:6088927, PMID:10815751