Adults, adolescents, and children over the age of 10 yEars and Nose with primary hypercholesterolemia (type IIA, including heterozygous familial hypercholesterolemia) or mixed dyslipidemia (type IIB) as a Supplement to the diet, when dieting and the use of other non-medicinal products (such as exercise, weight loss) is insufficient. In homozygous familial hypercholesterolemia as a Supplement to diet and other lipid-lowering treatments (for example, LDL apheresis) or in cases where such treatment is inappropriate. Prevention of cardiovascular disorders Prevention of significant cardiovascular disorders in patients who are estimated to be at high risk for the first case of cardiovascular disease (see the section “Pharmacodynamics”), in addition to correcting other risk factors.
Evoid №60 Storage
active substance: rosuvastatin;
1 tablet contains rosuvastatin calcium 5.2 mg, 10.4 mg, 20.8 mg or 41.6 mg, which is equivalent to rosuvastatin 5 mg, 10 mg, 20 mg or 40 mg;
Excipients: calcium citrate, microcrystalline cellulose, hydroxypropylcellulose, mannitol (E 421), lactose anhydrous, crospovidone, magnesium stearate;
film coating (tablets of 5 mg): polyvinyl alcohol, titanium dioxide (E 171), macrogol 3350, talc, tartrazine (E 102), yellow FCF (E 110), indigo carmine (E 132);
film coating (tablets of 10 mg, 20 mg, 40 mg): polyvinyl alcohol, titanium dioxide (E 171), macrogol 3350, talc, tartrazine (E 102), special red speaker (E 129), yellow FCF (E 110) ), indigo carmine (E 132).
Evoid №60 Dosage form
Basic physical and chemical properties:
5 mg tablets: round tablets with a biconvex surface, film-coated, yellow;
10 mg tablets: round tablets with a biconvex surface, film-coated, pink;
tablets of 20 mg: oval tablets with a biconvex surface, with a line on one side, covered with a film coating, pink;
tablets of 40 mg: oblong tablets with a biconvex surface, with a line on one side, covered with a film coating, pink.
Hypolipidemic drugs. HMG-CoA reductase inhibitors.
ATX code C10A A07.
Evoid №60 Pharmacological properties
Mechanism of action
Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, an enzyme that determines the reaction rate and converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol. The main site of action of rosuvastatin is the liver, a target organ for lowering cholesterol levels.
Rosuvastatin increases the number of LDL receptors on the surface of liver cells, enhancing LDL uptake and catabolism, and inhibits hepatic LDL synthesis, thereby reducing the total number of LDL and LDL particles.
Treatment of hypercholesterolemia
Adults, adolescents, and children over 10 years of age with primary hypercholesterolemia (type IIa, including heterozygous familial hypercholesterolemia) or mixed dyslipidemia (type IIb) as a dietary supplement when dieting and other non-drug use body weight) is insufficient.
In homozygous familial hypercholesterolemia as an adjunct to diet and other lipid-lowering treatments (eg LDL apheresis) or when such treatment is inappropriate.
Prevention of cardiovascular disorders
Prevention of significant cardiovascular events in patients who are estimated to be at high risk for the first case of cardiovascular events (see Pharmacodynamics) as an adjunct to correction of other risk factors.
patients with hypersensitivity to rosuvastatin or any of the excipients;
patients with active liver disease, including persistent elevations of serum transaminases of unknown etiology and any elevations of serum transaminases three times the upper limit of normal (ULN);
patients with severe renal impairment (creatinine clearance <30 ml / min);
patients with myopathy;
patients receiving concomitant cyclosporine;
during pregnancy and breastfeeding, as well as women of reproductive age who do not use appropriate contraceptives.
A dose of 40 mg is contraindicated in patients with a predisposition to myopathy / rhabdomyolysis.
Factors of such risk include:
moderate renal impairment (creatinine clearance <60 ml / min);
presence in the personal or family history of hereditary muscle diseases;
history of myotoxicity with other HMG-CoA reductase inhibitors or fibrates;
situations that may lead to increased plasma concentrations of the drug;
belonging to the Mongoloid race;
concomitant use of fibrates (see sections “Peculiarities of use”, “Interaction with other medicinal products and other forms of interaction” and “Pharmacokinetics”).