Each Film-coated tablet contains
rosuvastatin calcium equivalent to rosuvastatin......5mg
Each Film-coated tablet contains
rosuvastatin calcium equivalent to rosuvastatin....10mg
In clinical pharmacology studies in man, peak plasma concentrations of rosuvastatin were reached 3 to 5 hours following oral dosing. Both peak concentration (Cmax) and area under the plasma concentration-time curve (AUC) increased in approximate proportion to rosuvastatin dose. The absolute bioavailability of rosuvastatin is approximately 20%. Administration of rosuvastatin with food did not affect the AUC of rosuvastatin. The AUC of rosuvastatin does not differ following evening or morning drug administration.
Mean volume of distribution at steady-state of rosuvastatin is approximately 134 liters. Rosuvastatin is 88% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations.
Rosuvastatin is not extensively metabolized; approximately 10% of a radio labeled dose is recovered as metabolite. The major metabolite is N-desmethylrosuvastatin, which is formed principally by cytochrome P450 2C9, and in vitro studies have demonstrated that N-desmethylrosuvastatin has approximately one-sixth to one-half the HMG-CoA reductase inhibitory activity of rosuvastatin. Overall, greater than 90% of active plasma HMG-CoA reductase inhibitory activity is accounted for by rosuvastatin.
Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces(90%). The elimination half-life (t1/2) of rosuvastatin is approximately 19 hours. After an intravenous dose, approximately 28% of total body clearance was via the renal route, and 72% by the hepatic route.
Geriatric: There were no differences in plasma concentrations of rosuvastatin between the nonelderly and elderly populations (age > 65 years).
Renal Impairment: Mild to moderate renal impairment (creatinine clearance > 30mL/min/1.73m2) had no influence on plasma concentrations of rosuvastatin when oral doses of 20 mg rosuvastatin were administered for 14 days. However, plasma concentrations of rosuvastatin increased to a clinically significant extent (about 3-fold) in patients with severe renal impairment (CLcr < 30 mL/min/1.73m2) compared with healthy
Subjects (CLcr> 80 mL/min/1.73m2).
Hemodialysis: Steady-state plasma concentrations of rosuvastatin in patients on chronic hemodialysis were approximately 50% greater compared with healthy volunteer subjects with normal renal function.
Hepatic Impairment: In patients with chronic alcohol liver disease, plasma concentrations of rosuvastatin were modestly increased. In patients with Child-Pugh A disease, C max and AUC were increased by 60% and 5%, respectively, as compared with patients with normal liver function. In patients with Child-Pugh B disease, Cmax and AUC were increased 100% and 21%, respectively, compared with patients with normal liver function.
Hyperlipidemia and Mixed Dyslipidemia
Primary Dysbetalipoproteinemia (Type III hyperlipoproteinemia)
Homozygous Familial Hypercholesterolemia
Heterozygous Familial Hypercholesterolemia in Pediatrics (10 to 17 years)
Slowing of the Progression of Atherosclerosis
Primary Prevention of Cardiovascular Disease
Patients with a known hypersensitivity to any component of this product. Hypersensitivity reactions including rash, pruritus, Urticaria and angioedema have been reported with rosuvastatin
Patients with active liver disease, which may include unexplained persistent elevations of hepatic Transaminase levels
Women who are pregnant or may become pregnant.
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