Mertenil, pills 20mg, 30pcs

Composition

Active ingredient:

rosuvastatin calcium – 20 mg;

Auxiliary substances:

MCC 12 — 86.2 mg;

lactose monohydrate-174 mg;

magnesium hydroxide-15 mg;

crospovidone (type A) – 1 mg;

magnesium stearate-3 mg;

Film shell:

Opadry II white (talc-1.48 mg, macrogol 3350-2.02 mg,

titanium dioxide (E 171) – 2.5 mg,

polyvinyl alcohol 1,2/2/4/8 mg) – 10 mg

Pharmacological action

Mertenil – hypolipidemic.

Pharmacodynamics

Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, an enzyme that converts HMG-CoA to mevalonate, which is a precursor of cholesterol (CH). The main target of rosuvastatin action is the liver, where cholesterol synthesis and LDL catabolism are carried out.

Rosuvastatin increases the number of hepatic LDL receptors on the cell surface, increasing the uptake and catabolism of LDL.

It also inhibits the synthesis of VLDL cholesterol in liver cells, thereby reducing the total LDL content and VLDL.

Rosuvastatin reduces elevated levels of LDL cholesterol, total cholesterol and triglycerides( TG), increases HDL cholesterol, and also reduces the content of apolipoprotein B (apoB), HDL cholesterol (total cholesterol less HDL cholesterol), VLDL cholesterol, VLDL TG and increases the level of apolipoprotein A-I (ApoA-I). Rosuvastatin reduces the ratio of LDL/HDL cholesterol, total cholesterol/HDL cholesterol, non-HDL/HDL cholesterol, and apoB/ApoA-I.

The therapeutic effect can be achieved within 1 week after the start of treatment, after 2 weeks 90% of the maximum possible effect is achieved. Usually, the maximum possible therapeutic effect is achieved after 4 weeks and is maintained with further use of the drug.

Clinical efficacy

Rosuvastatin is effective in the treatment of adult patients with hypercholesterolemia with or without symptoms of hypertriglyceridemia, regardless of their race, gender or age, as well as in the treatment of a special category of patients, patients with diabetes mellitus or an inherited form of familial hypercholesterolemia.

Rosuvastatin is effective for the treatment of patients with Fredrickson type IIa and IIb hypercholesterolemia (mean baseline LDL-C level of about 4.8 mmol / L).80% of patients who received 10 mg of rosuvastatin achieved the LDL cholesterol target values set by the European Society for Research on Atherosclerosis (less than 3 mmol / L).

In patients with heterozygous familial hypercholesterolemia who received rosuvastatin in doses from 20 to 80 mg according to the forced titration scheme, all doses taken had a significant effect on changing the parameters characterizing the lipid content and on achieving the goal of therapy. As a result of titration of doses up to 40 mg / day (12 weeks of therapy), the LDL-C content decreased by 53%. In 33% of patients, LDL-C values were achieved that met the target values (below 3 mmol / L) of the guidelines of the European Society for the Study of Atherosclerosis.

In patients with homozygous familial hypercholesterolemia treated with rosuvastatin at doses of 20 and 40 mg, the average reduction in LDL cholesterol was 22%. In patients with hypertriglyceridemia with an initial TG concentration of 273 to 817 mg / dl, treated with rosuvastatin at a dose of 5 to 40 mg / day for 6 weeks, the concentration of TG in blood plasma significantly decreased.

The additive effect is observed in combination with fenofibrate in relation to the content of TG and nicotinic acid (more than 1 g / day) in relation to the content of HDL cholesterol.

Studies on the effect of rosuvastatin on reducing the number of complications caused by lipid disorders, such as coronary artery disease, have not yet been completed.

In patients with low-risk disease coronary artery disease (defined as Framingham risk less than 10% over a period of more than 10 years), with the average content of LDL cholesterol is 4 mmol/l (of 154.5 mg/DL) rosuvastatin at a dose of 40 mg/day significantly slowed the increase in the maximum values characterizing the wall thickening of the carotid artery in 12 segments, compared to a placebo at a speed of -0,0145 mm/year (95% confidence interval — CI — from -0,0196 to -0,0093, p

Pharmacokinetics

Absorption tmax — 5 hours after oral use of the appropriate dose. Absolute bioavailability is approximately 20%.

Distribution

Rosuvastatin is absorbed mainly by the liver, which is the main site of cholesterol synthesis and LDL cholesterol metabolism. The_{vd of} rosuvastatin is approximately 134 l. 90% of rosuvastatin binds to plasma proteins, mainly albumin.

Metabolism

It undergoes a limited metabolism (approximately 10%). Rosuvastatin is a fairly non-core substrate for metabolism by cytochrome P450 enzymes. CYP2C9 is the main isoenzyme involved in metabolism, while CYP2C19, CYP3A4, and CYP2D6 are less involved in metabolism. The main metabolite is N-desmethyl, which is 50% less active than rosuvastatin. Lactone metabolites are pharmacologically inactive. More than 90% of the pharmacological activity in inhibiting circulating HMG-CoA reductase is provided by rosuvastatin, the rest by its metabolites.

Deduction

Approximately 90% of the dose of rosuvastatin taken is excreted unchanged from the body through the intestines (including absorbed and non-absorbed rosuvastatin), and the remainder is excreted by the kidneys. T_1/2 is 19 hours, does not change with increasing dose of the drug. The average geometric plasma clearance is approximately 50 l / h (coefficient of variation 21.7%). As with other HMG-CoA reductase inhibitors, rosuvastatin is involved in the process of hepatic uptake by a membrane transporter of cholesterol across membranes — a transport protein from organic anions. This transporter plays an important role in the elimination of rosuvastatin by the liver.

Linearity

Systemic exposure to rosuvastatin increases in proportion to the dose. Changes in pharmacokinetic parameters when taking the drug several times a day are not observed.

Age and gender

They do not have a clinically significant effect on the pharmacokinetic parameters of rosuvastatin.

Ethnic groups

Comparative pharmacokinetic studies showed a twofold increase in the mean AUC and tmax values in patients of Asian descent (Japanese, Chinese, Filipino, Vietnamese, and Korean) compared to those of Caucasian race. The average AUC and cmax values were approximately 1.3 times higher in the Indianpopulation. At the same time, the analysis of pharmacokinetic parameters for the entire study population did not reveal clinically significant differences in the pharmacokinetics of the drug among representatives of the Caucasian, Negroid races, and Latin Americans.

Kidney failure

In patients with mild to moderate renal insufficiency, the plasma concentration of rosuvastatin or N-desmethyl metabolite does not change significantly. In patients with severe renal insufficiency (creatinine clearance less than 30 ml/min), the concentration of rosuvastatin in blood plasma is 3 times higher, and the concentration of N-desmethyl metabolite is 9 times higher than in healthy volunteers. The plasma concentration of rosuvastatin in patients undergoing hemodialysis was approximately 50% higher than in healthy volunteers.

Liver failure

In patients with varying degrees of hepatic insufficiency with a Child-Pugh score of 7 or lower, there was no increase in T_1/2 of rosuvastatin. However, in 2 patients with Child-Pugh scores of 8 and 9, an elongation of T_{1/2 was observed}, approximately 2 times higher than the same indicator for patients with lower Child-Pugh scores. There is no experience of using rosuvastatin in patients with a score higher than 9 on the Child-Pugh scale.

Indications

• hypercholesterolemia and combined (mixed) dyslipidemia States to reduce elevated concentrations of total cholesterol, LDL cholesterol, Apob, and TG in the serum as a Supplement to diet when diet and other non-pharmacological methods (e. g. exercise, weight reduction) are insufficient;
• family homozygous hypercholesterolemia as an adjunct to diet and other methods Lipetskaya therapy (e. g. LDL-apheresis) or if such therapy is not effective enough;
• hypertriglyceridemia (type IV according to Fredrickson) as a Supplement to the diet;
• to slow the progression of atherosclerosis as an adjunct to diet in patients who have shown therapy to reduce the concentration of total cholesterol and LDL cholesterol;
• primary prevention of major cardiovascular complications (cardiovascular death, stroke, heart attack, unstable angina and arterial revascularization) in adult patients without clinical signs of coronary heart disease but with an increased risk of its development (the age of 50 years for men and 60 years for women elevated concentrations of C-reactive protein ≥2 mg/l in the presence of at least one additional risk factors such as arterial hypertension, a low concentration of HDL-C, Smoking, family history of early coronary heart disease).

Use during pregnancy and lactation

The drug Mertenil® is contraindicated for use during pregnancy and lactation.

Women of childbearing age should use reliable and adequate contraceptives.

Since cholesterol and cholesterol biosynthetic products are important for fetal development, the potential risk of HMG-CoA reductase inhibition exceeds the benefit of its use during pregnancy.

If pregnancy occurs, the drug should be discontinued immediately. There are no data on the excretion of rosuvastatin in breast milk. If it is necessary to prescribe the drug during lactation, breastfeeding should be discontinued.

Contraindications

• hypersensitivity to rosuvastatin or to any component of the drug;
• liver disease in the active phase, including a persistent increase in liver transaminases, as well as any increase of transaminases in blood serum more than 3 times compared with CAH;
• severe impairment of renal function (Cl creatinine less than 30 ml/min);
• myopathy;
• concomitant use of cyclosporine;
• patients predisposed to the development myotoxicity complications;
• patients with hepatic impairment with a score above 9 on a scale child-Pugh;
• lactose intolerance, lactase deficiency or glucose-galactose malabsorption;
• pregnancy;
• lactation;
• women of childbearing age not using reliable contraception;
• the age of 18 years (effectiveness and safety not established).

Side effects

From the immune system: rarely — hypersensitivity reactions, including angioedema.

From the endocrine system: often — type 2 diabetes mellitus.

From the central nervous system: often — headache, dizziness.

From the digestive system: often-constipation, abdominal pain, nausea; rarely-pancreatitis.

From the side of the skin and subcutaneous fat: infrequently — skin pruritus, rash, urticaria.

Musculoskeletal and connective tissue disorders: often — myalgia; rarely-myopathy (including myositis), rhabdomyolysis.

Other services: often-asthenic syndrome.

As with other HMG-CoA reductase inhibitors, the frequency of side effects is dose-dependent.

The incidence of rhabdomyolysis, severe side effects from the kidneys and liver increases in patients taking rosuvastatin at a dose of 40 mg.

From the side of the kidneys and urinary tract: when taking rosuvastatin, proteinuria was observed, mainly of tubular origin. Changes in the protein content in the urine (from the absence or presence of trace amounts to ++ and higher) were found in less than 1% of patients taking 10 and 20 mg of rosuvastatin, and in approximately 3% of patients taking the drug at a dose of 40 mg.

A minimal change in the amount of protein in the urine, expressed as a change from zero or traces to+, was observed when taking the drug at a dose of 20 mg. In most cases, proteinuria decreased and passed independently during treatment. No causal association between proteinuria and acute or progressive kidney disease was found in the analysis of clinical trials.

A number of patients treated with rosuvastatin experienced hematuria, but data from clinical studies have shown that the incidence of such cases is very low.

From the musculoskeletal system: skeletal muscle effects that cause myalgia, myopathy (including myositis) and, in rare cases, rhabdomyolysis with or without acute renal failure have been observed in patients taking any dose of rosuvastatin, especially a dose higher than 20 mg. Increased CPK activity depending on the dose taken was detected in patients taking rosuvastatin, but in most cases these manifestations were insignificant, asymptomatic and temporary. If the CPK activity is 5 times higher than the ULN, then treatment should be discontinued (see “Special instructions”).

From the liver: as with other HMG-CoA reductase inhibitors, an increase in hepatic transaminase activity, depending on the dose taken, was detected in a small number of patients taking rosuvastatin. In most cases, this increase was moderate, asymptomatic, and transient.

Laboratory parameters: increased concentration of glucose, bilirubin, GGTP activity, alkaline phosphatase, thyroid function disorders.

Post-marketing application

From the digestive system: very rarely-jaundice, hepatitis; rarely-increased activity of hepatic transaminases; unspecified frequency-diarrhea.

From the musculoskeletal system: very rarely — arthralgia.

From the central nervous system: very rarely — polyneuropathy, memory loss.

Respiratory system disorders: unspecified frequency-cough, shortness of breath.

From the side of the kidneys and urinary tract: very rarely — hematuria.

From the side of the skin and subcutaneous fat: unspecified frequency-Stevens-Johnson syndrome

Other services: unspecified frequency-peripheral edema.

The following side effects have been reported with some statins — depression, sleep disorders including insomnia and nightmares, and sexual dysfunction. Isolated cases of interstitial lung disease have been reported, especially with long-term drug use.

Composition

Cyclosporine interaction – when rosuvastatin and cyclosporine were co-administered, the AUC of rosuvastatin increased 7-fold compared to the values obtained in healthy volunteers (see “Contraindications”). Combined use leads to an 11-fold increase in the concentration of rosuvastatin in blood plasma. No change in the concentration of cyclosporine in the blood plasma was detected with simultaneous use of drugs.

Vitamin K antagonists – as with other HMG-CoA reductase inhibitors, starting rosuvastatin therapy or increasing the dose of the drug in patients receiving concomitant vitamin K antagonists (for example, warfarin or other coumarin anticoagulants) may lead to an increase in MHO. Discontinuation or reduction of the rosuvastatin dose may cause a decrease in MHO. In such cases, the MHO should be monitored.

Ezetimibe — no change in AUC or cmax is observed when rosuvastatin and ezetimibe_{are co-administered} both drugs. However, the pharmacodynamic interaction of rosuvastatin and ezetimibe, which may cause undesirable effects, cannot be excluded.

Gemfibrozil and other lipid-lowering agents-simultaneous use of rosuvastatin and gemfibrozil leads to a 2-fold increase in the_cmax and AUC of rosuvastatin (see “Special instructions”).

Based on the data of a specific interaction study, no corresponding pharmacokinetic interaction with fenofibrates is expected, but a pharmacodynamic interaction is possible. Gemfibrozil, fenofibrate, other fibrates, and nicotinic acid in lipid-lowering doses (1 g or more per day) when taken concomitantly with HMG-CoA reductase inhibitors increased the risk of myopathy, possibly due to the fact that they can also cause myopathy when taken in monotherapy. Concomitant use of 40 mg of rosuvastatin and fibrates is contraindicated (see “Special instructions” and “Contraindications”). When taken concomitantly with gemfibrozil and other lipid-lowering agents, the initial dose of Mertenil®is it should not exceed 5 mg.

Protease inhibitors-although the exact mechanism of interaction is unknown, concomitant use of rosuvastatin with protease inhibitors may lead to an elongation of rosuvastatin T 1/2. In a pharmacokinetic study, concomitant use of 20 mg of rosuvastatin and a combination drug containing two protease inhibitors (400 mg of lopinavir/100 mg of ritonavir) in healthy volunteers revealed a 2 — fold increase in AUC_0-24 and 5-fold increase in_cmaxof rosuvastatin, respectively. Therefore, simultaneous use of rosuvastatin and protease inhibitors in the treatment of patients with HIV is not recommended.

Antacids-simultaneous use of rosuvastatin and antacids in suspensions containing aluminum or magnesium hydroxide may lead to a decrease in the concentration of rosuvastatin in blood plasma by about 50%. This effect is less pronounced if antacids are applied 2 hours after taking rosuvastatin. The clinical significance of this interaction has not been studied.

Erythromycin-concomitant use of rosuvastatin and erythromycin may result in a 20% decrease in rosuvastatin 0–t AUC and a 30% decrease in rosuvastatin cmax. This relationship may be caused by increased intestinal motility due to the use of erythromycin.

Oral contraceptives / hormone replacement therapy-concomitant use of rosuvastatin and oral contraceptives can lead to an increase in the AUC of ethinyl estradiol and norgestrel by 26 and 34%, respectively. Such an increase in plasma concentrations should be considered when choosing the dose of oral contraceptives. There are no pharmacokinetic data on the concomitant use of rosuvastatin and hormone replacement therapy drugs, so it is impossible to exclude a similar effect when using this combination. However, this combination of drugs was widely used by women in clinical trials and was well tolerated.

Other DRUGS — no clinically significant interaction is expected with simultaneous use of rosuvastatin and digoxin.

Cytochrome P450 isoenzymes-the results of in vitro and in vivo studies have shown that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a rather weak substrate for these enzymes. There was no clinically significant interaction between rosuvastatin and fluconazole (an inhibitor of the CYP2C9 and CYP3A4 isoenzymes) or ketoconazole (an inhibitor of the CYP2A6 and CYP3A4 isoenzymes). Co-use of itraconazole (a CYP3A4 inhibitor) and rosuvastatin increases the AUC of rosuvastatin by 28% (not clinically significant). Therefore, no drug interaction associated with cytochrome P450 metabolism is expected.

How to take, course of use and dosage

Inside, at any time of the day, regardless of food intake, without chewing or grinding, swallowing whole, washed down with water.

Before starting treatment, the patient should follow a standard diet with low CHOLESTEROL products, which should be continued throughout the entire treatment period. Doses of the drug should be selected individually, in accordance with the purpose of the treatment and the therapeutic response of the patient to the therapy, taking into account current generally accepted recommendations for target lipid levels.

The recommended starting dose of the drug is 5 or 10 mg once a day, both for patients who have not previously taken statins, and for patients transferred to taking this drug after therapy with other HMG-CoA reductase inhibitors.

When choosing the initial dose of the drug, the level of cholesterol in each individual patient should be taken into account, as well as the possible risk of developing cardiovascular complications and the potential risk of side effects. If necessary, a dose adjustment can be made after 4 weeks.

Due to the possible development of side effects when taking a dose of 40 mg compared to lower doses of the drug (see “Side effects”) final titration to a maximum dose of 40 mg should only be performed in patients with severe hypercholesterolemia and a high risk of cardiovascular complications (especially patients with hereditary hypercholesterolemia), who did not reach the target cholesterol level at a dose of 20 mg and who will be under medical supervision. When prescribing a dose of 40 mg, careful medical supervision is recommended. It is not recommended to prescribe a dose of 40 mg to patients who have not previously consulted a doctor.

Elderly patients

No age-related dose adjustment is required.

Patients with renal insufficiency

No dose adjustment is required in patients with mild or moderate renal insufficiency. The recommended starting dose of the drug is 5 mg for patients with moderate renal insufficiency (creatinine clearance less than 60 ml / min). The use of Mertenil® in any dose is contraindicated in patients with severe renal insufficiency (see “Contraindications”). In patients with moderate renal insufficiency, the use of the drug at a dose of 40 mg is contraindicated.

Patients with hepatic insufficiency

There was no increase in the systemic concentration of rosuvastatin in patients with a Child-Pugh score of 7 or lower. However, an increase in the systemic concentration of the drug was observed in patients with Child-Pugh scores of 8 and 9. In such patients, liver function should be monitored during therapy. There are no data on taking the drug in patients with a Child-Pugh score higher than 9. Mertenil® is contraindicated in patients with active liver disease.

Ethnic groups

In Asian patients, an increase in the systemic concentration of rosuvastatin is possible. When prescribing doses of 10 and 20 mg, the recommended initial dose of the drug for patients of Asian origin is 5 mg. The use of the drug at a dose of 40 mg in such patients is contraindicated (see “Contraindications”).

Patients predisposed to myopathy

When prescribing doses of 10 and 20 mg, the recommended initial dose of the drug for patients with a predisposition to myopathy is 5 mg. The use of the drug in a dose of 40 mg in such patients is contraindicated.

Special instructions

Application in pediatric practice. The efficacy and safety of the drug in children under 18 years of age has not been established. The experience of using the drug in pediatric practice is limited to a small number of children (8 years and older) with familial homozygous hypercholesterolemia. Currently, the drug Mertenil® it is not recommended for use in children under 18 years of age.

Renal effects. Proteinuria, mainly of tubular origin, was observed in patients receiving high doses of Mertenil®, especially 40 mg, but in most cases it was intermittent or short-term. It has been shown that such proteinuria does not mean the occurrence of acute or progressive existing kidney disease. The incidence of serious renal impairment increases with 40 mg of rosuvastatin. It is recommended to monitor the parameters of renal function during therapy with Mertenil®.

Musculoskeletal system. When using the drug Mertenil® in all dosages, and especially when taking the drug in a dose exceeding 20 mg, myalgia, myopathy and, in rare cases, rhabdomyolysis were detected. Very rarely, rhabdomyolysis occurred when ezetimibe was co-administered with HMG-CoA reductase inhibitors. In this case, a pharmacological interaction of the drugs cannot be excluded, so Mertenil® and ezetimibe should be used together with caution (see “Interaction”). The incidence of rhabdomyolysis increases with 40 mg of rosuvastatin.

Definition of CPK. Determination of CKD activity should not be performed after intense physical exertion that causes an increase in blood pressure. CKD, as this may make it difficult to interpret the results. If CPK activity increases more than 5 times the ULN before starting therapy, a second measurement should be performed after 5-7 days. If repeated measurement confirms the initial CPK value (5 times higher than ULN), Mertenil®therapy is recommended. you should not start.

Before starting therapy. Mertenil®, like other HMG-CoA reductase inhibitors, should be used with extreme caution in patients with existing risk factors for myopathy/rhabdomyolysis. These factors include:

– renal failure;

– hypothyroidism (for doses of 40 mg see “Contraindications”);

– private or family history of muscle diseases (for doses of 40 mg see “Contraindications”);

– a history of myotoxicity in patients receiving other inhibitors of HMG-COA reductase inhibitors or fibrates (for doses of 40 mg see “Contraindications”);

– alcohol (for a dose of 40 mg see “Contraindications”);

– age over 65 years;

– status with the increase of drug concentration in plasma (see “Interaction”, for the dose of 40 mg see “Contraindications”);

– simultaneous use of fibrates (for doses of 40 mg see “Contraindications”).

In such patients, the risk-benefit ratio of therapy should be evaluated and clinical monitoring should be carried out throughout the course of therapy.

During therapy. It is recommended that patients be informed of the need to immediately inform the doctor about cases of unexpected muscle pain, muscle weakness or spasms, especially in combination with malaise or fever.

In such patients, CPK activity should always be monitored. Treatment should be discontinued if CKD activity is more than 5 times higher than normal. ULN or muscle symptoms are pronounced and cause daily discomfort throughout the day (even if the activity of KFC is 5 times less than ULN). If symptoms disappear and CPK activity returns to normal, consideration should be given to re-prescribing Mertenil® or prescribing an alternative HMG-CoA reductase inhibitor in smaller doses, with careful monitoring of the patient. Regular monitoring of CPK activity in patients with no symptoms of rhabdomyolysis is impractical.

However, an increase in the number of cases of myositis and myopathy was found in patients taking other HMG-CoA reductase inhibitors together with fibroic acid derivatives, including gemfibrozil, cyclosporine, nicotinic acid in lipid-lowering doses, antifungal drugs, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when co-administered with certain HMG-CoA reductase inhibitors. Therefore, simultaneous use of rosuvastatin and gemfibrozil is not recommended. The risk-benefit ratio should be carefully evaluated when rosuvastatin is co-administered with fibrates or nicotinic acid in lipid-lowering doses (more than 1 g). Concomitant use of rosuvastatin at a dose of 40 mg and fibrates is contraindicated (see “Interaction” and “Side effects”).

The drug Mertenil® it should not be prescribed to patients with acute, severe diseases that suggest myopathy, or with the possible development of secondary renal failure (for example, sepsis, arterial hypertension, surgery, trauma, metabolic syndrome, seizures, endocrine disorders, electrolyte disorders-see With caution).

Liver. As with other HMG-CoA reductase inhibitors, Mertenil should be used with extreme caution in patients who abuse alcohol or have a history of liver disease. It is recommended to determine liver function indicators before and 3 months after the start of treatment.If the activity of hepatic transaminases in the blood serum is 3 times higher than the ULN, you should stop taking the drug or reduce the dose taken (see “Method of use and doses”). The frequency of serious liver function disorders (mainly associated with increased activity of hepatic transaminases) increases with taking 40 mg of the drug.

Secondary hypercholesterolemia. In patients with secondary hypercholesterolemia due to hypothyroidism, nephrotic syndrome, treatment of the underlying disease should be carried out before starting treatment with Mertenil®.

Special populations and ethnic groups. Pharmacokinetic studies revealed an increase in the systemic concentration of rosuvastatin among patients of Asian origin compared to the data obtained among patients of Caucasian race (see “Method of use and doses” and “Pharmacokinetics”).

Protease inhibitors. Concomitant use of rosuvastatin with protease inhibitors is not recommended (see “Interaction”).

Lactose. The drug should not be used in patients with lactase deficiency, galactose intolerance and glucose-galactose malabsorption.

Influence on the ability to drive vehicles and work with machinery. Studies on the effect of Mertenil® the ability to drive a vehicle and use technical means was not tested. However, based on the pharmacodynamic properties of the drug, it can be assumed that the drug Mertenil® it should not have such an impact. At the same time, when driving a vehicle or other mechanisms, it is necessary to take into account that dizziness may occur during treatment.

Composition

Tablet Form of production

Storage conditions

Store in a dry place, protected from light, at a temperature not exceeding 30 °C

Shelf life

2 years

Active ingredient

Rosuvastatin

Conditions of release from pharmacies

By prescription

Dosage form

Tablets

Purpose

For adults as directed by your doctor

Indications

Atherosclerosis, Prevention of heart attacks and strokes