Atorvastatin-SZ pills 10mg 30pcs

Composition

dosage 10 mg of Active ingredient:

atorvastatin calcium in terms of atorvastatin – 10 mg

excipients (core):

lactose monohydrate (milk sugar) – 62.0 mg; calcium carbonate – 33,0 mg; povidone K 30 (polyvinylpyrrolidone middle) – 6.0 mg; croscarmellose sodium (Primerose) was 6.75 mg; sodium fumarate – 1.5 mg; silicon dioxide colloidal (Aerosil) – 0.75 mg; microcrystalline cellulose was 30.0 mg;

auxiliary substances (shell):

Opadray II (polyvinyl alcohol, partially hydrolyzed – 2.2 mg; macrogol (polyethylene glycol) 3350 – 0.6175 mg; talc – 1.0 mg; titanium dioxide E 171 – 0.9585 mg; soy lecithin E 322 – 0.175 mg; aluminum varnish based on indigo carmine dye – 0.003 mg; aluminum varnish based on azorubin dye – 0.0255 mg; aluminum varnish based on crimson dye [Ponceau 4R] – 0.0205 mg).

Tablets covered with a film-coated pink color, round, biconvex.

On a cross-section, the tablet core is white or almost white in color.

Pharmacological action

Pharmacotherapeutic group of the medicinal product: Hypolipidemic agent-HMG-CoA reductase inhibitor ATX Code: [C 10 AA 05]Pharmacological Propertiespharmacodynamicatorvastatin is a selective competitive inhibitor of HMG-CoA reductase, a key enzyme that converts 3-hydroxy-3-methylglutaryl-CoA to mevalonate – a precursor of steroids, including cholesterol; synthetic hypolipidemic agent. In patients with homozygous and heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia, and mixed dyslipidemia, atorvastatin reduces plasma concentrations of cholesterol (CH), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein B (apo-B), as well as very low-density lipoprotein cholesterol (VLDL-C), and triglycerides (TG), causes an unstable increase in the concentration of high-density lipoprotein cholesterol (HDL-C). Atorvastatin reduces the concentration of cholesterol and lipoproteins in blood plasma, inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and increasing the number of” hepatic ” LDL receptors on the cell surface, which leads to increased uptake and catabolism of LDL-C. Atorvastatin reduces the formation of LDL-C and the number of LDL particles, causes a pronounced and persistent increase in the activity of LDL receptors in combination with favorable qualitative changes in LDL particles, and also reduces the concentration of LDL-C in patients with homozygous hereditary familial hypercholesterolemia resistant to therapy with other lipid-lowering agents. Atorvastatin in doses from 10 mg to 80 mg reduces the concentration of cholesterol by 30% – 46%, LDL-C – by 41% – 61%, apolipoproteins-on-B-by 34% – 50% and TG-by 14% – 33%. The results of therapy are similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia, including patients with type 2 diabetes mellitus. In patients with isolated hypertriglyceridemia, atorvastatin reduces the concentration of cholesterol, LDL-C, VLDL-C, apo-B and TG and increases the concentration of HDL-C. In patients with dysbetalipoproteinemia, atorvastatin reduces the concentration of intermediate-density lipoprotein cholesterol. In patients with hyperlipoproteinemia of type IIa and IIb according to the Fredrickson classification, the average increase in HDL-C concentration during treatment with atorvastatin (10-80 mg) compared to baseline is 5.1% – 8.7% and does not depend on the dose. There is a significant dose-dependent decrease in the total cholesterol/HDL-C and LDL-C/HDL-C ratios by 29% -44% and 37% -55%, respectively. The antisclerotic effect of atorvastatin is a consequence of its effect on the walls of blood vessels and blood components. Atorvastatin inhibits the synthesis of isoprenoids, which are growth factors of cells of the inner lining of blood vessels. Under the influence of atorvastatin, endothelium-dependent dilation of blood vessels improves, the concentration of LDL-C, apolipoprotein B, and TG decreases, and the concentration of HDL-C cholesterol and apolipoprotein A. Atorvastatin reduces the viscosity of blood plasma and the activity of certain coagulation and platelet aggregation factors. Thanks to this, it improves hemodynamics and normalizes the state of the coagulation system. HMG-CoA reductase inhibitors also have an effect on macrophage metabolism, block their activation and prevent the rupture of atherosclerotic plaque. Atorvastatin-SZ at a dose of 80 mg significantly reduces the risk of ischemic complications and mortality by 16% after a 16-week course, and the risk of repeated hospitalization for angina accompanied by signs of myocardial ischemia by 26%. In patients with different baseline LDL-C concentrations, Atorvastatin-SZ reduces the risk of ischemic complications and mortality (in patients with non-Q-wave myocardial infarction and unstable angina, as well as in men and women, and in patients younger and older than 65 years). A decrease in the concentration of LDL-C in the blood plasma correlates better with the dose of the drug than with its concentration in the blood plasma. The dose is selected taking into account the therapeutic effect (see the section “Dosage and use”). The therapeutic effect is achieved 2 weeks after the start of therapy, reaches a maximum in 4 weeks and persists throughout the entire period of therapy. Pharmacokinetics of absorption Atorvastatin is rapidly absorbed after oral use: the time to reach its maximum concentration (TCmax) in blood plasma is 1-2 hours. In women, the maximum concentration (Cmax) of atorvastatin is 20% higher, and the area under the concentration-time curve (AUC) is 10% lower than in men. The degree of absorption and plasma concentration increase in proportion to the dose. The absolute bioavailability is about 14%, and the systemic bioavailability of HMG-CoA reductase inhibitory activity is about 30%. Low systemic bioavailability is due to presystemic metabolism in the gastrointestinal mucosa and/or during “primary passage” through the liver. Food intake reduces the rate and degree of drug absorption (by 25% and 9%, respectively), as evidenced by the results of determining Cmax and AUC, but the decrease in LDL-C is similar to that when taking atorvastatin on an empty stomach. Despite the fact that after taking atorvastatin in the evening, its plasma concentration is lower (Cmax and AUC, approximately 30%) than after taking it in the morning, the decrease in LDL-C concentration does not depend on the time of day at which the drug is taken. Distribution The average volume of distribution of atorvastatin is about 381 liters. Binding to plasma proteins is not less than 98%. The ratio of the content in red blood cells/blood plasma is about 0.25, i. e. atorvastatin does not penetrate well into red blood cells. Metabolism Atorvastatin is largely metabolized to form ortho – and parahydroxylated derivatives and various beta-oxidation products. In vitro, ortho-and parahydroxylated metabolites have an inhibitory effect on HMG-CoA reductase comparable to that of atorvastatin. Approximately 70% of the decrease in HMG-CoA reductase activity occurs due to the action of active circulating metabolites. The results of initro studies suggest that the liver SURZA 4 isoenzyme plays an important role in the metabolism of atorvastatin. This fact is supported by an increase in the concentration of the drug in blood plasma with simultaneous use of erythromycin, which is an inhibitor of this isoenzyme. In vitro studies have also shown that atorvastatin is a weak inhibitor of the CYP3A4 isoenzyme. Atorvastatin does not have a clinically significant effect on the plasma concentration of terfenadine, which is mainly metabolized by the CYP4A4 isoenzyme, so its significant effect on the pharmacokinetics of other substrates of the CYP4A4 isoenzyme is unlikely (see the section “Interaction with other drugs”). Elimination Atorvastatin and its metabolites are mainly excreted in the bile after hepatic and / or extrahepatic metabolism (atorvastatin does not undergo significant enterohepatic recirculation). The half-life (T1 / 2) of atorvastatin is about 14 hours, while the inhibitory effect of the drug against HMG-CoA reductase is approximately 70% determined by the activity of circulating metabolites and persists for about 20-30 hours due to their presence. After oral use, less than 2% of the drug dose is detected in the urine. Special patient groupslong-lived patients Plasma concentrations of atorvastatin in patients over 65 years of age are higher (Cmax by about 40%, AUC by about 30%) than in young adult patients. There were no differences in the efficacy and safety of the drug, or achievement of the goals of lipid-lowering therapy in elderly patients compared to the general population. The pharmacokinetics of the drug in children have not been studied. Renal insufficiency Impaired renal function does not affect the concentration of atorvastatin in the blood plasma or its effect on lipid metabolism, and therefore a dose change in patients with impaired renal function is not required. Atorvastatin is not eliminated during hemodialysis due to intensive binding to plasma proteins. No studies have been conducted on the use of atorvastatin in patients with end-stage renal failure. Liver function insufficiency The concentration of the drug is significantly increased (Cmax approximately 16 times, AUC approximately 11 times) in patients with alcoholic cirrhosis of the liver (stage B on the Child-Pugh scale) (see the section “Contraindications”).

Indications

* Primary hypercholesterolemia (heterozygous familial and non-familial hypercholesterolemia (Fredrickson type IIa);

* Combined (mixed) hyperlipidemia (Fredrickson types IIa and IIb);

* Dysbetalipoproteinemia (type III according to the Fredrickson classification) (as an adjunct to diet);

• Familial endogenous hypertriglyceridemia (type IV according to the Fredrickson classification), resistant to diet•

* Homozygous familial hypercholesterolemia with insufficient effectiveness of diet therapy and other non-pharmacological methods of treatment;

• Prevention of cardiovascular diseases:

– Primary prevention of cardiovascular events in patients without clinical signs of coronary heart disease (CHD), but with multiple risk factors for its development: over 55 years of age, nicotine dependence, hypertension, diabetes mellitus, genetic predisposition, including on the background of dyslipidemia;

– Secondary prevention of cardiovascular events in patients with coronary artery disease to reduce total mortality, myocardial infarction, stroke, re-hospitalization for about angina and the need for revascularization.

Contraindications

Hypersensitivity to any component of the drug. Active liver disease or an increase in the activity of” hepatic ” transaminases in blood plasma of unknown origin by more than 3 times compared to the upper limit of normal. Age up to 18 years (insufficient clinical data on the effectiveness and safety of the drug in this age group). Lactose intolerance, lactase deficiency, glucose-galactose malabsorption. Hypersensitivity to soy and peanuts. Pregnancy and breast-feeding period. Use in women who are planning pregnancy and do not use reliable methods of contraception.

With caution

, the Abuse of alcohol, liver disease, a history of diseases of the muscular system (in history from the other representatives of the group of HMG-COA reductase inhibitors), severe violations of water-electrolyte balance, endocrine (hyperthyroidism) and metabolic disorders, severe acute infection (sepsis), hypotension, diabetes mellitus, uncontrolled epilepsy, extensive surgical intervention, trauma.

Side effects

In controlled clinical trials (n=2502), less than 2% of patients discontinued treatment due to atorvastatin-related side effects.

The most common adverse effects associated with atorvastatin were constipation, flatulence, dyspepsia, and abdominal pain.

From the nervous system and sensory organs: ≥2% – headache, asthenic syndrome, insomnia, dizziness;

From the cardiovascular system: ≥2% – chest pain; blood pressure, phlebitis, arrhythmia, angina pectoris, anemia, lymphadenopathy, thrombocytopenia.

Respiratory system disorders: ≥2% – sinusitis, pharyngitis, bronchitis, rhinitis;

From the digestive tract: ≥2% — abdominal pain, constipation or diarrhea, dyspepsia, flatulence, nausea;

Musculoskeletal disorders: ≥2% – arthralgia, myalgia, arthritis;

From the genitourinary system: ≥2% – urogenital infections, peripheral edema;

From the side of the skin:

Allergic reactions: ≥2% — skin rash;

Other: ≥2% – infections, accidental injury, flu-like syndrome, back pain; ALP, increased ALT or AST, exacerbation of gout.

Side effects reported in post-marketing studies with atorvastatin therapy: anaphylaxis, angioedema, bullous rash (including erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis), rhabdomyolysis, tendon rupture.

Interactions

the Risk of myopathy during treatment with inhibitors of HMG-COA reductase inhibitors is increased with simultaneous use of cyclosporine, fibrates, antibiotics (erythromycin, clarithromycin, dinoproston/dalfopristin), nefazodone, the HIV protease inhibitors (indinavir, ritonavir), colchicine, antifungals derivatives of asola, and nicotinic acid in Lipetskaya doses (more than 1 g/day) (see “Special instructions”).

Inhibitors of the SURZA 4 isoenzyme

Since atorvastatin is metabolized by the SURZA 4 isoenzyme, the combined use of atorvastatin with inhibitors of the SURZA 4 isoenzyme may lead to an increase in the concentration of atorvastatin in blood plasma. The degree of interaction and the potentiation effect are determined by the variability of the effect on the SURZA 4 isoenzyme.

Inhibitors of the OATP transport protein 1 In 1

Atorvastatin and its metabolites are substrates of the OATP 1-In-1 transport protein. OATP 1-In-1 inhibitors (for example, cyclosporine) can increase the bioavailability of atorvastatin. Thus, the combined use of atorvastatin at a dose of 10 mg and cyclosporine at a dose of 5.2 mg / kg / day leads to an increase in the concentration of atorvastatin in blood plasma by 7.7 times. If concomitant use with cyclosporine is necessary, the dose of Atorvastatin-SZ should not exceed 10 mg / day (see the section “Dosage and use”).

Erythromycin/Clarithromycin

Concomitant use of atorvastatin and erythromycin (500 mg 4 times a day) or clarithromycin (500 mg 2 times a day), which inhibit the SURZA 4 isoenzyme, increased the concentration of atorvastatin in blood plasma (see the section “Special instructions”). Caution should be exercised when using the lowest effective dose of atorvastatin in combination with clarithromycin.

Protease inhibitors

Concomitant use of atorvastatin with protease inhibitors, known as SURZA 4 inhibitors, is accompanied by an increase in the concentration of atorvastatin in blood plasma (when used simultaneously with erythromycin, the Cmax of atorvastatin increases by 40%).

Combination of protease inhibitors

Patients taking HIV protease inhibitors and hepatitis C inhibitors should exercise caution and use the lowest effective dose of atorvastatin. In patients taking telaprevir or a combination of tipranavir/ritonavir, the dose of Atorvastatin-SZ should not exceed 10 mg / day.

Patients taking the HIV protease inhibitor tipranavir plus ritonavir or the hepatitis C protease inhibitor telaprevir should avoid taking Atorvastatin-SZ concomitantly. Patients taking the HIV protease inhibitor lopinavir plus ritonavir should exercise caution when prescribing Atorvastatin-SZ and should be given the lowest required dose. In patients taking the HIV protease inhibitors saquinavir plus ritonavir, darunavir plus ritonavir, fosamprenavir or fosamprenavir plus ritonavir, the dose of Atorvastatin-SZ should not exceed 20 mg and the drug should be used with caution. In patients taking the HIV protease inhibitor nelfinavir or the hepatitis C protease inhibitor boceprevir, the dose of Atorvastatin-SZ should not exceed 40 mg and careful clinical monitoring is recommended.

Diltiazem

The combined use of atorvastatin at a dose of 40 mg with diltiazem at a dose of 240 mg leads to an increase in the concentration of atorvastatin in blood plasma.

Ketoconazole, spironolactone and cimetidine

Caution should be exercised when using atorvastatin concomitantly with drugs that reduce the concentration of endogenous steroid hormones, such as ketoconazole, spironolactone and cimetidine.

Itraconazole

Concomitant use of atorvastatin in doses from 20 mg to 40 mg and itraconazole in a dose of 200 mg resulted in an increase in the AUC of atorvastatin. Caution should be exercised and the lowest effective dose of atorvastatin should be used when co-administered with itraconazole.

Grapefruit juice

Since grapefruit juice contains one or more components that inhibit the SURZA 4 isoenzyme, excessive consumption (more than 1.2 liters per day) can cause an increase in the concentration of atorvastatin in blood plasma.

Inducers of the SURZA 4 isoenzyme

Concomitant use of atorvastatin with inducers of the SURZA 4 isoenzyme (for example, efavirenz, phenytoin, or rifampicin) may lead to a decrease in the concentration of atorvastatin in blood plasma. Due to the dual mechanism of interaction with rifampicin (an inducer of the SURZA 4 isoenzyme and an inhibitor of the hepatocyte transport protein OATP 1 In 1), simultaneous use of atorvastatin and rifampicin is recommended, since delayed use of atorvastatin after taking rifampicin leads to a significant decrease in the concentration of atorvastatin in blood plasma.

Antacids

Simultaneous oral use of a suspension containing magnesium hydroxide and aluminum hydroxide reduced the concentration of atorvastatin in blood plasma by about 35%, but the degree of decrease in LDL-C concentration did not change.

Phenazone

Atorvastatin does not affect the pharmacokinetics of phenazone, so interaction with other drugs metabolized by the same cytochrome isoenzymes is not expected.

Kolestipol

With simultaneous use of colestipol, the concentration of atorvastatin in blood plasma decreased by about 25%; however, the lipid-lowering effect of the combination of atorvastatin and colestipol exceeded that of each drug separately.

Digoxin

When digoxin and atorvastatin were re-administered at a dose of 10 mg, the steady-state plasma concentrations of digoxin did not change. However, when digoxin was used in combination with atorvastatin at a dose of 80 mg/day, the digoxin concentration increased by about 20%.

Patients receiving digoxin in combination with atorvastatin should be monitored accordingly.

Azithromycin

Concomitant use of atorvastatin at a dose of 10 mg once a day and azithromycin at a dose of 500 mg once a day did not change the concentration of atorvastatin in blood plasma.

Oral contraceptives

When atorvastatin was co-administered with an oral contraceptive containing norethisterone and ethinylestradiol, there was a significant increase in the AUC of norethisterone and ethinylestradiol by approximately 30% and 20%, respectively.This effect should be considered when choosing an oral contraceptive for a woman taking atorvastatin.

Terfenadine

There were no clinically significant changes in the pharmacokinetics of terfenadine when atorvastatin and terfenadine were co-administered.

Warfarin

Concomitant use of atorvastatin with warfarin may increase the effect of warfarin on blood clotting parameters in the first days (reduction of prothrombin time). This effect disappears after 15 days of simultaneous use of these drugs.

Amlodipine

Concomitant use of atorvastatin 80 mg and amlodipine 10 mg did not alter the pharmacokinetics of atorvastatin at steady state.

Other concomitant therapy

In clinical studies, atorvastatin was used in combination with antihypertensive agents and estrogens as part of replacement therapy; no clinically significant undesirable interactions were observed; interaction studies with specific drugs were not conducted.

How to take, course of use and dosage

Inside.

Take at any time of the day, regardless of food intake. Before starting treatment with Atorvastatin-SZ, an attempt should be made to control hypercholesterolemia through diet, exercise, and weight loss in obese patients, as well as therapy for the underlying disease.

When prescribing the drug, the patient should be recommended a standard hypocholesterolemic diet, which he should adhere to throughout the entire period of therapy.

The dose of the drug varies from 10 mg to 80 mg once a day and is titrated taking into account the initial concentration of LDL-C, the purpose of therapy and the individual effect on the therapy. The maximum daily dose of the drug for a single dose is 80 mg. At the beginning of treatment and/or during an increase in the dose of Atorvastatin-SZ, it is necessary to monitor the concentration of lipids in blood plasma every 2 to 4 weeks and adjust the dose accordingly.

Primary hypercholesterolemia and combined (mixed) hyperlipidemia

For most patients-10 mg once a day; the therapeutic effect is manifested within 2 weeks and usually reaches a maximum within 4 weeks. With long-term treatment, the effect persists.

Homozygous familial hypercholesterolemia

The initial dose is selected individually depending on the severity of the disease. In most cases, the optimal effect is observed when using the drug at a dose of 80 mg once a day (reducing the concentration of LDL-C by 18-45%).

Liver failure

In case of insufficient liver function, caution should be exercised (due to slowing down the elimination of the drug from the body). Clinical and laboratory parameters should be carefully monitored (regular monitoring of the activity of “hepatic” transaminases: aspartate aminotransferase (AST) and alanine aminotransferase (ALT)). With a significant increase in “hepatic” transaminases, the dose of Atorvastatin-SZ should be reduced or treatment should be discontinued.

Renal insufficiency

Impaired renal function does not affect the concentration of atorvastatin in blood plasma or the degree of decrease in LDL-C concentration during therapy with Atorvastatin-SZ, so no dose adjustment is required. Elderly patients There were no differences in the efficacy, safety or therapeutic effect of Atorvastatin-SZ in elderly patients compared to the general population and no dose adjustment is required (see section “Pharmacokinetics”).

Use in combination with other medicinal products

If concomitant use with cyclosporine, telaprevir or a combination of tipranavir/ritonavir is necessary, the dose of Atorvastatin-SZ should not exceed 10 mg / day. Caution should be exercised when using the lowest effective dose of atorvastatin concomitantly with HIV protease inhibitors, hepatitis C inhibitors, clarithromycin and itraconazole (see section “Special instructions”).

Overdose

In case of overdose, the following general measures are necessary: monitoring and maintaining the vital functions of the body, as well as preventing further absorption of the drug (gastric lavage, taking activated charcoal or laxatives). If myopathy develops, followed by rhabdomyolysis and acute renal failure (a rare but severe side effect), the drug should be immediately discontinued and an infusion of diuretic and sodium bicarbonate should be initiated. If necessary, hemodialysis should be performed. Rhabdomyolysis can lead to hyperkalemia, which requires intravenous use of a calcium chloride solution or a calcium gluconate solution, infusion of 5% dextrose (glucose) solution with insulin, and the use of potassium exchange resins. Since the drug actively binds to plasma proteins, hemodialysis is ineffective.

Special instructions

Before starting therapy with Atorvastatin, the patient should be prescribed a standard hypocholesterolemic diet, which he must follow during the entire treatment period. The use of HMG-CoA reductase inhibitors to reduce blood lipids may lead to changes in biochemical parameters that reflect liver function.

Liver function should be monitored before starting therapy,6 weeks,12 weeks after starting Atorvastatin and after each dose increase, as well as periodically, for example, every 6 months. An increase in the activity of “liver” enzymes in the blood serum can be observed during therapy with Atorvastatin. Patients with elevated enzyme levels should be monitored until their enzyme levels return to normal.

If the values of alanine aminotransferase (ALT) or asparagine aminotransferase (AST) are more than 3 times higher than the upper permissible limit, it is recommended to reduce the dose of Atorvastatin or discontinue treatment. Atorvastatin should be used with caution in patients who abuse alcohol and / or have liver disease.

Active liver disease or a persistent increase in the activity of aminotransferases of unknown origin serve as contraindications to the appointment of Atorvastatin. Treatment with Atorvastatin may cause myopathy. The diagnosis of myopathy (muscle pain and weakness combined with an increase in creatine phosphokinase (CPK) activity more than 10 times higher than the upper limit of normal) should be discussed in patients with advanced myalgia, muscle soreness or weakness, and/or a marked increase in CPK activity. Patients should be warned that they should immediately inform the doctor about the appearance of unexplained pain or weakness in the muscles, if they are accompanied by malaise or fever.

Atorvastatin therapy should be discontinued if there is a marked increase in CKD activity or if there is a confirmed or suspected myopathy. The risk of myopathy associated with other drugs in this class was increased with concomitant use of cyclosporine, fibrates, erythromycin, nicotinic acid, or azole antifungal agents. Many of these drugs inhibit cytochrome P450-3A4-mediated metabolism and / or drug transport.

Atorvastatin is biotransformed by CYP 3A4. When prescribing Atorvastatin in combination with fibrates, erythromycin, immunosuppressive agents, azole antifungal agents or nicotinic acid in hypolipidemic doses, the expected benefit and risk of treatment should be carefully weighed and patients should be regularly monitored for muscle pain or weakness, especially during the first months of treatment and during periods of increasing the dose of any drug. In such situations, periodic monitoring of CPK activity can be recommended, although such monitoring does not prevent the development of severe myopathy.

When using Atorvastatin, as well as other drugs of this class, cases of rhabdomyolysis with acute renal failure due to myoglobinuria have been described. Atorvastatin therapy should be temporarily discontinued or completely discontinued if there are signs of possible myopathy or a risk factor for developing renal failure due to rhabdomyolysis (for example, severe acute infection, hypotension, serious surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures).

Before starting therapy with Atorvastatin, it is necessary to try to achieve control of hypercholesterolemia by adequate diet therapy, increased physical activity, weight loss in obese patients, and treatment of other conditions. Patients should be warned to seek immediate medical attention if they experience unexplained muscle pain or weakness, especially if they are accompanied by malaise or fever.

Form of production

Tablets

Storage conditions

Store in a dry place protected from light, out of reach of children, at a temperature of 15 C to 30 C.

Shelf

life is 2 years.

Active ingredient

Atorvastatin

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