Active substanceAcetylsalicylic acid + DipyridamoleAcetylsalicylic acid + Dipyridamole
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  • AgrenoX®
    capsules inwards 
  • Dosage form: & nbspmodified release capsules
    Composition:

    1 capsule contains:

    Tablets of acetylsalicylic acid

    Active substance

    Acetylsalicylic acid 25 mg

    Excipients

    Lactose monohydrate; microcrystalline cellulose; corn starch dried; silicon dioxide colloidal; aluminum stearate; sucrose; acacia gum; titanium dioxide; talc

    Pellet of dipyridamole

    Active substance

    Dipyridamole 200 mg

    Excipients

    Tartaric acid, spherical; tartaric acid, powder; povidone (Kollidon 25); methacrylic acid and methyl methacrylate copolymer; hypromellose phthalate HP 55; hypromellose; glycerol triacetate (Triacetin); dimethicone 350; stearic acid; talc; arabic gum

    Volatiles:

    Purified water (volatilized); isopropyl alcohol (volatilized); ethanol 96% (volatilized)

    capsule hard gelatin size 0:

    gelatin, titanium dioxide, iron oxide yellow (dye), iron oxide red (dye)

    Description:Hard gelatin capsules, size 0. The cap is red-brown, opaque, ivory-colored, opaque.Contents of the capsules: yellow pellets and round white biconvex tablet, coated with a shell, with smooth edges.
    Pharmacotherapeutic group:Antiaggregant agent
    ATX: & nbsp

    B.01.A.C   Inhibitors of platelet aggregation (excluding heparin)

    Pharmacodynamics:

    The antiaggregant effect of the combination of acetylsalicylic acid and dipyridamole is due to various biochemical mechanisms.

    Acetylsalicylic acid inactivates in the platelets enzyme cyclooxygenase, and thus prevents the formation of thromboxane A2 - a powerful inducer of platelet aggregation and vasoconstriction.

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

    Dipyridamole inhibits phosphodiesterase (PDE) in various tissues.As long as the inhibition of c-AMP-PDE is weak, therapeutic concentrations inhibit c-HMF-PDE, and therefore contribute to an increase in c-HMF induced by RFEV (a relaxing factor released from the endothelium identified as N0). Adenosine has no vasodilating effect, which is one of the mechanisms by which dipyridamole causes vasodilation. Dipyridamole stimulates biosynthesis and release of prostacyclin by endothelium. Dipyridamole reduces thrombogenicity of subendothelial structures, increasing the concentration of the protective mediator 13-GODE (13-hydroxyoctadecadienoic acid). Thus, in response to various stimulants, for example, TAF, collagen and ADP, aggregation of platelets is suppressed. Reduction of platelet aggregation leads to normalization of adenosine consumption by platelets.

    If acetylsalicylic acid inhibits only aggregation of platelets, then dipyridamole further inhibits the activation and adhesion of platelets. Therefore, a combination of these two drugs can be expected to have an additional effect.

    Pharmacokinetics:

    Between sustained-release dipyridamole pellets and acetylsalicylic acid, there is no significant pharmacokinetic interaction. Therefore, the pharmacokinetics of the drug AGRENOX is characterized by the pharmacokinetics of the individual components.

    Dipyridamole

    Most of the data on pharmacokinetics was obtained in studies on healthy volunteers.

    Dipyridamole is characterized by a linear dependence of the pharmacokinetics on the applied dose.

    For long-term treatment with dipyridamole, modified-release capsules have been developed, which include pellets. Dependence of the solubility of dipyridamole on pH, preventing the dissolution of dipyridamole in the lower gastrointestinal tract (where sustained release preparations still have to release the active substance), was overcome by its combination with tartaric acid. Delayed release is achieved through the use of a diffusion membrane, which is sprayed onto pellets as a spray. Various kinetic studies in the equilibrium state have shown that according to the pharmacokinetic parameters characterizing the modified release preparations,Dipiridamole capsules with modified release, which are taken 2 times a day, are either equivalent, or by some parameters, superior to dipyridamole tablets, which take 3-4 times a day. Bioavailability is slightly higher, the maximum concentrations are the same, the concentrations between receptions are much higher, fluctuations in peak concentrations between receptions are reduced.

    Suction

    Absolute bioavailability is about 70%. Since at the primary passage about 1/3 of the dose administered is removed, we can assume almost or complete absorption of dipyridamole after taking the drug.

    The maximum concentration of dipyridamole in the plasma after taking a daily dose of 400 mg (200 mg twice a day) is observed 2-3 hours after taking the drug. The mean maximum concentrations at the equilibrium state are 1.98 μg / ml (range 1.01 to 3.99 μg / ml) and the concentrations between the receipts are 0.53 μg / ml (range 0.18-1.01 μg / ml) .

    Food intake does not affect the pharmacokinetics of dipyridamole in the preparation AGRENOX

    Distribution

    Due to its high lipophilicity, log P 3.92 (p-octanol / 0.1 p, NaOH), Dipyridamole is distributed in many organs.

    In animals dipyridamole mainly distributed in the liver, as well as in the lungs, kidneys, spleen and heart.

    The rapid phase of the distribution observed with intravenous administration can not be determined by oral administration.

    The apparent volume of distribution in the central compartment (Vc) is about 5 liters (similar to the volume of the plasma). The apparent volume of the distribution at the equilibrium state is about 100 liters, reflecting the distribution in different compartments. The drug does not penetrate the blood-brain barrier in a significant amount. Penetration of the drug through the placental barrier is very low.

    In one case, breast milk was found to contain an amount of 1/17 of its concentration in the plasma.

    The binding of dipyridamole with proteins is about 97% -99%, mainly it binds to alpha-1-acid glycoprotein and albumin.

    Metabolism

    The metabolism of dipyridamole occurs in the liver. Dipyridamole is mainly metabolized by conjugation with glucuronic acid with the formation of mainly monoglycuronide and only small amounts of diglucuronide. In plasma, about 80% of the total is present in the form of the starting compound, and 20% of the total amount in the form of monoglycuronide.The pharmacodynamic activity of dipyridamole glucuronides is significantly lower than that of dipyridamole.

    Excretion

    The dominant half-life for oral administration, as for intravenous administration, is about 40 minutes.

    Excretion of the drug unchanged through the kidneys is negligible (<0.5%). Excretion of the metabolite glucuronide in the urine is low (5%), metabolites are mainly (about 95%) excreted through bile with feces, while intestinal-hepatic recirculation is observed. The total clearance is about 250 ml / min, the average residence time in the body is about 11 hours determined on the basis of its own average residence time in the body of about 6.4 hours and an average suction time of 4.6 hours).

    As with intravenous administration, a prolonged period of final half-life is observed, which is about 13 hours. This final elimination phase has a relatively small value, since it is an insignificant part of the total area under the pharmacokinetic curve (AUC), which is confirmed by the fact that when receiving capsules with a modified release 2 times a day, the equilibrium state is reached within 2 days.

    With repeated administration of a dose, no appreciable accumulation of the drug is observed.

    Kinetics in the elderly

    The concentrations of dipyridamole in plasma (determined by AUC) in the elderly (> 65 years) were approximately 50% higher for tablets and about 30% higher for capsules with a modified release of AGRENOX than for young (<55 years) subjects. This difference is mainly due to reduced clearance, because it turned out that the intake was the same.

    Kinetics in patients with renal insufficiency

    Due to low deducing through the kidneys (5%), it can be assumed that there is no change in pharmacokinetics in the case of kidney failure. In the study ESPS2 in patients with a creatinine clearance in the range of about 15 ml / min and up to> 100 ml / min, changes in the pharmacokinetics of dipyridamole or its metabolite-glucuronide dipyridamole - were not observed provided that the data were adjusted to the age difference.

    Kinetics in patients with hepatic impairment

    In patients with hepatic insufficiency, there was no change in plasma dipyridamole concentrations, but an increase in glucuronide concentrations with low pharmacodynamic activity was noted. Therefore, adjusting the dose of dipyridamole is necessary only in the case of clinically confirmed decompensation of liver function.

    Acetylsalicylic acid

    Suction

    Acetylsalicylic acid is rapidly and completely absorbed. Maximum plasma concentrations after taking a daily dose of 50 mg of acetylsalicylic acid in the preparation of AGRENOX (25 mg twice daily) are observed after 30 minutes, and the maximum plasma concentration in the equilibrium state is 319 ng / ml (range 175-463 ng / ml). Maximum concentrations of salicylic acid in plasma are reached after 60-90 minutes.

    30-40% of the dose of acetylsalicylic acid undergoes primary metabolism with cleavage to salicylic acid, which is the main pathway of metabolism. Pharmacodynamics of acetylsalicylic acid in the composition of AGRENOX does not depend on the intake of food.

    Distribution

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

    Metabolism

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

    Excretion

    The half-life of acetylsalicylic acid is 15-20 minutes; the half-life of the main metabolite (salicylic acid) is 2-3 hours, can increase to 5-18 hours at high doses (> 3 g) because of the saturation of the enzyme.

    About 90% of acetylsalicylic acid is excreted in the form of metabolites through the kidneys.

    Kinetics in patients with renal insufficiency

    In severe disturbances of kidney function (glomerular filtration rate less than 10 ml / min), acetylsalicylic acid should not be administered.

    An increase in the half-life of 2-3 times in patients with kidney disease has been reported.

    Kinetics in patients with hepatic impairment

    With severe liver failure, acetylsalicylic acid should not be prescribed.

    Indications:

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

    Contraindications:

    - Hypersensitivity to any component of the drug or salicylates.

    - Stomach ulcer or duodenal ulcer in the stage of exacerbation or with a tendency to bleeding.

    - Pregnancy (III trimester).

    - Children and adolescence under 18 years.

    Carefully:

    Along with other properties dipyridamole has a vasodilating effect. The drug should be administered with caution to patients with severe coronary heart disease, including with unstable angina and recently suffered myocardial infarction, as well as with difficulty in ejection of blood from the left ventricle or instability of hemodynamics (eg, in decompensated heart failure).

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

    In addition, caution is recommended for patients with hypersensitivity to nonsteroidal anti-inflammatory drugs.

    Pregnancy and lactation:

    Data on the safety of the use of dipyridamole and acetylsalicylic acid in low dose during pregnancy in humans is not enough. In preclinical studies, no adverse effects were identified.

    Dipyridamole and salicylates are excreted in breast milk.


    The drug AGRENOX can be taken in
    I-II trimesters of pregnancy or during lactation and only if the benefit to the mother exceeds the potential risk for the fetus (child). The drug is contraindicated in the III trimester of pregnancy.
    Dosing and Administration:

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

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

    Side effects:

    There have been reports of hypersensitivity reactions (rash, hives, severe bronchospasm and angioedema) with respect to dipyridamole and acetylsalicylic acid. In very rare cases, after taking acetylsalicylic acid, a decrease in the number of thrombocytes (thrombocytopenia) can be observed.There were also reports of individual cases of thrombocytopenia observed with dipyridamole treatment.

    Hemorrhages on the skin, such as bruising, ecchymosis and bruising can occur when the drug is used.

    The undesirable effects of dipyridamole in therapeutic doses are usually mild and transient. When treated with dipyridamole, vomiting, diarrhea and symptoms such as dizziness, nausea, headache, migraine-like headache (especially at the beginning of treatment) and myalgia were noted. These symptoms usually disappear with prolonged use of the drug.

    As a consequence of the vasodilator effect of dipyridamole, hypotension, flushing and tachycardia may occur. Symptoms of coronary heart disease worsened. Acetylsalicylic acid increases the time of bleeding, also after taking dipyridamole in very rare cases, there was an increase in bleeding during and after surgery.

    When taking acetylsalicylic acid, there may be pain in the epigastrium, nausea and vomiting, a stomach ulcer or duodenal ulcershkand erosive gastritis, which can lead to serious gastrointestinal bleeding.

    As a result of latent bleeding, especially when taking acetylsalicylic acid for a long period of time, iron deficiency anemia may develop.

    Overdose:

    Symptoms

    Due to the ratio of doses of dipyridamole and acetylsalicylic acid in case of an overdose of Agrohnox, the signs and symptoms of an overdose of dipyridamole will probably prevail.

    Experience with respect to an overdose of dipyridamole is limited due to a small number of observations. Presumably, symptoms such as fever, hot flashes, sweating, agitated state, weakness, dizziness and symptoms of angina pectoris should be observed. A sharp drop in blood pressure and tachycardia may occur.

    Symptoms of a minor acute overdose of acetylsalicylic acid are hyperventilation, ringing in the ears, nausea, vomiting, visual and hearing impairment, dizziness and blurred vision.

    Dizziness and ringing in the ears, especially in patients of senile age, may be symptoms of an overdose.

    Treatment

    Symptomatic treatment, gastric lavage.The introduction of xanthine derivatives (eg, aminophylline) can neutralize the hemodynamic effects of an overdose of dipyridamole.

    Because dipyridamole widely distributed in tissues and, basically, is eliminated by the liver, it is not excreted by hemodialysis.

    Interaction:

    When using dipyridamole in combination with acetylsalicylic acid or with warfarin, precautions for these drugs should be taken into account. Acetylsalicylic acid can enhance the effect of anticoagulants (for example, coumarin derivatives and heparin), drugs inhibiting platelet aggregation (clopidogrel, ticlopidine), valproic acid and increase the risk of side effects from the gastrointestinal tract when used simultaneously with NSAIDs or with corticosteroids, as well as in the systematic use of alcohol. The combined use of dipyridamole and acetylsalicylic acid does not increase the frequency of bleeding.

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

    Dipyridamole increases the concentration of adenosine in the plasma and enhances its cardiovascular effects.The need to adjust the dose of adenosine should be considered. With the combined use of dipyridamole and warfarin, the frequency and severity of bleeding was no more than when only one warfarin was administered.

    Dipyridamole may enhance the antihypertensive effect of drugs that lower blood pressure and reverse the anticholinesterase effect of cholinesterase inhibitors, and as a consequence cause a worsening of the course of the malignant myasthenia gravis.

    The effect of hypoglycemic drugs and the toxicity of methotrexate may be enhanced when combined with acetylsalicylic acid. Acetylsalicylic acid can reduce the natriuretic effect of spironolactone and inhibit the effect of uricosuric medicines (eg, probenecid, sulfinpyrazone).

    Simultaneous 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.

    Caution is advised to prescribe the drug to patients who receive treatment with drugs that increase the risk of bleeding - inhibiting the aggregation of platelets (clopidogrel, ticlopidine) or selective serotonin reuptake inhibitors (SSRI).

    Special instructions:

    Clinical experience suggests that patients receiving dipyridamole and who also requires a pharmacological stress test with intravenous administration of dipyridamole, should stop taking medications containing dipyridamole, 24 hours before the test. Otherwise, the sensitivity of the test may be impaired.

    In patients with malignant myasthenia, after changing the dose of dipyridamole, an adjustment of the basic therapy may be required (see Interactions).

    In a small number of cases it was shown that unconjugated diPIridamol is incorporated to varying degrees in gallstones (up to 70% of the dry weight of the stone). All patients were senile. They had ascending cholangitis and they received dipyridamole for many years. Evidence that dipyridamole was the initiating factor in the formation of gallstones, is not available. Probably, the presence of dipyridamole in the gallstones can be explained by bacterial deglucuronidation of conjugated dipyridamole in bile.

    The dose of acetylsalicylic acid in the preparation AGRENOX (25 mg) was not investigated by the indication of the prevention of myocardial infarction.

    Contains 106 mg of lactose and 22.5 mg of sucrose in the maximum daily dose. Do not use in patients with hereditary intolerance to fructose and / or galactose, for example, galactosemia.

    Form release / dosage:Capsules with modified release.
    Packaging:For 30 or 60 capsules in a polypropylene tube, sealed with a plastic stopper with a desiccant or in a polypropylene vial, sealed with a plastic screw cap with an opening control from the children, with a desiccant. Tube or bottle with instructions for use in a cardboard box.
    Storage conditions:

    Store at a temperature not exceeding 25 ° C in a place inaccessible to children.

    Shelf life:

    3 years.

    Do not use the product after the expiry date printed on the package.

    Terms of leave from pharmacies:On prescription
    Registration number:LSR-001959/07
    Date of registration:07.08.2007/14.11.2013
    Expiration Date:Unlimited
    The owner of the registration certificate:Boehringer Ingelheim International GmbHBoehringer Ingelheim International GmbH Germany
    Manufacturer: & nbsp
    Representation: & nbspBERINGER INGELCHAIM INTERNATIONAL GmbH BERINGER INGELCHAIM INTERNATIONAL GmbH Germany
    Information update date: & nbsp21.01.2017
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