Dipyridamole 25 mg 100 tablets, film-coated

• Treatment and prevention of ischemic type cerebrovascular disorders;

• Primary and secondary prevention of ischemic heart disease (IHD), especially in cases of acetylsalicylic acid (ASA) intolerance;

• Discircular encephalopathy;

• Prevention of arterial and venous thrombosis and their complications;

• Prevention of thromboembolism after heart valve replacement surgery;

• Prevention of placental insufficiency in complicated pregnancies;

• As part of combination therapy for microcirculation disorders of any origin;

• As an interferon inducer and immunomodulator for the prevention and treatment of influenza and acute respiratory viral infections (ARVI).

Tablets are taken orally, on an empty stomach, with a small amount of water, without breaking or chewing. The dosage of the medication is determined based on the indications, severity of the disease, and the patient's response to treatment. The duration of the treatment course is determined by the physician.

To reduce platelet aggregation, it is recommended to take the medication at a daily dose of 75-225 mg.

In severe cases, the daily dose may be increased to 600 mg.

For the prevention of placental insufficiency, it is recommended to take Dipyridamole at a dose of 25 mg or 75 mg (1 tablet 3 times a day). The maximum recommended daily dose is 225 mg.

For the prevention and treatment of cerebrovascular disorders, the daily dose of dipyridamole is 225-450 mg (1 tablet of 75 mg of Dipyridamole 3-6 times a day).

Patients with ischemic heart disease are recommended to take Dipyridamole at 75 mg 3 times a day. If necessary, the dose may be increased under medical supervision.

For the prevention of influenza and other acute respiratory viral infections, especially during epidemics, it is recommended to take Dipyridamole according to the following scheme: 50 mg (2 tablets of 25 mg) once every 7 days for 4-5 weeks.

For the prevention of recurrences in patients frequently suffering from respiratory viral infections, it is recommended to take Dipyridamole according to the following scheme: 100 mg (2 tablets of 25 mg 2 times a day with an interval of 2 hours) once a week for 8-10 weeks.

Dipyridamole is suitable for long-term treatment courses.

Composition per tablet:
Dosage 25 mg
Active ingredient: dipyridamole - 25.00 mg.
Excipients: lactose monohydrate (milk sugar) - 32.10 mg; microcrystalline cellulose (MCC-101) - 30.00 mg; copovidone - 4.00 mg;
sodium croscarmellose - 3.00 mg; magnesium stearate - 0.90 mg.
Coating composition: hypromellose - 1.24 mg; polysorbate 80 - 0.24 mg; yellow quinoline dye - 0.02 mg; titanium dioxide - 0.50 mg.

Round, biconvex tablets coated with a yellow film; a cross-section reveals two layers: a core ranging from yellow to bright yellow and a film coating.

• Increased sensitivity to the components of the drug;

• Lactose intolerance, lactase deficiency, glucose-galactose malabsorption syndrome;

• Acute myocardial infarction;

• Unstable angina;

• Widespread stenosing atherosclerosis of the coronary arteries;

• Subaortic stenosis;

• Decompensated heart failure;

• Severe arterial hypotension; collapse;

• Severe arterial hypertension;

• Severe cardiac rhythm disorders;

• Chronic obstructive pulmonary disease (COPD);

• Decompensated renal failure;

• Liver failure;

• Hemorrhagic diatheses;

• Diseases with a tendency to bleeding (peptic ulcer disease of the stomach and duodenum, etc.);

• Children under 12 years of age (efficacy and safety not studied).

With caution:
Caution is advised when prescribing to elderly patients, as it may cause orthostatic hypotension.
Pregnancy and lactation:
The use of dipyridamole during pregnancy and breastfeeding is possible only if the expected benefit to the mother outweighs the potential risk to the fetus and child. The duration of treatment is determined by the physician.

Xanthine derivatives (coffee, tea, theophylline derivatives) may weaken the vasodilatory effect of dipyridamole.

Dipyridamole may enhance the effect of anticoagulants and acetylsalicylic acid when used concurrently.

Dipyridamole enhances the effect of antihypertensive medications.

It weakens the properties of cholinesterase inhibitors, which may lead to exacerbation of myasthenia gravis.

Cephalosporins enhance the antithrombotic effect of dipyridamole.

Antacids reduce the maximum concentration of dipyridamole due to decreased absorption.

Special instructions:
The drug is not recommended for children under 12 years of age.

During treatment, it is advisable to avoid the consumption of coffee and tea.

In patients with myasthenia gravis, after changing the dose of dipyridamole, dose adjustment of medications used in the complex therapy of myasthenia may be required.

Patients who are continuously taking dipyridamole orally should not be additionally prescribed it intravenously.

If it is necessary to perform a dipyridamole stress test intravenously for the diagnosis of coronary artery diseases, oral administration of the drug should be discontinued 24 hours prior to the procedure.

In the case of coronary steal syndrome, the use of aminophylline is indicated to improve intracardiac blood flow.

Effect on the ability to drive vehicles and operate machinery:
Due to the possible decrease in blood pressure and the occurrence of dizziness during the use of the drug, the ability to concentrate and the speed of psychomotor reactions in patients may be reduced. Therefore, caution should be exercised when driving vehicles and engaging in potentially dangerous activities that require increased attention and quick psychomotor responses during the treatment with dipyridamole.

When the drug is used at therapeutic doses, side effects are usually mild and transient.

Possible side effects when using the drug are listed below in descending order of frequency: often (> 1/100, 1/1000, 1/10000, < 1/1000), very rarely (< 1/10000), including individual reports.Cardiovascular system:Infrequently: tachycardia, flushing of the face, decreased blood pressure (especially when used in conjunction with other vasodilators), coronary steal syndrome (when used at doses greater than 225 mg/day).Gastrointestinal system:Infrequently: nausea, vomiting, diarrhea, epigastric pain. These side effects usually appear at the beginning of treatment and disappear with prolonged use of the drug.Blood and homeostasis system:Infrequently: thrombocytopenia, changes in platelet function, bleeding.Very rarely: increased bleeding after surgical interventions.Immune system:Rarely: allergic reactions, such as skin rash, urticaria.Others: weakness, dizziness, headache, facial skin hyperemia, arthritis, myalgia, rhinitis.Individual reports: exacerbation of symptoms of ischemic heart disease (IHD), such as angina, myocardial infarction.Symptoms: pronounced decrease in blood pressure, development or exacerbation of angina attacks, tachycardia, sensation of heat, "flushing" of the face, increased sweating, anxiety, weakness, and dizziness.Treatment: induction of vomiting, gastric lavage, use of adsorbents to reduce absorption (activated charcoal, etc.). The undesirable vasodilatory effect of the drug can be countered by slow intravenous administration of aminophylline (50-100 mg/min). In case of angina symptoms, sublingual administration of nitroglycerin is indicated.Xanthine derivatives (coffee, tea, theophylline derivatives) may weaken the vasodilatory effect of dipyridamole. Dipyridamole may enhance the effect of anticoagulants and acetylsalicylic acid when used concurrently. Dipyridamole enhances the effect of antihypertensive medications. It weakens the properties of cholinesterase inhibitors, which may lead to exacerbation of myasthenia gravis. Cephalosporins enhance the antithrombotic effect of dipyridamole. Antacids reduce the maximum concentration of dipyridamole due to decreased absorption.

Dipyridamole inhibits platelet aggregation and adhesion, improves microcirculation, and has a mild vasodilatory effect.

The mechanism by which dipyridamole exerts an inhibitory effect on platelet aggregation is associated with the suppression of the reuptake of adenosine (a platelet reactivity inhibitor) by endothelial cells, erythrocytes, and platelets; activation of adenylate cyclase; and inhibition of platelet phosphodiesterase. Thus, dipyridamole prevents the release from platelets of aggregation activators - thromboxane (TxA2), ADP, serotonin, and others. Dipyridamole increases the synthesis of prostacyclin PgI2 by the vascular wall endothelium, normalizes the ratio of PgI2 to TxA2, preventing platelet aggregation; enhances the synthesis of endothelial nitric oxide (NO). Dipyridamole reduces platelet adhesiveness, prevents thrombus formation in blood vessels, and stabilizes blood flow in the ischemic area.

Dipyridamole dose-dependently prolongs the pathologically shortened lifespan of platelets.

Due to its vasodilatory properties, dipyridamole helps reduce total peripheral vascular resistance, improves microcirculation, and has angioprotective effects. These effects are due to the increased activity of endogenous adenosine (adenosine affects the smooth muscle of blood vessels and prevents the release of norepinephrine). Dipyridamole has both angiogenic and arteriogenic activity, stimulating the formation of new capillaries and collateral arteries.

Dipyridamole normalizes venous outflow, reduces the incidence of deep vein thrombosis in the postoperative period. It improves microcirculation in the retina and renal glomeruli.

In neurological practice, the pharmacodynamic effects of dipyridamole include reduced tone of cerebral vessels and improved cerebral blood circulation. According to angiographic studies, the use of dipyridamole in combination with acetylsalicylic acid (ASA) can slow the progression of atherosclerosis.

In obstetric practice, dipyridamole is used to improve placental blood flow and prevent dystrophic changes in the placenta, eliminate tissue hypoxia in the fetus, and promote glycogen accumulation in fetal tissues.

When taken orally, dipyridamole is rapidly absorbed from the gastrointestinal tract: most absorption occurs in the stomach and partially in the small intestine. The bioavailability is 37-66%, and the time to reach maximum concentration (Tmax) in plasma is approximately 2 hours. Dipyridamole is almost completely bound to plasma proteins.

After oral administration, a biphasic pattern of dipyridamole concentration reduction in plasma is observed. The half-life of the drug in the initial phase is 20-30 minutes, while in the terminal elimination phase it is 10-12 hours. Dipyridamole is metabolized in the liver by conjugation with glucuronic acid. It is primarily excreted in bile and eliminated through the intestines as monoglucuronide. A small amount of dipyridamole (1-3%) is excreted by the kidneys.