Atorvastatin-SZ, 20 mg 60 pcs
€9.13 €7.99
Pharmacotherapeutic drug group:
Hypolipidemic drug – HMG-CoA reductase inhibitor
ATX code: [C10AA05]
Pharmacological properties
Pharmacodynamics
Atorvastatin 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; a synthetic hypolipidemic agent.
. In patients with homozygous and heterozygous familial hypercholesterolemia, nonfamilial forms of hypercholesterolemia and mixed dyslipidemia, atorvastatin reduces plasma 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 unstable increase in high density lipoprotein cholesterol (HDL-C). Atorvastatin reduces plasma concentrations of cholesterol and lipoproteins by 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 capture and catabolism of LDL-C.
Atorvastatin decreases formation of LDL-C and the number of LDL particles, causes a pronounced and sustained increase in LDL receptor activity in combination with favorable qualitative changes of LDL particles and decreases LDL-C concentration in patients with homozygous hereditary familial hypercholesterolemia resistant to therapy with other hypolipidemic agents.
Atorvastatin at doses of 10 mg to 80 mg reduces cholesterol concentration by 30% to 46%, LDL-C by 41% to 61%, apolipoprotein-b by 34% to 50% and TG by 14% to 33%. Therapy results were similar in patients with heterozygous familial hypercholesterolemia, nonfamilial forms of hypercholesterolemia and mixed hyperlipidemia, including patients with type 2 diabetes. In patients with isolated hypertriglyceridemia, atorvastatin reduces cholesterol, LDL-C, LDL-C, apo-B and TG concentrations and increases HDL-C concentration. In patients with dysbetalipoproteinemia, atorvastatin reduces the concentration of intermediate-density lipoprotein cholesterol.
In patients with hyperlipoproteinemia of type IIa and IIb according to Fredrickson classification mean increase of HDL-C concentration during treatment with atorvastatin (10-80 mg) in comparison with baseline is 5.1 % – 8.7 % and it is not dose dependent. There is a significant dose-dependent decrease of total cholesterol/CHD-LDL and LDL-C/CHD-LDL ratios by 29 % – 44 % and 37 % – 55 %, respectively. Antisclerotic effect of atorvastatin is a consequence of its effect on the vascular wall and blood components. Atorvastatin inhibits the synthesis of isoprenoids, which are growth factors of the cells of the inner membrane of blood vessels. Under the effect of atorvastatin endothelium-dependent dilation of blood vessels is improved, concentration of HDL-C, apolipoprotein B, TG is reduced, concentration of HDL-C and apolipoprotein A cholesterol is increased. Atorvastatin reduces plasma viscosity and activity of some clotting and platelet aggregation factors. Due to this it improves hemodynamics and normalizes the state of the clotting system. HMG-CoA reductase inhibitors also affect the metabolism of macrophages, block their activation and prevent the rupture of atherosclerotic plaque.
Atorvastatin-CZ at a dose of 80 mg significantly reduces the risk of coronary complications and mortality rate by 16% after a 16-week course, and the risk of readmission for angina with signs of myocardial ischemia by 26%. In patients with different baseline concentrations of LDL-C, Atorvastatin NW causes a decrease in the risk of ischemic complications and mortality (in patients with myocardial infarction without Q-wave and unstable angina, as well as in men and women, and in patients aged younger and older than 65 years). Decrease in plasma concentration of LDL-C better correlates with the drug dose than with its plasma concentration. The dose is selected taking into account the therapeutic effect (see section “Dosage and administration”). Therapeutic effect is achieved 2 weeks after the start of therapy, reaches a maximum after 4 weeks and is maintained during the entire period of therapy.
Pharmacokinetics
Eabsorption
Atorvastatin is quickly absorbed after oral administration: time of reaching its maximum concentration (TSmax) in plasma is 1-2 hours. In women maximal concentration (CMax) of atorvastatin is 20% higher and area under curve “concentration-time” (AUC) is 10% lower than in men. The degree of absorption and plasma concentration increase in proportion to the dose. Absolute bioavailability is about 14% and systemic bioavailability of HMG-CoA reductase inhibitory activity is about 30%. Low systemic bioavailability is due to presystemic metabolism in the mucosa of the gastrointestinal tract 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 Cmax and AUC determination, but decrease of LDL-C is similar to that of atorvastatin on an empty stomach. Despite the fact that after Atorvastatin administration in the evening its concentration in plasma is lower (Cmax and AUC, approximately by 30%) than after administration in the morning, decrease of LDL-C concentration does not depend on the time of day, when the drug is taken.
Distribution
The mean volume of distribution of atorvastatin is about 381 liters. The binding to plasma proteins is at least 98%. The ratio of content in erythrocytes/plasma is about 0.25, i.e. atorvastatin poorly penetrates into erythrocytes.
Metabolism
Atorvastatin is largely metabolized with the formation of ortho- and parahydroxylated derivatives and various β-oxidation products. In vivo ortho- and parahydroxylated metabolites have an inhibitory effect on HMG-CoA reductase comparable with that of atorvastatin. Approximately 70% of the decrease of HMG-CoA reductase activity is due to the action of active circulating metabolites. The results of in vitro studies suggest that hepatic CYPCA4 isoenzyme plays an important role in atorvastatin metabolism. This fact is supported by increased plasma concentrations of the drug with concomitant administration of erythromycin, which is an inhibitor of this isoenzyme. Studies have also shown that atorvastatin is a weak inhibitor of CYP3A4 isoenzyme. Atorvastatin has no clinically significant effect on plasma concentrations of terfenadine, which is metabolized primarily by CYPCA4 isoenzyme, therefore its significant effect on pharmacokinetics of other substrates of CYPCA4 isoenzyme is unlikely (see section “Interaction with other medicinal products”).
Atorvastatin and its metabolites are excreted mainly with bile after hepatic and/or extrahepatic metabolism (atorvastatin does not undergo marked hepatic recirculation). The half-life (T1/2) of atorvastatin is about 14 h, while its inhibitory effect 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 administration, less than 2% of the administered dose of the drug is detected in the urine.
Patient special groups
Elderly patients
Atorvastatin concentrations in plasma of patients over 65 years old are higher (Cmax
by about 40%, AUC by about 30%) than those of adult patients of younger age. No differences in efficacy and safety of the drug, or in achieving the goals of hypolipidemic therapy in elderly patients compared to the general population were found.
Children
There have been no studies of pharmacokinetics of the drug in children.
Inadequate renal function
Induced renal function has no effect on plasma concentrations of atorvastatin or its effect on lipid metabolism parameters; therefore, no dose change is required in patients with impaired renal function.
Atorvastatin is not excreted during hemodialysis due to intense binding to plasma proteins.
There have been no studies of atorvastatin use in patients with end-stage renal failure.
Liver function insufficiency
The drug concentration is significantly increased (Cmax approximately 16-fold, AUC approximately 11-fold) in patients with alcoholic cirrhosis (stage B on the Child-Pugh scale) (see section “Contraindications”).
Indications
– Combined (mixed) hyperlipidemia (Fredrickson classification types IIa and IIb);
– Dysbetalipoproteinemia (Fredrickson classification type III) (as a supplement to the diet);
– Familial endogenous hypertriglyceridemia (Fredrickson classification type IV), resistant to diet;
– Homozygous familial hypercholesterolemia with insufficient effectiveness of diet therapy and other non-pharmacological treatments;
– Prevention of cardiovascular disease:
– Primary prevention of cardiovascular complications in patients without clinical signs of coronary heart disease (CHD) but who have several risk factors for its development: Age over 55 years, nicotine addiction, arterial hypertension, diabetes mellitus, genetic predisposition, including on the background of dyslipidemia;
– Secondary prevention of cardiovascular complications in patients with CHD to reduce the total mortality rate, myocardial infarction, stroke, repeated hospitalization for angina and need for revascularization.
Active ingredient
Composition
1 film-coated tablet contains:
active ingredient:
atorvastatin calcium in terms of atorvastatin – 20 mg
auxiliary substances (core):
Lactose monohydrate (milk sugar) – 124.0 mg;
Calcium carbonate – 66.0 mg;
povidone K 30 (polyvinylpyrrolidone medium molecular weight) – 12.0 mg;
croscarmellose sodium (primellose) – 13.5 mg;
sodium stearyl fumarate – 3.0 mg;
colloidal silicon dioxide (aerosil) – 1.5 mg;
Microcrystalline cellulose – 60.0 mg;
excipients (coating):
Opadray II (polyvinyl alcohol, partially hydrolyzed, 3.96 mg; macrogol (polyethylene glycol) 3350, 1.1115 mg; talc, 1.8 mg; titanium dioxide E 171, 1.7253 mg; soy lecithin E 322, 0.315 mg; aluminum varnish on the basis of the dye indigo carmine – 0.0054 mg; aluminum varnish on the basis of the dye azorubin – 0.0459 mg; aluminum varnish on the basis of the dye crimson [Ponceau 4R] – 0.0369 mg).
How to take, the dosage
Ingestion.
Take at any time of the day regardless of meals. Before starting treatment with Atorvastatin-SZ, an attempt should be made to achieve control of hypercholesterolemia by diet, exercise and weight reduction in obese patients, as well as by therapy of the underlying disease.
The standard hypocholesterolemic diet should be recommended to the patient when prescribing the drug and should be followed during the entire period of therapy.
The dose of the drug varies from 10 mg to 80 mg once daily and is titrated taking into account baseline concentration of LDL-C, purpose of therapy and individual effect on therapy. Maximum daily dose of the drug for single administration is 80 mg. At the beginning of treatment and / or during increasing the dose of Atorvastatin-SZ it is necessary to monitor plasma lipid concentrations every 2 to 4 weeks and adjust the drug dose accordingly.
Primary hypercholesterolemia and combined (mixed) hyperlipidemia
For most patients, 10 mg once daily; the therapeutic effect is seen within 2 weeks and usually reaches a maximum within 4 weeks. With prolonged treatment, the effect persists.
Homozygous familial hypercholesterolemia
The initial dose is adjusted individually depending on the severity of the disease. In most cases the optimal effect is observed when using the drug in a dose of 80 mg once daily (decrease of HDL-C concentration by 18-45%).
Inadequate liver function
Inadequate liver function requires caution (due to delayed elimination of the drug from the body). Clinical and laboratory parameters should be carefully monitored (regular monitoring of “hepatic” transaminases activity: aspartate aminotransferase (AST) and alanine aminotransferase (ALT)). In case of significant increase in “hepatic” transaminases, the dose of Atorvastatin-CZ should be decreased or the treatment should be discontinued.
Kidney function impairment does not affect the plasma concentration of atorvastatin or the degree of decrease in LDL-C concentration during therapy with Atorvastatin-SZ, so no dose adjustment is required. Elderly patients No differences in efficacy, safety or therapeutic effect of Atorvastatin-SZ have been found in elderly patients compared to the general population and no dose adjustment is required (see section “Pharmacokinetics”).
The use in combination with other medicinal products
If simultaneous use with cyclosporine, telaprevir or tipranavir/ritonavir combination is necessary, the dose of Atorvastatin-SZ should not exceed 10 mg/day. Caution should be exercised and the lowest effective dose of atorvastatin used concomitantly with HIV protease inhibitors, hepatitis C inhibitors, clarithromycin and itraconazole. (see section “Special indications”).
Interaction
The risk of myopathy during treatment with HMG-CoA reductase inhibitors is increased with concomitant use of cyclosporine, fibrates, antibiotics (erythromycin, clarithromycin, quinupristine/dalfopristine), nefazodone, HIV protease inhibitors (indinavir, ritonavir), colchicine, antifungal agents – azole derivatives – and nicotinic acid at lipid-lowering doses (more than 1 g/day) (see See section “Special Precautions”).
SYPCA4 isoenzyme inhibitors
Since atorvastatin is metabolized by CYPCA4 isoenzyme, co-administration of atorvastatin with CYPCA4 isoenzyme inhibitors may increase Atorvastatin plasma concentrations. The degree of interaction and potentiation effect are determined by the variability of effect on CYPCA4 isoenzyme.
OATP1B1 transport protein inhibitors
Atorvastatin and its metabolites are substrates of OATP1B1 transport protein. OATP1B1 inhibitors (e.g., cyclosporine) may increase the bioavailability of atorvastatin. Thus, co-administration of atorvastatin at a dose of 10 mg and cyclosporine at a dose of 5.2 mg/kg/day leads to an increase in plasma concentration of atorvastatin by 7.7 times. If concomitant use with cyclosporine is necessary, the dose of Atorvastatin-SZ should not exceed 10 mg/day (see section “Dosage and administration”).
Eritromycin/clarithromycin
Concomitant administration of atorvastatin with erythromycin (500 mg 4 times daily) or clarithromycin (500 mg 2 times daily), which inhibit CYPCA4 isoenzyme, was observed to increase Atorvastatin plasma concentration (see sect. See section “Special indications”). Caution should be exercised and the lowest effective dose of atorvastatin should be used concomitantly with clarithromycin.
Protease inhibitors
Simultaneous use of atorvastatin with protease inhibitors, known as CYPZA4 isoenzyme inhibitors, is accompanied with increase of plasma concentration of atorvastatin (concomitant use with erythromycin increases Atorvastatin Cmax 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 tipranavir/ritonavir combination drugs, the dose of Atorvastatin-CZ should not exceed 10 mg/day.
Patients taking the HIV protease inhibitor tipranavir plus ritonavir or the hepatitis C protease inhibitor telaprevir should avoid concomitant administration of Atorvastatin-SZ. Patients taking HIV protease inhibitors lopinavir plus ritonavir should be careful when prescribing Atorvastatin-CZ and the lowest dose necessary should be prescribed. In patients taking HIV protease inhibitors saquinavir plus ritonavir, darunavir plus ritonavir, fosamprenavir or fosamprenavir plus ritonavir, the dose of Atorvastatin-ZS 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-CZ should not exceed 40 mg and close clinical monitoring is recommended.
Diltiazem
The co-administration of atorvastatin at a dose of 40 mg with diltiazem at a dose of 240 mg, leads to increased plasma concentrations of atorvastatin.
Ketoconazole, spironolactone and cimetidine
Caution should be exercised when concomitant use of atorvastatin with drugs that reduce the concentration of endogenous steroid hormones, such as ketoconazole, spironolactone and cimetidine.
Itraconazole
The concomitant use of atorvastatin in doses from 20 mg to 40 mg and itraconazole in dose 200 mg led to increase of AUC of atorvastatin. Caution should be exercised and the lowest effective dose of atorvastatin should be used concomitantly with itraconazole.
Grapefruit juice
Since grapefruit juice contains one or more components that inhibit CYPCA4 isoenzyme, its excessive consumption (more than 1.2 liters per day) may cause increase of plasma concentration of atorvastatin.
CYPCA4 isoenzyme inducers
The co-administration of atorvastatin with CYPCA4 isoenzyme inducers (e.g., efavirenz, phenytoin or rifampicin) may lead to decreased plasma concentration of atorvastatin. Due to dual mechanism of interaction with rifampicin (inducer of CYPCA4 isoenzyme and inhibitor of hepatocyte transport protein OATP1B1), simultaneous use of atorvastatin and rifampicin is recommended, since delayed administration of atorvastatin after rifampicin administration leads to significant decrease of plasma concentration of atorvastatin.
Antacids
Concomitant oral administration of suspension containing magnesium hydroxide and aluminum hydroxide decreased plasma concentration of atorvastatin by approximately 35%, but the degree of decrease in LDL-C concentration was not changed.
Phenazone
Atorvastatin does not affect the pharmacokinetics of phenazone, so no interaction with other drugs metabolized by the same cytochrome isoenzymes is expected.
Colestipol
Concomitant use of colestipol decreased plasma concentrations of atorvastatin by approximately 25%; however, the hypolipidemic effect of combining atorvastatin and colestipol was superior to that of each drug alone.
Digoxin
The equilibrium plasma concentrations of digoxin and atorvastatin at a dose of 10 mg did not change when digoxin and atorvastatin were repeatedly administered. However, when digoxin was used in combination with atorvastatin at a dose of 80 mg/day, digoxin concentrations increased by approximately 20%.
Patients receiving digoxin in combination with atorvastatin require appropriate monitoring.
Azithromycin
The concomitant use of atorvastatin in dose of 10 mg once daily and azithromycin in dose of 500 mg once daily did not change concentration of atorvastatin in plasma.
In concomitant use of atorvastatin and oral contraceptive containing norethisterone and ethinylestradiol a significant increase in AUC of norethisterone and ethinylestradiol by approximately 30% and 20%, respectively, was observed. 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 concomitant use of atorvastatin and terfenadine.
Warfarin
The concomitant use of atorvastatin with warfarin may in the first days increase the effect of warfarin on blood clotting (decrease in prothrombin time). This effect disappears after 15 days of concomitant use of these drugs.
Amlodipine
The pharmacokinetics of atorvastatin at a dose of 80 mg and amlodipine 10 mg have not changed in equilibrium.
Other concomitant therapy
In clinical trials atorvastatin was used in combination with hypotensive agents and estrogens within substitution therapy; no signs of clinically significant adverse interaction were observed; no studies of interaction with specific drugs were conducted.
Special Instructions
Before starting therapy with Atorvastatin, the patient should be prescribed a standard hypocholesterolemic diet, which should be followed during the entire period of treatment.
The use of HMG-CoA reductase inhibitors to reduce blood lipid levels may lead to changes in biochemical parameters reflecting liver function. Liver function should be monitored before the start of therapy, at 6 weeks, 12 weeks after the start of Atorvastatin administration and after each dose increase as well as periodically, e.g., every 6 months. Elevation of serum hepatic enzymes activity may be observed during Atorvastatin therapy. Patients with increased enzyme levels should be monitored until enzyme levels return to normal. In case if values of alanine aminotransferase (ALT) or asparagine aminotransferase (AST) exceed more than 3 times the upper allowable limit, it is recommended to reduce Atorvastatin dose or discontinue treatment.
Atorvastatin should be used with caution in patients who abuse alcohol and/or have liver disease. Active liver disease or persistent increase in aminotransferase activity of unclear genesis are contraindications to Atorvastatin administration.
Treatment with Atorvastatin may cause myopathy. The diagnosis of myopathy (pain and weakness in muscles combined with an increase in creatine phosphokinase (CPK) activity more than 10 times the upper limit of normal) should be discussed in patients with widespread myalgia, muscle soreness or weakness and/or a marked increase in CPK activity. Patients should be warned to inform their physician immediately of unexplained muscle pain or weakness if accompanied by malaise or fever.
Atorvastatin therapy should be discontinued if there is a marked increase in CPK activity or if there is confirmed or suspected myopathy. Risk of myopathy during treatment by other drugs of 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 benefits and risks of treatment should be carefully weighed and patients should be regularly observed to detect muscle pain or weakness, especially during the first months of treatment and during periods of increasing doses of any drug. In such situations, periodic determination of CPK activity may be recommended, although such monitoring does not prevent the development of severe myopathy.
In Atorvastatin, as well as other drugs of this class, there have been cases of rhabdomyolysis with acute renal failure due to myoglobinuria. Atorvastatin therapy should be temporarily discontinued or completely discontinued in case of signs of possible myopathy or in presence of risk factor of renal failure during rhabdomyolysis (for example, severe acute infection, arterial hypotension, serious surgery, trauma, severe metabolic, endocrine and electrolyte disorders and uncontrolled convulsions).
Before starting therapy with Atorvastatin, an attempt should be made to control hypercholesterolemia through adequate diet therapy, increasing physical activity, reducing body weight in obese patients and treating other conditions.
Patients should be warned to seek immediate medical attention if they experience unexplained muscle pain or weakness, especially if accompanied by malaise or fever.
Contraindications
Hypersensitivity to any component of the drug.
Active liver disease or an increase in plasma “hepatic” transaminases of unclear origin of more than 3 times the upper limit of normal.
Age before 18 years of age (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 the period of breastfeeding.
The use in women who are planning a pregnancy and do not use reliable methods of contraception.
With caution:
Alcohol abuse, history of liver disease, diseases of the muscular system (history of other representatives of the group of HMG-CoA reductase inhibitors), severe water-electrolyte balance disorders, endocrine (hyperthyroidism) and metabolic disorders, severe acute infections (sepsis), arterial hypotension, diabetes, uncontrolled epilepsy, extensive surgical interventions, injuries.
Side effects
World Health Organization (WHO) Frequency Classification of side effects: Very common (â¥1/10), common (â¥1/100 to < 1/10), infrequent (â¥1/1000 to < 1/100), rare (â¥1/10 000 to < 1/1000), very rare (from < 1/10 000, including individual reports), frequency unknown – adverse reactions with unknown frequency (cannot be calculated from available data).
Nervous system disorders: frequent – headache, insomnia, dizziness, paresthesia, asthenic syndrome; infrequent – peripheral neuropathy, amnesia, hypoesthesia, nightmares.
Hearing organ: infrequent – tinnitus.
Cardiovascular system disorders: palpitations, vasodilation symptoms, migraine, postural hypotension, increased BP, phlebitis, arrhythmia.
Hematopoietic system disorders: infrequent – thrombopitopenia.
Respiratory system disorders: rarely – nasopharyngitis, nasal bleeding.
The digestive system: frequently – constipation, dyspepsia, nausea, diarrhea, flatulence (bloating), abdominal pain; infrequently – disorder of taste perception, vomiting, pancreatitis, belching; rarely – hepatitis, cholestatic jaundice; very rarely – liver failure.
Urinary system disorders: common – urinary tract infections; infrequent – secondary renal failure.
Perior genital system and mammary gland: infrequent – decrease in potency.
Muscular system: often – myalgia, arthralgia, joint swelling; infrequent – myopathy, muscle cramps; rarely – myositis, rhabdomyolysis, tendopathy (in some cases with tendon rupture).
Skin and subcutaneous tissue: often – skin rash, itching; infrequently – alopecia.
Allergic reactions: infrequent – urticaria; very rare – angioedema, bullous rash, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, anaphylaxis;
Laboratory disorders: infrequent – increased ACT activity, ALT, increased serum CPK activity, leukocyturia; very rare – hyperglycemia, hypoglycemia.
Others: often – peripheral edema, chest pain, back pain; infrequent – weakness, fatigue, fever, anorexia, weight gain, appearance of “black eyes”.
In postmarketing use of statins the following adverse effects have been reported: loss or reduction of memory, depression, sexual dysfunction, gynecomastia, increased concentration of glycosylated hemoglobin, single cases of interstitial lung disease (especially with long-term use), cases of immune-mediated necrotic myopathy.
The causal association of some adverse effects with the use of Atorvastatin-CZ, which are rated as “very rare”, has not been established.
In case of severe adverse effects, the use of Atorvastatin-SZ should be discontinued.
Overdose
Similarities
Weight | 0.200 kg |
---|---|
Shelf life | 3 years. |
Conditions of storage | In a dry, light-protected place at a temperature not exceeding 25 ° C. |
Manufacturer | North Star NAO, Russia |
Medication form | pills |
Brand | North Star NAO |
Other forms…
Related products
Buy Atorvastatin-SZ, 20 mg 60 pcs with delivery to USA, UK, Europe and over 120 other countries.