Rosuvastatin FT tablets p/o 20mg №10×3

Name:
Rosuvastatin ft.
Description:
Dosage 200 mg: round, biconvex, scored on one side, pink film-coated tablets. The main active ingredient Rosuvastatin Release form film-coated tablets 10 tablets in a blister pack. Each 3 blister packs, together with the leaflet, are placed in a pack of cardboard. Dosage 10 mg Pharmacological action Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase. HMG-CoA reductase is a rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate. Mevalonate is a cholesterol precursor. The main site of action of rosuvastatin is the liver, which is a target organ for lowering the concentration of cholesterol in the blood. Rosuvastatin increases the number of hepatic LDL receptors on the cell surface, thus stimulating the uptake and catabolism of LDL. Rosuvastatin also inhibits the synthesis of VLDL in the liver, thereby reducing the total number of VLDL and LDL particles. Rosuvastatin reduces elevated concentrations of LDL cholesterol, total cholesterol and triglycerides and increases the concentration of HDL cholesterol. Also, rosuvastatin reduces the content of ApoB, non-HDL-cholesterol, VLDL cholesterol, VLDL triglycerides and increases the level of ApoA-I. Rosuvastatin reduces the ratio of LDL cholesterol / HDL cholesterol, total cholesterol / HDL cholesterol, non-HDL-cholesterol / HDL-cholesterol and ApoB / ApoA-I. The therapeutic effect is manifested within the first week from the start of taking the drug. 90% of the maximum possible response is achieved within 2 weeks. The maximum possible response is usually achieved by the 4th week of taking rosuvastatin and then maintained at the achieved level with further drug administration. ROSUVASTATIN FT is effective in adults with hypercholesterolemia with or without triglyceridemia, regardless of race, sex, age, and in such special categories of patients as patients with diabetes mellitus and patients with familial hypercholesterolemia. Rosuvastatin is extensively taken up by the liver, which is the main site for cholesterol synthesis and LDL cholesterol clearance. The systemic exposure of rosuvastatin increases in proportion to the dose. When taking rosuvastatin several times a day, no changes in pharmacokinetic parameters are observed. There was no clinically significant effect of age or gender on the pharmacokinetics of rosuvastatin in adults. Pharmacokinetic studies demonstrate an approximately 2-fold increase in median AUC and Cmax in patients of Asian origin (Japanese, Chinese, Filipinos, Vietnamese and Koreans) compared with those in Caucasians; in Southeast Asians, an increase in median AUC and Cmax by approximately 1.3 times was noted. Population pharmacokinetic analysis did not reveal clinically significant differences in the pharmacokinetics of rosuvastatin in Caucasians, representatives of Latin America, the Caribbean, and people of African descent. In a study in patients with varying degrees of impaired renal function, mild to moderate renal disease had no effect on plasma concentrations of rosuvastatin or its N-desmethyl metabolite. In patients with severe renal impairment (creatinine clearance less than 30 ml / min), a 3-fold increase in the concentration of rosuvastatin in blood plasma and a 9-fold increase in the concentration of the N-desmethyl metabolite were observed compared with healthy volunteers. Steady-state plasma concentrations of rosuvastatin in patients undergoing hemodialysis were approximately 50% higher than in healthy volunteers. In a study in patients with varying degrees of hepatic impairment, there was no evidence of an increase in rosuvastatin exposure in patients with a Child-Pugh score of 7 or less. Two patients with scores of 8 and 9 experienced an increase in systemic exposure of at least 2-fold compared with patients who scored lower. There are no data on the features of the pharmacokinetics of rosuvastatin in patients with a score of more than 9 according to the Child-Pugh criteria, since there is no experience in this category of patients. The pharmacokinetics of HMG-CoA reductase inhibitors, including rosuvastatin, involve transport proteins OATP1B1 and BCRP. Patients with SLCO1B1 (OATP1B1) and/or ABCG2 (BCRP) genetic polymorphisms are at risk of increased exposure to rosuvastatin. The individual polymorphisms SLCO1B1 c.521CC and ABCG2 c.421AA are associated with increased exposure (AUC) of rosuvastatin compared to the genotypes SLCO1B1 c.521TT or ABCG2 c.421CC. This specific genotyping has not been implemented in clinical practice protocols, however, patients who are known to have these types of polymorphisms are advised to prescribe a lower daily dose of rosuvastatin. Pharmacokinetic studies involving children and adolescents 10-17 and 6-17 years old with heterozygous familial hypercholesterolemia have shown that the exposure of rosuvastatin in children and adolescents is comparable or less than that in adult patients. Indications for use 1. Treatment of hypercholesterolemia – primary hypercholesterolemia (type IIa, including heterozygous familial hypercholesterolemia) or mixed dyslipidemia (type IIb) in adults, adolescents, and children 6 years of age and older as an adjunct to diet when the effect of diet and other non-drug treatments (eg, exercise, weight loss) is insufficient; Homozygous familial hypercholesterolemia in adults, adolescents, and children aged 6 years and older as an adjunct to diet and other lipid-lowering therapies (eg, LDL apheresis), or when such therapies do not work as expected effect. 2. Primary prevention of cardiovascular disease Primary prevention of severe cardiovascular disease (stroke, myocardial infarction, diseases requiring arterial revascularization) in patients without clinical evidence of coronary heart disease (CHD) who are considered to be at increased risk development of cardiovascular disease (age men ≥ 50 years and age women ≥ 60 years, concentration of highly sensitive C-reactive protein (hsCRP) ≥ 2 mg/l and the presence of at least one of the additional risk factors for the development of cardiovascular disease, such as hypertension, low HDL cholesterol, smoking, or early development of CAD in family members). Dosage and administration Before starting the use of the drug ROSUVASTATIN FT, the patient should be prescribed a standard diet aimed at lowering cholesterol levels. This diet should be followed throughout the entire period of therapy with rosuvastatin. The dose of the drug should be adjusted individually depending on the goal of therapy and the patient’s response to the drug, taking into account current generally accepted recommendations for target lipid levels and patient management. ROSUVASTATIN FT should be taken once a day. The tablet should be swallowed whole without chewing and washed down with water. ROSUVASTATIN FT can be taken at any time of the day, regardless of meals. It is advisable to take the tablet at the same time every day. Treatment of hypercholesterolemia The recommended starting dose of ROSUVASTATIN FT is 5 mg or 10 mg once daily for both patients who have not previously taken statins and for patients who are switched to rosuvastatin after using another HMG-CoA reductase inhibitor. When choosing an initial dose, individual cholesterol levels, the predicted risk of cardiovascular disease, and the potential risk of developing adverse reactions should be taken into account (see the “Side effect” section). Dose adjustment upwards under the control of lipid metabolism can be made after 4 weeks from the start of the current dose, if necessary; this is due to the fact that the maximum possible effect when taking rosuvastatin at a certain dose is usually achieved by the 4th week of therapy and is maintained at the achieved level with further use of the drug (see section “Pharmacological properties”). When using a dose of 40 mg, there is a higher frequency of reports of adverse reactions than when using lower doses (see section “Side Effects”). Therefore, final titration up to the maximum daily dose (40 mg) should only be considered in patients with severe hypercholesterolemia associated with high CV risk (particularly in patients with familial hypercholesterolemia) who fail to achieve their individual therapy goals with taking the drug at a dose of 20 mg and for which regular routine medical supervision can be carried out (see section “Special instructions and precautions”). At the start of the 40 mg dose, a doctor’s supervision is recommended. Prevention of cardiovascular disease In a study to reduce the risk of cardiovascular disease, rosuvastatin was used at a dose of 20 mg per day. Children and adolescents The appointment of rosuvastatin to children and adolescents should be made only by qualified specialists. Children and adolescents aged 6 to 17 years (Tanner stage 70 years is 5 mg (see section “Special Instructions and Precautions”). No other dose adjustment is required due to age. Patients with renal insufficiency Dose adjustment in patients with Mild to moderate renal impairment is not required.The recommended starting dose for patients with moderate renal impairment (creatinine clearance < 60 ml/min) is 5 mg. The 40 mg dose is contraindicated in patients with moderate renal impairment. The use of the drug ROSUVASTATIN FT at any dose is contraindicated in patients with severe renal impairment (see sections "Contraindications" and "Pharmacological properties"). Patients with impaired liver function There was no increase in systemic exposure of rosuvastatin in patients with a Child criteria - I drink 7 or less.However, an increase in systemic exposure was observed b in patients with a Child-Pugh score of 8 and 9 (see section "Pharmacological properties"). In these patients, an assessment of liver function should be carried out (see section "Special instructions and precautions"). There is no experience of use in patients with a score of more than 9 according to the Child-Pugh criteria. ROSUVASTATIN FT is contraindicated in patients with active liver disease (see section "Contraindications"). Race An increase in the systemic exposure of rosuvastatin is observed in patients of Asian origin (see sections "Contraindications", "Special instructions and precautions", "Pharmacological properties"). The recommended starting dose for patients in this group is 5 mg. The 40 mg dose is contraindicated in Asian patients. Genetic polymorphisms Special types of genetic polymorphisms are known that can lead to an increase in the exposure of rosuvastatin (see the section "Pharmacological properties"). For patients known to have these specific types of polymorphisms, a lower daily dose of ROSUVASTATIN FT is recommended. Patients with factors predisposing to the development of myopathy The recommended starting dose for patients with factors predisposing to the development of myopathy is 5 mg (see section "Special Instructions and Precautions"). The 40 mg dose is contraindicated in some of these patients (see Contraindications section). Concomitant drug therapy Rosuvastatin is a substrate for various transport proteins (eg, OATP1B1 and BCRP). The risk of myopathy (including rhabdomyolysis) is increased when ROSUVASTATIN FT is co-administered with certain medicinal products that may increase plasma concentrations of rosuvastatin due to interactions with these transport proteins (eg, cyclosporine and certain protease inhibitors, including combinations of ritonavir with atazanavir, lopinavir and / or tipranavir; see sections "Special instructions and precautions", "Interaction with other medicinal products and other forms of interaction"). Whenever possible, consideration should be given to prescribing alternative medicinal products and, if necessary, consider temporarily discontinuing rosuvastatin therapy. In situations where the co-administration of these drugs and rosuvastatin cannot be avoided, the benefit / risk ratio of concurrent therapy and the need for dose adjustment of the drug ROSUVASTATIN FT should be carefully assessed (see section "Interaction with other drugs and other forms of interaction"). If you have taken a higher dose of rosuvastatin than was prescribed to you by your doctor, you should seek advice from your doctor or the nearest medical facility. When you are hospitalized and / or when you are being treated for any other disease / pathological condition, you must inform the medical staff that you are currently taking rosuvastatin. Don't worry if you miss your next dose of rosuvastatin; take your next scheduled dose at the usual time. It is not allowed to take a double dose in order to compensate for the missed one! If you wish to temporarily suspend / stop therapy with rosuvastatin, you must first notify your doctor and follow his recommendations. When therapy with rosuvastatin is discontinued, cholesterol levels may rise again. Use during pregnancy and lactation Pregnancy ROSUVASTATIN FT is contraindicated during pregnancy (see section "Contraindications"). Women of childbearing potential should use appropriate contraception while taking rosuvastatin. Since cholesterol and other products of cholesterol biosynthesis are essential for fetal development, the potential risk associated with inhibition of HMG-CoA reductase is of higher significance than the benefits of using rosuvastatin during pregnancy. Animal studies provide limited data on reproductive toxicity. If the patient becomes pregnant while taking ROSUVASTATIN FT, treatment should be discontinued. The period of breastfeeding ROSUVASTATIN FT is contraindicated during the period of breastfeeding (see section "Contraindications"). It has been established that rosuvastatin is excreted in breast milk in rats. There are no data on the allocation of rosuvastatin with breast milk in humans. If it is necessary to prescribe a drug during lactation, breastfeeding should be stopped. Precautions Effects on the kidneys Proteinuria, detected by dipstick analysis and mainly of tubular origin, has been observed in patients treated with high doses of rosuvastatin, in particular the 40 mg dose; in most cases, proteinuria was transient or intermittent. It has not been established that proteinuria has a prognostic value in relation to the occurrence of acute or progression of an existing kidney disease (see section "Side effects"). Based on post-marketing data from rosuvastatin-based medicinal products, the incidence of serious renal impairment is higher in the 40 mg dose population. Renal function should be assessed as part of the routine medical follow-up of patients taking rosuvastatin 40 mg. Effects on skeletal muscle Skeletal muscle disorders (eg, myalgia, myopathy and, in rare cases, rhabdomyolysis) have been reported with rosuvastatin at any dose, and especially at doses above 20 mg. Very rare cases of rhabdomyolysis have been described with the use of the combination "ezetimibe + HMG-CoA reductase inhibitor". Pharmacodynamic interactions between these active substances cannot be excluded (see section "Interaction with other medicinal products and other forms of interaction"); therefore, care should be taken when using them together. According to data obtained during the post-marketing use of drugs based on rosuvastatin (as well as on the basis of other inhibitors of HMG-CoA reductase), the incidence of rhabdomyolysis associated with taking rosuvastatin is higher with a dose of 40 mg. Creatine Kinase Measurement Creatine kinase measurement should not be taken after strenuous physical activity or if there are other possible causes of an increase in creatine kinase levels - this may lead to an erroneous interpretation of the test result. If before the start of therapy with rosuvastatin, the level of creatine kinase is significantly increased (the value is more than 5 times the value of the upper limit of normal), a re-analysis should be performed after 5-7 days. If, in the reanalysis, the value of the creatine kinase level is also more than 5 times the upper limit of normal, treatment with rosuvastatin should not be started. Prior to treatment, Rosuvastatin, like other HMG-CoA reductase inhibitors, should be administered with caution to patients with risk factors for myopathy/rhabdomyolysis. These factors include: - impaired renal function; - hypothyroidism; - the presence in a personal or family history of hereditary muscular pathology; - a history of manifestations of myotoxicity while taking another inhibitor of HMG-CoA reductase or fibrate; - alcohol abuse; - age over 70 years; - situations in which an increase in the concentration of rosuvastatin in the blood plasma is possible (see sections "Method of application and doses", "Interaction with other drugs and other forms of interaction", "Pharmacological properties"); - Asian origin; - concomitant use of fibrates. In such patients, the ratio of expected benefits and possible risks associated with the use of rosuvastatin should be carefully assessed. If it is decided to prescribe a drug, regular medical monitoring of the patient is recommended throughout the entire course of therapy. If the creatine kinase level determined in a patient before the start of rosuvastatin use is significantly (more than 5 times) higher than the upper limit of normal, treatment with ROSUVASTATIN FT should not be started. During treatment Patients who are prescribed ROSUVASTATIN FT should be informed of the need to immediately notify the attending physician of the occurrence of unexplained muscle pain, muscle weakness, cramps, especially if these symptoms are combined with a feeling of general malaise or with fever. In such patients, the level of creatine kinase in the blood serum should be determined. Therapy with rosuvastatin is recommended to be interrupted if the level of creatine kinase in the blood serum is significantly elevated (the value of the level of creatine kinase is more than 5 times the value of the upper limit of normal). Also, therapy should be interrupted if muscle symptoms are significant and cause daily discomfort (even if the value of the creatine kinase level is not more than 5 times the value of the upper limit of normal). If, after discontinuation of rosuvastatin, the symptoms disappeared and the level of creatine kinase returned to normal values, then consideration should be given to resuming the use of rosuvastatin or another HMG-CoA reductase inhibitor at a minimum dose and with careful monitoring of the patient's condition. Routine monitoring of serum creatine kinase levels in asymptomatic patients is neither practical nor required. Very rarely, immune-mediated necrotizing myopathy has been reported during or after treatment with statins, including rosuvastatin. Immune-mediated necrotizing myopathy is clinically characterized by proximal muscle weakness and increased serum creatine kinase levels; these symptoms persist despite discontinuation of the statin. In clinical trials involving a small number of patients, more pronounced skeletal muscle disorders were not observed during the use of rosuvastatin and concomitant therapy. However, an increase in the incidence of myositis and myopathy has been observed in patients receiving other HMG-CoA reductase inhibitors in combination with fibric acid derivatives (including gemfibrozil), cyclosporine, nicotinic acid, azole antifungals, protease inhibitors, and antibiotics from the macrolides. Gemfibrozil increases the risk of myopathy when given concomitantly with certain HMG-CoA reductase inhibitors. Therefore, the combination "rosuvastatin + gemfibrozil" is not recommended. The benefit of further lipid management through the use of rosuvastatin + fibrate or rosuvastatin + niacin should be carefully weighed against the potential risks associated with the use of such combinations. The use of rosuvastatin at a dose of 40 mg in combination with a drug from the fibrate group is prohibited (see sections "Interaction with other drugs and other forms of interaction" and "Side effects"). Rosuvastatin should not be administered simultaneously with fusidic acid in dosage forms that involve systemic action; also, rosuvastatin should not be administered within 7 days after discontinuation of fusidic acid. In patients in whom the use of systemic fusidic acid is considered essential, statin therapy should be interrupted while fusidic acid is being used. Cases of rhabdomyolysis (including fatal cases) have been reported in patients who used both fusidic acid and a statin at the same time (see the section "Interaction with other medicinal products and other forms of interaction"). It is necessary to inform patients about the need to immediately seek medical help if muscle weakness, muscle pain, painful muscle sensitivity appear. Statin therapy can be resumed 7 days after the last dose of fusidic acid. In exceptional cases, when prolonged use of fusidic acid in dosage forms that involve systemic action is required (for example, for the treatment of severe infections), the question of the possibility of simultaneous use of rosuvastatin and fusidic acid should be considered on an individual basis; patients who are prescribed this combination should be under close medical supervision. Rosuvastatin should not be administered to any patient with an acute, severe condition that suggests myopathy or predisposes to the development of renal failure due to rhabdomyolysis. Such conditions include, for example, sepsis, hypotension, pathology requiring extensive surgical intervention, trauma, severe metabolic, endocrine and electrolyte disturbances, or uncontrolled seizures. Effects on the liver As with other HMG-CoA reductase inhibitors, rosuvastatin should be used with caution in patients who abuse alcohol and/or have a history of liver disease. It is recommended to conduct a laboratory and instrumental assessment of liver function before and within 3 months after the start of rosuvastatin therapy. Rosuvastatin should be discontinued or its dose adjusted downward if serum transaminase levels are more than 3 times the upper limit of normal. According to post-marketing data, the incidence of severe liver disorders (which manifest themselves mainly as an increase in liver transaminase levels) is higher in the group of patients taking rosuvastatin at a dose of 40 mg. In patients with secondary hypercholesterolemia due to hypothyroidism or nephrotic syndrome, the underlying (underlying secondary hypercholesterolemia) pathological condition should be corrected before starting therapy with rosuvastatin. Race According to pharmacokinetic studies, there is an increase in the systemic exposure of rosuvastatin in people of Asian origin compared with representatives of the Caucasian race (see sections "Method of application and doses", "Contraindications" and "Pharmacological properties"). Protease inhibitors An increase in the systemic exposure of rosuvastatin was observed in patients receiving rosuvastatin simultaneously with various protease inhibitors in combination with ritonavir. During the period of initiation of therapy and when titrating the dose upwards in patients taking protease inhibitors, the benefit of lowering lipid levels through the use of rosuvastatin in HIV-infected patients receiving protease inhibitors should be carefully weighed against the potential risks associated with an increase in the concentration of rosuvastatin in blood plasma. The concomitant use of rosuvastatin and certain protease inhibitors is not recommended; if necessary, simultaneous use should be carefully titrated dose of rosuvastatin. Lactose intolerance This medicinal product contains lactose. Patients with rare hereditary problems of galactose intolerance, lactase deficiency or glucose/galactose malabsorption should not take ROSUVASTATIN FT. A doctor's consultation is required. Interstitial lung disease There are isolated reports of the development of interstitial lung disease against the background of the use of some statins, especially when taking them for a long time (see section "Side effects"). The group of symptoms may include dyspnea, non-productive cough and deterioration in general condition (fatigue, weight loss, fever). If there is a suspicion that the patient has developed interstitial lung disease, statin therapy should be discontinued. Diabetes mellitus Some evidence suggests that statins increase blood glucose levels and, in some patients at high risk of developing diabetes, may lead to a level of hyperglycemia for which standard antidiabetic agents are justified. However, this risk is inferior in importance to the benefit of reducing the risk of vascular complications with statins. Therefore, it is hardly advisable to cancel statin therapy due to the potential risk of developing hyperglycemia. For patients at risk for the development of hyperglycemia (fasting blood glucose concentration in the range of 5.6-6.9 mmol / l, body mass index of more than 30 kg / m2, an increase in serum triglyceride levels, hypertension), dynamic monitoring should be carried out, which provides for a physical examination, instrumental and laboratory studies. This observation should be carried out in accordance with current national clinical protocols. Children and adolescents Assessment of height, body weight, body mass index and development of secondary signs of puberty (according to the Tanner scale) in patients aged 6 to 17 years who took rosuvastatin was carried out for 2 years. After a 2-year study, no effect of rosuvastatin therapy on height, body weight, body mass index or puberty was recorded. In one clinical study, children and adolescents received rosuvastatin for 52 weeks. According to the analysis of the results of the study, an increase in the level of creatine kinase more than 10 times the upper limit of the norm, muscle symptoms after training or increased physical activity were observed more often compared with similar observations in clinical studies involving adults (see section "Side Effects"). Use in children The safety and efficacy of rosuvastatin in children under 6 years of age have not been studied. Therefore, ROSUVASTATIN FT is not recommended for use in children under 6 years of age. Influence on the ability to drive a car or other moving mechanisms Studies of the effect of rosuvastatin on the ability to drive a car or other moving mechanisms have not been conducted. However, given the pharmacodynamic properties of rosuvastatin, it is unlikely that the drug ROSUVASTATIN FT will affect this ability. When driving vehicles or working with moving mechanisms, as well as when planning such activities, it should be borne in mind that during therapy with rosuvastatin, dizziness and other undesirable reactions may occur that may affect the ability to drive a car or other moving mechanisms (see section " Side effect”) Interaction with other drugs Effect of concomitant drugs on rosuvastatin Inhibitors of transport proteins Rosuvastatin is a substrate for several transport proteins, including the transport protein OATP1B1, which is responsible for the uptake and movement of substances into the liver cells, and the efflux transport protein BCRP. The simultaneous use of rosuvastatin and drugs that inhibit these transport proteins can lead to an increase in the concentration of rosuvastatin in the blood plasma and, thereby, to an increase in the risk of developing myopathy (see sections "Method of application and doses", "Special instructions and precautions" , table 1 in the section "Interaction with other medicinal products and other forms of interaction"). Cyclosporine During the period of simultaneous use of rosuvastatin and cyclosporine, the AUC values of rosuvastatin were on average 7 times higher than those observed in healthy volunteers (see table 1). Rosuvastatin is contraindicated in patients taking cyclosporine (see section "Contraindications"). Simultaneous use does not affect the concentration of cyclosporine in plasma. Protease inhibitors Although the exact mechanism of interaction is unknown, the simultaneous use of a protease inhibitor and rosuvastatin can significantly increase the exposure of rosuvastatin (see table 1). For example, in a pharmacokinetic study, the simultaneous use of 10 mg rosuvastatin and a combination drug containing two protease inhibitors (300 mg atazanavir/100 mg ritonavir) in healthy volunteers was accompanied by an approximately 3-fold increase in AUC of rosuvastatin and an approximately 7-fold increase in Cmax of rosuvastatin. The combined use of the drug ROSUVASTATIN FT and certain combinations of protease inhibitors can only be carried out after careful consideration of the need to adjust the dose of rosuvastatin, based on the expected increase in exposure to rosuvastatin (see sections "Method of administration and doses", "Special instructions and precautions", table 1 in the section "Interaction with other medicinal products and other forms of interaction"). Gemfibrozil and other lipid-lowering agents The simultaneous use of rosuvastatin and gemfibrozil led to an increase in AUC and Cmax of rosuvastatin by 2 times (see section "Special instructions and precautions"). Based on data from specific drug interaction studies, a pharmacokinetically significant interaction between rosuvastatin and fenofibrate should not be expected, but a pharmacodynamic interaction may occur. Gemfibrozil, fenofibrate, other fibrates and niacin (nicotinic acid) at lipid-lowering doses (greater than or equal to 1 g/day) increase the risk of myopathy when used concomitantly with HMG-CoA reductase inhibitors. This is probably due to the fact that these drugs can cause myopathy when used as monotherapy. It is forbidden to take rosuvastatin at a dose of 40 mg simultaneously with fibrates (see sections "Contraindications", "Special instructions and precautions"). Patients who are taking any drugs from the fibrate group should start taking the drug ROSUVASTATIN FT at a dose of 5 mg. Ezetimibe The simultaneous use of rosuvastatin at a dose of 10 mg and ezetimibe at a dose of 10 mg in patients with hypercholesterolemia led to an increase in the AUC of rosuvastatin by 1.2 times (see table 1). The possibility of a pharmacodynamic interaction between rosuvastatin and ezetimibe, leading to the development of side effects, cannot be excluded (see section "Special Instructions and Precautions"). Antacids Simultaneous administration of rosuvastatin with an antacid suspension containing aluminum hydroxide and magnesium hydroxide resulted in a decrease in the plasma concentration of rosuvastatin by approximately 50%. This effect weakened when taking an antacid 2 hours after taking rosuvastatin. The clinical significance of this interaction