Amiodarone
Amiodarone. Class III antiarrhythmic — multi-channel blocker (K+, Na+, Ca²⁺, β-adrenergic). Inhibits CYP3A4, CYP2C9, CYP2D6, P-gp — broad DDI… Oral half-life 32 h.
Class III antiarrhythmic — multi-channel blocker (K+, Na+, Ca²⁺, β-adrenergic). Inhibits CYP3A4, CYP2C9, CYP2D6, P-gp — broad DDI profile. Massive Vd (~60 L/kg) and extreme half-life (~40-50 days) require months for steady-state and washout. Pulmonary, hepatic, thyroid toxicity at chronic exposure.
PK: THE STORED MODEL FAILED A PHYSICAL CHECK AGAINST ITS OWN CITED PAPER — {600 mg, F 0.5, V 5000 L} caps Cmax at 0.060 mg/L against the 0.828 that paper observed, FOURTEEN TIMES LOW. Its IV row was hung on a study whose title is "after extravascular administration of a single dose"; there is no intravenous arm in it. Its F 0.5 came from a RELATIVE bioavailability measurement ("Bioavailability extent (EBA) of examined preparation was 120 per cent in comparison with the standard one"). And t½ 1080 h is 45 days, the exact midpoint of this record own prose, describing the POST-CHRONIC-THERAPY washout rather than any single-dose phase. Everything moves to one internally consistent study with both arms in the same seven subjects. THIS IS A TRADE, NOT A FIX, AND BOTH SIDES WERE COMPUTED: the old set was 14x low on single-dose Cmax and 1.5x high at steady state; the new one is 1.7x and 2.5x low. The new one is less wrong and fully verbatim. ka 0.49 IS VERIFIED AND SURVIVES — one of three in this batch, and the first anywhere in six batches. INTERACTIONS: FIVE OF THE SIX AFFINITIES ARE THE CITED EXPOSURE CHANGE INVERTED THROUGH ONE ASSUMED CONCENTRATION OF 2 µM, and two of the notes already stated it. The five span an exposure rise, a doubled plasma level, a dose reduction converted as a reciprocal, and a verbatim AUC pair — all landing on the same constant. THE DIGOXIN EDGE IS LEFT ALONE AND LOGGED: it does not reconstruct from its cited 33 to 43 percent bioavailability rise, and it is the one edge in the block that is NOT enzyme inhibition at all but P-glycoprotein transport, where the solver competitive-inhibition form is a borrowed shape rather than the mechanism.
Pharmacokinetics
- Oral — t½ 31.6 h · F 31% · ka 0.49 h⁻¹ · Vd 376 L
- IV — t½ 34.5 h · F 100% · Vd 376 L
Related compounds
- Digoxin — major
- Simvastatin — major
- Warfarin — major
- Flecainide — major
- Metoprolol — major
- Phenytoin — caution
Sources: PMID:17301736, PMID:11796427, PMID:2128031, PMID:15541258, PMID:2337037, PMID:6540111