Aspirin® c

INSTRUCTIONS FOR MEDICAL USE OF THE MEDICINAL PRODUCT ASPIRIN® C (ASPIRIN® C)

Composition:

Active substances: acetylsalicylic acid and ascorbic acid;

One tablet contains 400 mg of acetylsalicylic acid and 240 mg of ascorbic acid (vitamin C);

Excipients: sodium dihydrogen citrate, sodium hydrogencarbonate, citric acid, sodium carbonate.

Pharmaceutical form. Effervescent tablets.

Main physicochemical properties: white tablets with an embossment of the "Bayer cross" on one side of the tablet.

Pharmacotherapeutic group. Nervous system. Other analgesics and antipyretics. Salicylic acid and derivatives. Acetylsalicylic acid.

ATC code N02BA01.

Pharmacological Properties.

Pharmacodynamics.

Acetylsalicylic acid belongs to the group of non-steroidal anti-inflammatory drugs (NSAIDs) with analgesic, antipyretic, and anti-inflammatory properties. Its mechanism of action involves irreversible inactivation of cyclooxygenase enzymes, which play an important role in the synthesis of prostaglandins.

Oral acetylsalicylic acid in doses from 0.3 g to 1 g is used to relieve pain and feverish conditions such as colds, to reduce fever and alleviate joint and muscle pain.

Acetylsalicylic acid inhibits platelet aggregation by blocking the synthesis of thromboxane A2.

Water-soluble ascorbic acid is part of the body's protective system against oxygen radicals and other oxidants of both endogenous and exogenous origin, which play a significant role in inflammatory processes and leukocyte function.

Results of in vitro and ex vivo studies have shown that ascorbic acid positively influences the human leukocyte immune response.

Ascorbic acid is necessary for the synthesis of intracellular substances (mucopolysaccharides), which together with collagen fibers maintain the integrity of capillary walls and thus reduce vascular permeability.

The addition of ascorbic acid to acetylsalicylic acid reduces gastrointestinal tract damage and oxidative stress. These benefits may be due to improved tolerability profile of the combination of acetylsalicylic acid with ascorbic acid compared to acetylsalicylic acid administered alone.

Pharmacokinetics.

After oral administration, acetylsalicylic acid is rapidly and completely absorbed from the gastrointestinal tract. During and after absorption, it is converted into its main active metabolite, salicylic acid. Typically, maximum plasma concentration of acetylsalicylic acid is reached within 15–30 minutes, and of salicylates within 0.72–2 hours. The addition of ascorbic acid results in either minimal variability or no variability at all in the pharmacokinetic parameters of acetylsalicylic acid.

Acetylsalicylic acid and salicylic acid are completely bound to plasma proteins and rapidly distributed throughout the body.

Salicylic acid crosses the placenta and is excreted in breast milk.

Salicylic acid is metabolized in the liver. Metabolites of salicylic acid include salicyluric acid, salicyl phenol glucuronide, salicyl acyl glucuronide, gentisic acid, and gentisuric acid. Ascorbic acid is partially metabolized via dehydroascorbic acid to oxalic acid.

The elimination kinetics of salicylic acid are dose-dependent, as metabolism is limited by hepatic enzyme activity. The elimination half-life depends on the dose and increases from 2–3 hours with low doses to 15 hours with high doses. Salicylic acid and its metabolites are primarily excreted by the kidneys.

After oral administration, ascorbic acid is absorbed in the intestine via a Na⁺-dependent active transport system, most actively in the proximal segment of the intestine. Absorption is not proportional to the dose. As the daily oral dose of ascorbic acid increases, its concentration in plasma and other body fluids does not increase proportionally but tends to approach an upper limit.

Ascorbic acid is filtered by the glomerular system of the kidneys and reabsorbed by the proximal tubules via an active Na⁺-dependent process. The main metabolites are excreted in urine as oxalates and diketogulonic acid.

Clinical characteristics.

Indications.

• Mild or moderate pain, such as headache, toothache, menstrual pain, and pain symptoms associated with colds (e.g., headache, sore throat, limb pain).
• Fever.

Contraindications.

Acetylsalicylic acid and ascorbic acid are contraindicated in the following cases:

• Hypersensitivity to acetylsalicylic acid, other salicylates, ascorbic acid, or any component of the drug.
• Bronchial asthma induced by salicylates or other NSAIDs in the patient's history.
• Acute gastrointestinal ulcers.
• Haemorrhagic diathesis.
• Severe kidney disease; pronounced renal insufficiency.
• Nephrolithiasis.
• Severe hepatic insufficiency.
• Severe heart failure.
• Predisposition to thrombosis, thrombophlebitis.
• Diabetes mellitus.
• Nephrolithiasis or history of nephrolithiasis.
• Hyperoxaluria.
• Haemochromatosis.
• Combination with methotrexate at doses of 15 mg/week or higher (see section "Interaction with other medicinal products and other types of interactions").
• Third trimester of pregnancy (see section "Use during pregnancy or lactation").

Interaction with other medicinal products and other types of interactions.

Contraindicated combinations.

The use of acetylsalicylic acid with methotrexate at doses of 15 mg/week or higher increases the hematological toxicity of methotrexate (due to reduced renal clearance of methotrexate by anti-inflammatory agents and displacement of methotrexate from plasma protein binding by salicylates).

Combinations requiring caution.

When acetylsalicylic acid is used with methotrexate at doses less than 15 mg/week, the hematological toxicity of methotrexate increases (due to reduced renal clearance of methotrexate by anti-inflammatory agents and displacement of methotrexate from plasma protein binding by salicylates).

Concomitant use of ibuprofen interferes with the irreversible inhibition of platelets by acetylsalicylic acid. Treatment with ibuprofen in patients at risk of cardiovascular diseases may reduce the cardioprotective effect of acetylsalicylic acid.

Concomitant use of acetylsalicylic acid with NSAIDs increases the risk of gastrointestinal ulcers and gastrointestinal bleeding due to a mutually enhancing effect.

Concomitant use of Aspirin® C and anticoagulants/thrombolytics increases the risk of bleeding. Therefore, patients requiring thrombolytic therapy should be monitored for signs of external or internal bleeding.

Platelet aggregation inhibitors (ticlopidine, clopidogrel): increased risk of bleeding.

Concomitant use with uricosuric agents, such as benzbromarone, probenecid, reduces uric acid excretion (due to competition for renal tubular excretion of uric acid).

When used concomitantly with digoxin, its plasma concentration increases due to reduced renal excretion.

Concomitant use of high doses of acetylsalicylic acid and oral antidiabetic sulfonylurea derivatives or insulin enhances the hypoglycemic effect of the latter due to the hypoglycemic effect of acetylsalicylic acid and displacement of sulfonylurea from plasma protein binding.

Diuretics in combination with acetylsalicylic acid reduce glomerular filtration due to decreased synthesis of renal prostaglandins, and also reduce the diuretic effect.

Systemic glucocorticosteroids (except hydrocortisone used for replacement therapy in Addison's disease). When acetylsalicylic acid is used concomitantly with corticosteroids, the level of salicylates in blood decreases, increasing the risk of overdose after discontinuation of treatment, and also increasing the risk of gastrointestinal bleeding.

ACE inhibitors in combination with acetylsalicylic acid cause reduced glomerular filtration due to inhibition of vasodilatory prostaglandins and reduced antihypertensive effect.

Selective serotonin reuptake inhibitors (SSRIs): increased risk of upper gastrointestinal bleeding due to possible synergistic effect.

When used concomitantly with valproic acid, acetylsalicylic acid displaces it from plasma protein binding, increasing its toxicity.

Ethanol promotes damage to the gastrointestinal mucosa and prolongs bleeding time due to synergism between acetylsalicylic acid and alcohol.

Ascorbic acid reduces the toxicity of sulfonamide drugs, reduces the effect of heparin and indirect anticoagulants, promotes absorption of iron, enhances absorption of penicillin, ethinylestradiol, and aluminum (this should be considered when used concomitantly with antacids containing aluminum); enhances the adverse effects of salicylates (risk of crystalluria). Quinolone derivatives, calcium chloride, salicylates, glucocorticosteroids reduce vitamin C stores in the body during prolonged use. Concomitant use of ascorbic acid reduces the chronotropic effect of isoprenaline; at high doses, it increases renal excretion of mexiletine. Barbiturates and primidone increase urinary excretion of ascorbic acid. Ascorbic acid reduces the therapeutic effect of neuroleptics (phenothiazine derivatives), tubular reabsorption of amphetamine and tricyclic antidepressants. Administration of ascorbic acid together with deferoxamine increases tissue toxicity of iron, especially in cardiac muscle, which may lead to circulatory decompensation. Vitamin C may be taken 2 hours after deferoxamine injection. High doses of ascorbic acid affect the resorption of vitamin B12. Ascorbic acid increases oxalate excretion in urine, thus increasing the risk of calcium oxalate stone formation in urine.

Effect on laboratory test parameters

Since vitamin C is a reducing agent (i.e., an electron donor), it may interfere with laboratory tests involving oxidation/reduction reactions, such as tests for glucose, creatinine, carbamazepine, urinary and serum uric acid, and occult blood in stool. Vitamin C may interfere with tests measuring glucose levels in blood and urine, leading to false results, although it does not affect the actual blood glucose level.

Special precautions for use.

Acetylsalicylic acid

Aspirin® C should be used with caution in:

• hypersensitivity to analgesics, anti-inflammatory, or antirheumatic agents, as well as in the presence of allergy to other substances;
• history of peptic ulcers, including chronic or recurrent peptic ulcer disease or gastrointestinal bleeding;
• concomitant use of anticoagulants;
• renal function impairment or circulatory disorders (such as renal vascular disease, congestive heart failure, dehydration, major surgical procedures, sepsis, or significant blood loss), since acetylsalicylic acid may further increase the risk of kidney damage and cause acute renal failure;
• hepatic function impairment.

In patients with allergic complications, including bronchial asthma, allergic rhinitis, urticaria, skin pruritus, mucosal edema, nasal polyps, or their combination with chronic respiratory tract infections, and in patients with hypersensitivity to NSAIDs, treatment with Aspirin® C may provoke bronchospasm, asthma attacks, or other hypersensitivity reactions.

Due to its inhibitory effect on platelet aggregation, which persists for several days after administration, acetylsalicylic acid may increase the risk of bleeding during and after surgical procedures (including minor surgeries such as tooth extraction).

When low doses of acetylsalicylic acid are used, excretion of uric acid may be reduced. This may lead to gout in patients with impaired uric acid excretion.

In patients with glucose-6-phosphate dehydrogenase deficiency, acetylsalicylic acid may cause hemolysis or hemolytic anemia. Factors increasing the risk of hemolysis include, for example, high-dose administration, fever, or acute infections.

Prolonged use of analgesics may lead to the development of headache.

Frequent use of analgesics may cause temporary kidney dysfunction with a risk of developing renal failure (analgesic nephropathy). The risk is particularly high when multiple different analgesics are used simultaneously.

One effervescent tablet of Aspirin® C contains 466.4 mg of sodium, corresponding to 23% of the maximum daily intake (2 g per day) recommended by WHO for adults. This should be taken into account for patients on a sodium-restricted diet.

Ascorbic acid

Ascorbic acid should be used with caution in patients predisposed to calcium-oxalate nephrolithiasis or with recurrent nephrolithiasis.

When high doses are used or the drug is administered for prolonged periods, renal function, arterial blood pressure, and pancreatic function should be monitored.

The drug should be used cautiously in patients with a history of mild to moderate kidney disease.

Since ascorbic acid enhances iron absorption, its use in high doses may be hazardous in patients with hemochromatosis, thalassemia, polycythemia, leukemia, or sideroblastic anemia. Patients with high body iron stores should use the drug at minimal doses.

Absorption of ascorbic acid is reduced when taken simultaneously with fruit or vegetable juices or alkaline drinks.

Absorption of ascorbic acid may also be impaired in intestinal dyskinesia, enteritis, and achylia. Ascorbic acid, as a reducing agent, may interfere with laboratory test results, for example, in determining blood glucose, bilirubin, transaminase activity, lactate dehydrogenase, etc.

Since ascorbic acid has a mild stimulating effect, the drug is not recommended for administration at the end of the day.

Long-term use of high doses of ascorbic acid may accelerate its own metabolism, leading to paradoxical hypovitaminosis after discontinuation of treatment. The recommended dose should not be exceeded.

The drug should not be used simultaneously with other medications containing acetylsalicylic acid and vitamin C.

The drug should be used with caution in polycythemia and leukemia.

The result of fecal occult blood testing may be falsely negative.

Use during pregnancy or breastfeeding.

Pregnancy.

Aspirin® C may be used during pregnancy only if other medications are ineffective and only after careful assessment of the benefit-risk ratio.

Inhibition of prostaglandin synthesis may adversely affect pregnancy and/or embryonic/fetal development. Epidemiological data indicate an increased risk of miscarriage and congenital heart defects and gastroschisis following use of prostaglandin synthesis inhibitors in early pregnancy. The absolute risk of congenital heart defects increases from <1% to 1.5%. This risk is considered to increase with dose and duration of treatment.

Animal studies have shown that prostaglandin synthesis inhibitors cause increased pre- and post-implantation loss and embryonic/fetal death. Cases of various developmental abnormalities, including cardiovascular malformations, have been reported in animals treated with prostaglandin synthesis inhibitors during organogenesis.

Use of acetylsalicylic acid from the 20th week of pregnancy may cause oligohydramnios (low amniotic fluid) due to fetal renal dysfunction. This may occur soon after initiation of treatment and is usually reversible upon discontinuation of therapy. Additionally, cases of fetal ductus arteriosus constriction have been reported after use in the second trimester, most of which resolved after stopping treatment. Therefore, acetylsalicylic acid should be used only if necessary during the first and second trimesters. In women attempting to conceive or during the first and second trimesters of pregnancy, the dose of acetylsalicylic acid-containing products should be as low as possible and the duration of treatment as short as possible. Prenatal monitoring for oligohydramnios and ductus arteriosus constriction should be considered after exposure to acetylsalicylic acid starting from the 20th week of pregnancy. Treatment should be discontinued if oligohydramnios or ductus arteriosus constriction is detected.

During the third trimester of pregnancy, all prostaglandin synthesis inhibitors may affect the fetus as follows:

• cardiopulmonary toxicity (with premature constriction/closure of the ductus arteriosus and pulmonary hypertension);
• renal dysfunction with potential progression to renal failure and oligohydramnios.

In late pregnancy, prostaglandin synthesis inhibitors may affect the mother and fetus as follows:

• prolonged bleeding time, anti-aggregatory effect, which may occur even after very low doses;
• inhibition of uterine contractions, potentially leading to delayed or prolonged labor.

Therefore, acetylsalicylic acid is contraindicated during the third trimester of pregnancy.

Breastfeeding.

Salicylates and their metabolites pass into breast milk in small amounts. Since no adverse effects in infants have been observed so far, interruption of breastfeeding is not necessary if the drug is used occasionally. However, breastfeeding should be discontinued during prolonged use or use of high doses of the drug.

Fertility.

There is some evidence that drugs which inhibit prostaglandin synthesis may impair female reproductive function by affecting ovulation. This effect is reversible and resolves after discontinuation of treatment.

Ability to influence reaction speed when driving or operating machinery.

No effects on the ability to drive vehicles or operate machinery have been reported.

Method of Administration and Dosage.

Aspirin® C is taken orally after meals.

Effervescent tablets should be dissolved in 1 glass of water immediately before use. The dose of the medication is calculated based on acetylsalicylic acid.

Aspirin® C must not be used for longer than 4 days without consulting a physician.

Adults and children aged 15 years and older.

1–2 effervescent tablets as a single dose. Repeat dosing may be performed if necessary, but not sooner than every 4 hours. The daily dose is 3–6 effervescent tablets. The maximum daily dose of acetylsalicylic acid must not exceed 3 g.

Warning.

Dosage reduction or prolonged dosing intervals are required for patients with concomitant hepatic or renal function impairment.

Children. The medication is indicated for children aged 15 years and older.

Medicinal products containing acetylsalicylic acid should not be used in children with acute respiratory viral infections (ARVI), whether or not accompanied by fever, without prior medical consultation. In certain viral diseases, particularly influenza A, influenza B, and varicella, there is a risk of Reye’s syndrome—a very rare but life-threatening condition requiring urgent medical intervention. The risk may be increased when acetylsalicylic acid is used concomitantly; however, a causal relationship has not been established. If the aforementioned conditions are accompanied by persistent vomiting, this may be a sign of Reye’s syndrome.

Overdose.

Salicylate toxicity (administration exceeding 100 mg/kg/day for more than 2 days may cause toxicity) may result from chronic intoxication due to prolonged therapy, or from acute intoxication (overdose), which is potentially life-threatening and may be caused, for example, by accidental ingestion in children or overdose. Elderly individuals and children are at higher risk of salicylate poisoning.

Chronic intoxication with salicylates may have an insidious onset, as its symptoms are nonspecific. Moderate chronic intoxication, or salicylism, typically occurs only after repeated administration of high doses.

Symptoms. Dizziness, tinnitus, hearing loss, sweating, nausea and vomiting, headache, confusion. These symptoms may be controlled by reducing the dose. Tinnitus may occur at plasma salicylate concentrations above 150–300 µg/mL. More serious adverse reactions occur at plasma salicylate concentrations exceeding 300 µg/mL.

Acute intoxication is characterized by pronounced disturbances in acid-base balance, which vary depending on patient age and severity of intoxication. In children, metabolic acidosis is the most typical manifestation. The severity of the condition cannot be assessed based solely on plasma salicylate concentration. Absorption of acetylsalicylic acid may be delayed due to delayed gastric emptying, formation of gastric concretions, or ingestion of enteric-coated tablets.

Due to complex pathophysiological effects, signs and symptoms of salicylate poisoning may include:

Mild to moderate intoxication – tachypnea, hyperpnea, respiratory alkalosis. Sweating, nausea, vomiting.

Moderate to severe intoxication – respiratory alkalosis accompanied by compensatory metabolic acidosis, hyperpyrexia. Respiratory system: from hyperpnea, non-cardiogenic pulmonary edema, to respiratory arrest and asphyxia. Cardiovascular system: from arrhythmia, hypotension, to cardiac arrest. Dehydration, oliguria progressing to renal failure; glucose metabolism disturbances, ketosis; gastrointestinal hemorrhage; hematological changes – from platelet inhibition to coagulopathies. Nervous system: toxic encephalopathy and CNS depression, manifesting as drowsiness, depressed consciousness, coma, and seizures.

Laboratory and other test abnormalities: alkalemia, alkaluria, acidemia, aciduria, blood pressure changes, ECG changes, hypokalemia, hypernatremia, hyponatremia, renal function changes, hyperglycemia, hypoglycemia (especially in children). Elevated ketone bodies, hypoprothrombinemia.

Overdose of ascorbic acid.

Ascorbic acid is a water-soluble vitamin, and excess amounts are excreted in urine.

Cases of acute or chronic overdose have been reported, which may also cause vitamin C-related toxicity.

General manifestations of vitamin C overdose may include gastrointestinal disturbances such as diarrhea, nausea, and vomiting, which resolve after discontinuation.

Clinical signs, symptoms, laboratory findings, and consequences of overdose depend on individual susceptibility and treatment circumstances (i.e., dose, duration of use, time to diagnosis).

If symptoms of overdose occur, administration of the medication should be discontinued and medical advice sought. Acute or chronic overdose of vitamin C (> 2 g/day in adults) may significantly increase urinary oxalate levels. In some cases, this leads to hyperoxaluria, calcium oxalate crystallization, kidney stone formation, calcium oxalate deposition, tubulointerstitial nephropathy, and acute renal failure.

Prolonged high-dose vitamin C use may suppress pancreatic islet function, requiring monitoring of pancreatic function.

Elevated oxalate levels have been shown to cause calcium deposition in patients undergoing dialysis.

Vitamin C overdose in individuals with glucose-6-phosphate dehydrogenase deficiency (> 3 g/day in children and > 15 g/day in adults) may lead to erythrocyte hemolysis, disseminated intravascular coagulation, and significant increases in serum and urinary oxalate levels.

Treatment.

In cases of acetylsalicylic acid poisoning, immediate hospitalization in a specialized unit is required. Treatment of intoxication due to acetylsalicylic acid overdose is determined by severity and clinical symptoms and includes standard poisoning management measures (gastric lavage, activated charcoal, forced diuresis). All interventions should aim to accelerate drug elimination and restore electrolyte and acid-base balance. Infusion of electrolyte solutions should be administered based on acid-base and electrolyte status. Alkaline diuresis should be maintained until urine pH reaches between 7.5 and 8. Forced alkaline diuresis should be considered if plasma salicylate concentration exceeds 500 mg/L (3.6 mmol/L) or 300 mg/L (2.2 mmol/L) in children. Hemodialysis is indicated in severe poisoning cases. Adequate fluid resuscitation and symptomatic treatment must be ensured.

Adverse Reactions

Below is a list of all known adverse reactions during treatment with acetylsalicylic acid, including those observed with long-term use of high doses in patients with rheumatism. The frequency of adverse reactions is classified as follows: very common (≥ 1/10), common (≥ 1/100, < 1/10), uncommon (≥ 1/1,000, < 1/100), rare (≥ 1/10,000, < 1/1,000), very rare (< 1/10,000), and frequency not known (cannot be estimated from available data).

Gastrointestinal system disorders. Common: Dyspepsia, epigastric pain, abdominal pain, heartburn, diarrhea, nausea, vomiting, stomach cramps. Rare: Inflammation of the gastrointestinal tract, erosive and ulcerative lesions of the gastrointestinal tract, which may lead to gastrointestinal bleeding and perforation, with corresponding laboratory and clinical manifestations. Frequency not known: Diaphragmatic intestinal disease (particularly with long-term treatment). Very rare: Transient hepatic insufficiency with elevated liver transaminase levels.

Blood and lymphatic system disorders. Due to its antiplatelet effect, acetylsalicylic acid may increase the risk of bleeding and potentially prolong bleeding time. This effect may persist for 4–8 days after administration of acetylsalicylic acid. Rare: Perioperative bleeding, hematomas, urogenital bleeding, epistaxis, gingival bleeding. Very rare: Severe bleeding events such as gastrointestinal hemorrhage and cerebral hemorrhage (especially in patients with uncontrolled arterial hypertension and/or concomitant use of anticoagulant agents), which in rare cases may be life-threatening.

Bleeding may lead to acute and chronic post-hemorrhagic anemia/iron-deficiency anemia (due to so-called occult microbleeding), with corresponding laboratory findings and clinical symptoms such as asthenia, pallor of the skin, and hypoperfusion.

In patients with severe glucose-6-phosphate dehydrogenase deficiency, hemolysis and development of hemolytic anemia have been reported.

Immune system disorders. Aspirin-induced respiratory disease may occur. Rare: In patients with individual hypersensitivity to salicylates, allergic reactions involving the respiratory system, gastrointestinal tract, and cardiovascular system may develop, including symptoms such as rash, urticaria, pruritus, eczema, rhinitis, nasal congestion, and hypotension. Frequency not known: Severe hypersensitivity reactions, including anaphylactic shock.

Nervous system disorders. Headache, dizziness, hearing impairment; tinnitus and confusion may be signs of overdose. Sleep disturbances.

Other: Feeling of warmth.

Skin and subcutaneous tissue disorders. Uncommon: Hypersensitivity reactions of the skin. Rare: Severe hypersensitivity skin reactions (exudative multiform erythema).

With long-term use at high doses, the following may occur: Glomerular kidney damage, formation of urate and/or oxalate calculi in the kidneys and urinary tract, kidney injury; damage to the islet apparatus of the pancreas (hyperglycemia, glucosuria) and impaired glycogen synthesis up to the development of diabetes mellitus; myocardial dystrophy; thrombocytosis, hyperprothrombinemia, erythrocytopenia, neutrophilic leukocytosis, hemolytic anemia; decreased capillary permeability (possible worsening of tissue trophism, increased arterial pressure); in patients with glucose-6-phosphate dehydrogenase deficiency of blood cells, hemolysis of erythrocytes may occur; oral dysbiosis; disturbances in zinc and copper metabolism.

Reporting of adverse reactions after marketing authorization is of great importance. It enables continuous monitoring of the benefit-risk balance of the medicinal product. Healthcare professionals, pharmacists, patients, or their legal representatives are encouraged to report all suspected adverse reactions and lack of efficacy via the Automated Pharmacovigilance Information System at: https://aisf.dec.gov.ua.

Shelf life.

3 years.

Do not use after the expiry date stated on the packaging.

Storage conditions.

Store out of reach of children at a temperature not exceeding 25°C.

Incompatibilities.
Concomitant use of methotrexate at doses of 15 mg/week or higher increases the hematological toxicity of methotrexate (due to reduced renal clearance of methotrexate by anti-inflammatory agents and displacement of methotrexate from plasma protein binding by salicylates).

Packaging.

2 tablets per strip. 5 strips per cardboard box.

Prescription status.
Over-the-counter (without prescription).

Manufacturer.

Bayer Bitterfeld GmbH.

Manufacturer's address and place of business.

Ortsteil Greppin, Salegaster Chaussee 1, 06803 Bitterfeld-Wolfen, Germany.