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Aggrenox (Acetylsalicylic acid + Dipyridamole) 30 capsules (modified release)

Aggrenox (Acetylsalicylic acid + Dipyridamole) 30 capsules (modified release)


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  • Aggrenox (Acetylsalicylic acid + Dipyridamole) 30 capsules (modified release) Aggrenox (Acetylsalicylic acid + Dipyridamole) 30 capsules (modified release)

Aggrenox (Acetylsalicylic acid + Dipyridamole) 30 capsules (modified release)

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Aggrenox (Acetylsalicylic acid + Dipyridamole) 30 capsules (modified release) Anti-aggregants

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The composition and form of issue:

Capsules with modified release 1 capsule.

1 capsule contains:

Tablet of acetylsalicylic acid, 1 tab.

active substance:

acetylsalicylic acid 25 mg

auxiliary substances: lactose monohydrate microcrystalline starch, corn silicon dioxid dried colloidal aluminium stearate sucrose acacia gum, titanium dioxide, talc

Dipyridamole pellets 1 Pell.

active substance:

dipyridamole 200 mg

auxiliary substances: tartaric acid, spherical tartaric acid, powder povidone (Kollidon 25) of methacrylic acid and methyl methacrylate copolymer hypromellose phthalate HP 55 hypromellose glycerol triacetate (Triacetin) Dimethicone 350, stearic acid, talc Arabian gum

volatile substances: purified water (evaporates) isopropyl alcohol (evaporates) ethanol 96% (disappears)

hard gelatin capsule, size 0 gelatin titanium dioxide iron oxide yellow (colorant) iron oxide red (colorant)

Capsules with modified release: tube polypropylene, capped plastic tube with desiccants or polypropylene bottle, sealed with a plastic screw cap with tamper-evident bags from kids with a desiccant at 30 or 60 pieces per cardboard box 1 tube or bottle of 30 or 60 PCs.

Description pharmaceutical form:

Hard gelatin capsule, size 0. Cap red-brown, opaque, the body colors are ivory, opaque. The contents of the capsules: yellow pellets and round white biconvex tablet, film-coated, with smooth edges.


Between pellets of dipyridamole with sustained release and acetylsalicylic acid is not there is a significant pharmacokinetic interaction. Therefore, the pharmacokinetics of the drug Aggrenox characterized the pharmacokinetics of individual components.


Most pharmacokinetic data obtained in studies in healthy volunteers.

For dipyridamole characteristic linear dependence of the pharmacokinetics of the applied dose.

For long-term treatment with dipyridamole was designed capsules with modified release, comprising pellets. The dependence of solubility of dipyridamole from pH preventing dissolution of the dipyridamole in the lower gastrointestinal tract (where drugs with a slow release have yet to release the active substance) was overcome by combination with tartaric acid. Delayed release is achieved through the use of a diffusion membrane which is spray applied to pellets. Various kinetic studies at steady state showed that the pharmacokinetic parameters for drugs with modified-release capsules dipyridamole modified-release, which take 2 times a day, or equivalent, or on some indicators, surpass pills dipyridamole that take 3-4 times a day. The bioavailability is somewhat higher maximum concentrations are the same concentration between doses considerably higher fluctuations of peak concentrations between doses is reduced.

Suction. The absolute bioavailability is about 70%. Since the primary passage is removed about 1/3 of the administered dose, it can be assumed almost or complete absorption of dipyridamole after taking the drug.

Maximum concentration of dipyridamole in plasma after administration of a daily dose of 400 mg (200 mg 2 times per day) are observed 2-3 h after administration of the drug. Average maximum concentrations at steady state are of 1.98 µg/ml (range of 1.01–to 3.99 µg/ml) and concentrations between doses are of 0.53 mcg/ml (range of 0.18 to 1.01 µg/ml).

Food intake has no effect on the pharmacokinetics of dipyridamole in the drug Aggrenox.

Distribution. Due to its high lipophilicity, log P of 3.92 (n-octanol/0.1 n NaOH), dipyridamole is distributed in many bodies.

In animals, dipyridamole is distributed mainly in the liver and also in lungs, kidney, spleen and heart.

A fast phase distribution observed at/in the introduction, it is impossible to determine if oral administration.

Apparent Vd in the Central compartment is about 5 l (similar to plasma volume). The apparent Vss is about 100 l, reflecting distribution to various compartments. The drug does not penetrate the BBB in significant amounts. The penetration of the drug through the placental barrier is very low.

In one case, in human milk was discovered the drug in an amount of 1/17 part from its concentration in plasma.

The protein binding of dipyridamole is about 97-99%, primarily it is associated with &alpha-1-acid glycoprotein and albumin.

Metabolism. Metabolism of dipyridamole occurs in the liver. Dipyridamole is metabolized mainly by coniugali with glucuronic acid to form mainly monoglucuronide and only small amounts of diglucuronide. In plasma about 80% of the total number present in the form of the parent compound and 20% of the total amount in the form of monoglucuronide. Pharmacodynamic activity of dipyridamole glucuronides is considerably lower than the activity of dipyridamole.

Excretion. The dominant T1/2 after oral administration, as with on/in the introduction, is about 40 min.

Excretion of the drug in unchanged form via the kidneys is negligible (<0.5 percent). The urinary excretion of the glucuronide metabolite is low (5%), the metabolites are mostly (about 95%) excreted via bile in the feces, there is enterohepatic recirculation. Full Cl is about 250 ml/min, the average residence time in the body is about 11 h are determined on the basis of their own average time of stay in the body for about 6.4 h and a mean time of absorption of 4.6 h.

As with on/in the introduction there is prolonged period of the final half-life of about 13 h. This final phase of elimination has a relatively small impact, as it forms a minor part of the AUC, as evidenced by the fact that if capsules are modified-release, 2 times a day the equilibrium condition is reached within 2 days.

Repeated dose noticeable accumulation of PM is not observed.

Kinetics in the elderly. The concentration of dipyridamole in plasma (determined by AUC) in elderly (>65 years) were about 50% higher in the treatment with pills and approximately 30% higher when capsules are modified-release drug Aggrenox than in young (<55 years) subjects. This difference is mainly due to reduced ground clearance, because it turned out that the absorption was the same.

Kinetics in patients with renal insufficiency. Due to the low excretion via the kidneys (5%), it is possible to assume the absence of changes in the pharmacokinetics in case of kidney failure. In the ESPS2 study in patients with Cl creatinine in the range of from about 15 ml/min to >100 ml/min changes in the pharmacokinetics of dipyridamole or its metabolite — glucuronide dipyridamole — have not been observed, provided that adjustments to data to account for differences in age.

Kinetics in patients with hepatic insufficiency. In patients with liver failure changes in the concentration of dipyridamole in plasma was not observed, but there was an increase in the concentration of glucuronides, has low pharmacodynamic activity. Therefore, the adjustment of doses of dipyridamole are required only if clinically confirmed decompensation of liver function.

Acetylsalicylic acid

Suction. Acetylsalicylic acid is rapidly and completely absorbed. The maximum concentration in plasma after administration of a daily dose of 50 mg acetylsalicylic acid in a preparation Aggrenox (25 mg 2 times a day) are observed after 30 min, and the maximum concentration in plasma at steady state is 319 ng/ml (range 175-463 ng/ml). The maximum concentration of salicylic acid in plasma achieved through 60-90 min.

30-40% of the dose of the acetylsalicylic acid undergoes primary metabolism with the splitting up of salicylic acid that is the main way of metabolism. Pharmacodynamics of acetylsalicylic acid in the composition of Aggrenoxe not depend on food intake.

Distribution. Aspirin is poorly bound to plasma proteins and its apparent volume of distribution is small (10 l). Metabolite of acetylsalicylic acid — salicylic acid is largely bound to plasma proteins, but binding depends on the concentration (non-linear). At low concentrations (<100 µg/ml) about 90% salicylic acid associated with albumin. Salicylic acid is well distributed in all tissues and body fluids including the Central nervous system, breast milk and fetal tissue.

Metabolism. Acetylsalicylic acid is rapidly metabolized under the action of nonspecific esterases in liver, and to a lesser extent in the stomach to salicylic acid with subsequent formation hydroxyhippuric acid by reaction with glycine.

Excretion. T1/2 acetylsalicylic acid is 15-20 min T1/2 the main metabolite (salicylic acid) is 2-3 hours, may increase to 5-18 h at high doses (>3 g) due to saturation of the enzyme. About 90% of acetylsalicylic acid is in the form of metabolites via the kidneys.

Kinetics in patients with renal insufficiency. In severe renal impairment (glomerular filtration rate <10 ml/min) should not be administered acetylsalicylic acid. There is a reported increase in the duration of T1/2 in 2-3 times in patients with kidney disease.

Kinetics in patients with hepatic insufficiency. In severe deficiency of the liver should not be administered acetylsalicylic acid.

Description pharmacological action:

Antiplatelet effect of the combination of acetylsalicylic acid and dipyridamole due to various biochemical mechanisms.

Acetylsalicylic acid inactivates the platelet COX enzyme and thus prevents the formation of TX A2, a potent inducer of platelet aggregation and vasoconstriction.

Dipyridamole inhibits the capture of adenosine into erythrocytes, platelets and endothelial cells in vivo and in vitro inhibition reaches a maximum of 80%, in therapeutic concentrations (0.5 and 2 µg/ml) is dose-dependent. As a result, there occurs a local increase in the concentration of adenosine, which acts at A2 receptors of platelets, stimulating platelet adenylate cyclase and thus increasing the level of C-AMP of platelets.

Dipyridamole inhibits phosphodiesterase (PDE) in various tissues. As long as the inhibition of C-AMP-PDE is weak, therapeutic concentrations inhibit C-GMP-PDE, and thus contribute to an increase in C-GMP under the influence of HVA (relaxing factor released from the endothelium, identified as NO). Adenosine exerts a vasodilator effect, which is one of the mechanisms by which dipyridamole causes vasodilation. Dipyridamole stimulates the biosynthesis and release of prostacyclin by the endothelium. Dipyridamole reduces thrombogenicity subendothelial structures by increasing the concentration of the protective mediator 13-YEAR (13-hydroxyoctadecadienoic acid). Thus, in response to various stimulants, such as FAT, collagen and ADP, inhibiting platelet aggregation. Reduction of platelet aggregation leads to normalization of the consumption of adenosine by thrombocytes.

If acetylsalicylic acid inhibits only platelet aggregation, dipyridamole additionally inhibits the activation and adhesion of platelets. Therefore, the combination of these two drugs can be expected an additional effect.


Secondary prevention of ischemic stroke according to the mechanism of thrombosis and transient ischemic attacks.


  • hypersensitivity to any component of the drug or salicylates
  • peptic ulcer or duodenal ulcer in the acute stage or with a tendency to bleeding
  • pregnancy (III trimester)
  • childhood and adolescence till 18 years.

With caution

Among other properties dipyridamole has a vasodilatory effect. The drug should be administered with caution to patients with severe coronary artery disease, including unstable angina and recent myocardial infarction, and also in the difficulty of the ejection of blood from the left ventricle or hemodynamic instability (e.g. decompensated heart failure).

As one component of the drug is acetylsalicylic acid, the drug Aggrenox should be used with caution in patients with bronchial asthma, allergic rhinitis, nasal polyposis, recurrent ulcers of the stomach or duodenum, with impaired renal function or hepatic insufficiency or glucose-6-phosphate dehydrogenase.

In addition, it is recommended to exercise caution in patients with hypersensitivity to NSAIDs.

Application of pregnancy and breast-feeding:

Data on the safety of dipyridamole and acetylsalicylic acid in low dose in pregnancy person is not enough. In preclinical studies the negative impact have not been identified.

Dipyridamole and salicylates are excreted in breast milk.

Drug Aggrenox can be taken in the I–II trimesters of pregnancy or during lactation only if the benefit for mother exceeds potential risk for fetus (child). The drug is contraindicated in the third trimester of pregnancy.

Side effects:

Reported hypersensitivity reactions (rash, urticaria, severe bronchospasm and angioedema) in respect of dipyridamole , and in respect of acetylsalicylic acid. In very rare cases after administration of acetylsalicylic acid may experience a decrease in the number of platelets (thrombocytopenia). It was also reported on individual cases of thrombocytopenia observed in the treatment of dipyridamole.

Hemorrhages on the skin, such as bruises, ekhimozy and hematomas can occur with the use of the drug.

Adverse effects of dipyridamole in therapeutic doses are usually weak and transient. In the treatment of dipyridamole was observed vomiting, diarrhoea and symptoms such as dizziness, nausea, headache, migrenepodobna headache (especially at the beginning of treatment) and myalgia. These symptoms usually disappear with prolonged use of the drug.

As a consequence of the vasodilating effect of dipyridamole may cause hypotension, flushing and tachycardia. It was noted the worsening of symptoms of coronary artery disease. Acetylsalicylic acid increases bleeding time, also after taking dipyridamole in very rare cases, there was increased bleeding during and after surgery.

When taking acetylsalicylic acid may experience epigastric pain, nausea and vomiting, gastric ulcer or duodenal ulcer and erosive gastritis that can lead to serious gastrointestinal bleeding.

The result of concealed haemorrhage, especially when acetylsalicylic acid for a long period of time, can develop iron-deficiency anemia.

Drug interactions:

When using dipyridamole in combination with acetylsalicylic acid or with warfarin should be considered precautions for these drugs. Acetylsalicylic acid may potentiate the effects of anticoagulants (e.g. coumarin derivatives and heparin), drugs inhibiting platelet aggregation (clopidogrel, tiklopidin), valproic acid and increase the risk of side effects from the gastrointestinal tract with concomitant use with NSAIDs or with a COP, and the systematic use of alcohol. The combined use of dipyridamole and acetylsalicylic acid does not increase the frequency of bleeding.

Selective inhibitors of serotonin reuptake (SSRI) may increase the risk of bleeding.

Dipyridamole increases the concentration of adenosine in the plasma and enhances its cardiovascular effects. Consider the need to adjust doses of adenosine.

When used together, dipyridamole and warfarin, the frequency and severity of bleeding was not more than the introduction of only one of warfarin.

Dipyridamole may increase the hypotensive effect of drugs that reduce blood pressure and to provide reverse anticholinesterase effect of cholinesterase inhibitors, and as a consequence cause worsening of myasthenia gravis malignant.

The effect of hypoglycemic drugs and toxicity of methotrexate can be amplified when combined with acetylsalicylic acid.

Acetylsalicylic acid can reduce the natriuretic effect of spironolactone and inhibit the effect of uricosuric drugs (e.g. probenecid, sulfinpirazon).

Concurrent administration of ibuprofen (but not other NSAIDs or paracetamol) in patients with an increased risk of cardiovascular disease may limit the beneficial effect of aspirin on the cardiovascular system.

Should be cautiously prescribed to patients who are receiving treatment with drugs that increase the risk of bleeding — inhibiting platelet aggregation (clopidogrel, tiklopidin) or selective inhibitors of serotonin reuptake (SSRI).

Method of application and dose:

The recommended dose is 1 capsule. 2 times a day, usually take 1 caps. in the morning and 1 caps. in the evening, regardless of meals.

Capsules should be swallowed whole without chewing, with a glass of water.



Due to the ratio of doses of dipyridamole and acetylsalicylic acid in case of overdose Aggrenox likely to dominate the signs and symptoms of dipyridamole overdose.

Experience with dipyridamole overdose is limited due to the small number of observations. Supposed to experience symptoms such as hot flashes, hot flushes, sweating, restlessness, weakness, dizziness and symptoms of angina. Can be observed a sharp decrease in blood pressure and tachycardia.

Minor symptoms of acute aspirin overdose are hyperventilation, tinnitus, nausea, vomiting, disorders of vision and hearing, dizziness and blurred consciousness.

Dizziness and ringing in the ears, especially in elderly patients, can be symptoms of overdose.


Symptomatic treatment, gastric lavage. Introduction xanthine derivatives (e.g. aminophylline) may counteract haemodynamic effects of dipyridamole overdose.

As dipyridamole is widely distributed in tissues, and mostly eliminated by the liver, it is not displayed by hemodialysis.


Clinical experience suggests that patients receiving dipyridamole and inside which also requires a pharmacological stress test with I/V introduction of dipyridamole, should discontinue use of drugs that contain dipyridamole for 24 h before the test. Otherwise, the sensitivity of the test may be broken.

In patients with malignant myasthenia after a change in dose dipyridamole may be necessary to adjust primary therapy (see “Interactions”).

In a small number of cases it has been shown that nikanorovna dipyridamole in varying degrees, is embedded into the gallstones (up to 70% of the dry weight of stone). All patients were elderly. They had ascending cholangitis, and they received dipyridamole for many years. Evidence that dipyridamole was the initiating factor in the formation of gallstones. Probably, the presence of dipyridamole in gallstones can explain the bacterial dglucuronidase kongugirovannah dipyridamole in bile.

Dose acetylsalicylic acid in the drug Aggrenox (25 mg) were not studied for the indication of prevention of myocardial infarction.

Contains 106 mg lactose and 22.5 mg of sucrose in the maximum daily dose. It should not be used in patients with hereditary fructose intolerance and/or galactose, such as galactosemia.

Additional Information

SKU ml5144
Manufacturer Boehringer
The purpose of the medication Anti-aggregants
Weight kg. 0.05

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