Rosuvastatin
Rosuvastatin. Same HMG-CoA-R inhibition mechanism; hydrophilic (low CNS penetration → theoretically fewer cognitive side effects). Primarily… Oral half-life 19 h.
Same HMG-CoA-R inhibition mechanism; hydrophilic (low CNS penetration → theoretically fewer cognitive side effects). Primarily renal + minor CYP2C9 metabolism — fewer CYP interactions than atorvastatin / simvastatin. Most potent statin by mg — 5 mg ≈ atorvastatin 10 mg.
PK: F 0.2 is right but its cited paper is an oral-only mass-balance study with NO INTRAVENOUS ARM and could not have measured it; the real crossover exists, was uncited, and gives 20.1% alongside a steady-state volume of 134 L that is intravenous-derived, so the pairing is legitimate. V 140 L appears in no source. ka 0.595 is BACK-DERIVED rather than measured: against the stored half-life it reproduces a time to peak of exactly 5.00 h, and 5 h is itself the UPPER endpoint of a stated 3 to 5 h range; it is dropped. The half-life of 19 h is a genuine disposition value but is label-sourced, which is now recorded rather than attributed to a paper that does not state it. AN UNMODELLED TWOFOLD COVARIATE: exposure is 1.6 to 2.3 times higher in Chinese, Malay and Indian subjects than in white subjects — and, refuting the obvious explanation, the transporter genotype "did not account for the observed pharmacokinetic differences". THE EFFECT-COMPARTMENT VALUE IS REMOVED: the target is inside the hepatocyte, concentrated there by a transporter, and the clinical endpoint is cholesterol at four weeks, which no equilibration rate can bridge.
Pharmacokinetics
- Oral — t½ 19 h · F 20% · Vd 134 L
Sources: PMID:14693307, PMID:12773150, PMID:14667956, PMID:16198652