Active substanceGlimepirideGlimepiride
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  • Dosage form: & nbsppills
    Composition:

    Dosage 1 mg

    active substance: glimepiride - 1.0 mg;

    Excipients: lactose monohydrate 79.5 mg, cellulose microcrystalline 12.0 mg, carboxymethyl starch sodium (sodium starch glycolate) 5.0 mg, povidone K-30 1.0 mg, polysorbate 80 0.5 mg, magnesium stearate 1.0 mg.

    Dosage 2 mg

    active substance: glimepiride 2.0 mg;

    Excipients: lactose monohydrate 159.0 mg, cellulose microcrystalline 24.0 mg, carboxymethyl starch sodium (sodium starch glycolate) 10.0 mg, povidone K-30 2.0 mg, polysorbate 80 1.0 mg, magnesium stearate 2.0 mg.

    Dosage 3 mg

    active substance: glimepiride 3.0 mg;

    Excipients: lactose monohydrate - 117.6 mg, cellulose microcrystalline - 18.0 mg, carboxymethyl starch sodium (sodium starch glycolate) 7.5 mg, povidone K-30 1.5 mg, polysorbate 80 0.9 mg, magnesium stearate 1.5 mg.

    Dosage 4 mg

    active substance: glimepiride - 4.0 mg;

    Excipients: lactose monohydrate 237.5 mg, cellulose microcrystalline 36.0 mg, carboxymethyl starch sodium (sodium starch glycolate) 15.0 mg, povidone K-30 3.0 mg, polysorbate 80 1.5 mg. magnesium stearate - 3.0 mg.

    Dosage 6 mg

    active substance: glimepiride - 6.0 mg;

    Excipients: lactose monohydrate 235.2 mg, cellulose microcrystalline 36.0 mg, carboxymethyl starch sodium (sodium starch glycolate) 15.0 mg, povidone K-30 3.0 mg, polysorbate 80-1.8 mg, magnesium stearate 3.0 mg.

    Description:

    Round flat cylindrical tablets of white or almost white color, with a facet (1 mg, 2 mg, 3 mg), with a facet and a risk (6 mg), with a facet and a crosswise risk (4 mg).

    Pharmacotherapeutic group:Hypoglycemic agent for oral use of the sulfonylurea group of the third generation
    ATX: & nbsp

    A.10.B.B.12   Glimepiride

    Pharmacodynamics:

    Glimepiride reduces the concentration of glucose in the blood, mainly by stimulating the release of insulin from the beta cells of the pancreas. Its effect is mainly associated with improving the ability of beta cells of the pancreas to respond to physiological stimulation with glucose. Compared to glibenclamide, the administration of glimepiride in low doses causes the release of less insulin when the blood glucose concentration is approximately the same. This fact testifies in favor of the presence in glimepiride of extrapancreatic hypoglycemic effects (increase of sensitivity of tissues to insulin and insulinomimetic effect).

    Secretion of insulin

    Like all other sulfonylureas, glimepiride regulates the secretion of insulin through interaction with ATP-sensitive potassium channels on the membranes of beta cells. Unlike other derivatives of sulfonylurea, glimepiride selectively binds to a protein having a molecular weight of 65 kilodaltons (kDa). located in the membranes of beta cells of the pancreas. This interaction of glimepiride with the protein binding it regulates the opening or closing of ATP-sensitive potassium channels.

    Glimepiride closes potassium channels. This causes depolarization of beta cells and leads to the discovery of voltage-sensitive calcium channels and the intake of calcium into the cell. As a result, an increase in the intracellular calcium concentration activates the secretion of insulin by exocytosis.

    Glimepiride much faster and, accordingly, more often enters into a bond and is released from the connection with the protein that binds it, than glibenclamide. It is assumed that this property of a high rate of metabolism of glimepiride with the protein binding to it determines its pronounced effect of sensitization of beta cells to glucose and their protection from desensitization and premature exhaustion.

    The effect of increasing the sensitivity of tissues to insulin

    Glimepiride enhances insulin effects on glucose uptake by peripheral tissues.

    Insulinomimetic effect

    Glimepiride has effects similar to insulin effects on glucose uptake by peripheral tissues and glucose output from the liver. Absorption of glucose by peripheral tissues is carried out by its transport inside the muscle cells and adipocytes. Glimepiride directly increases the amount of glucose-transporting molecules in the plasma membranes of muscle cells and adiocytes. Increasing the intake of glucose in the cells leads to the activation of glycosylphosphatidyliositol-specific phospholipase C. As a result, the intracellular calcium concentration decreases, causing a decrease in the activity of protein kypase A, which in turn leads to stimulation of glucose metabolism. Glimepiride inhibits glucose output from the liver by increasing the concentration of fructose-2,6-bisphosphate, which inhibits gluconeogenesis.

    Effect on platelet aggregation

    Glimepiride reduces platelet aggregation in vitro and in vivo. This effect appears to be due to the selective inhibition of cyclooxygenase, which is responsible for the formation of thromboxane A, an important endogenous platelet adhesion factor.

    Aptiaterogenic effect of the drug

    Glimepiride promotes the normalization of lipid content, reduces the concentration of malonic aldehyde in the blood, which leads to a significant decrease in lipid peroxidation.

    In animals glimepiride leads to a significant decrease in the formation of atherosclerotic plaques.

    Reducing the severity of oxidative stress, which is constantly present in patients with diabetes mellitus 2 tina. Glimepiride increases the concentration of α-tocopherol, the activity of catalase, glutathione peroxidase and superoxide dismutase.

    Cardiovascular Effects

    Through the ATP-sensitive potassium channels (see above), the sulfoiyl urea derivatives also affect the cardiovascular system. Compared with the traditional derivatives of sulfoiylurea, glimepiride has a significantly lesser effect on the cardiovascular system, which can be explained by the specific nature of its interaction with the ATP-sensitive protein of the potassium channel binding to it.

    The effect of glimepiride is dose-dependent and reproducible.Physiological response to physical activity (reduced secretion of insulin) with the intake of glimepiride is preserved.

    There are no significant differences in the effect, depending on whether the drug was taken 30 minutes before meals or just before meals. In patients with diabetes mellitus, sufficient metabolic control can be achieved within 24 hours with a single dose of the drug. In patients with renal insufficiency (creatinine clearance 4-79 ml / min), sufficient metabolic control can also be achieved.

    Combined therapy with metformin

    In patients with insufficient metabolic control, a combination therapy with glimeniride and metformin can be initiated with the maximum dose of glimepiride. In two studies, combined therapy showed improved metabolic control compared with that in the treatment of each of these drugs individually.

    Combination therapy with insulin

    In patients with insufficient metabolic control, simultaneous insulin therapy can be initiated with maximum doses of glimepiride.Combined therapy requires a lower dose of insulin.

    Use in children

    There is insufficient data but long-term efficacy and safety of the drug in children.

    Pharmacokinetics:

    Suction and distribution

    With repeated administration of glimepiride in a daily dose of 4 mg, the maximum concentration (Cmax) of glimepiride in blood plasma is reached after approximately 2.5 hours and is 309 ng / ml. There is a linear relationship between dose and Cmax glimepiride in the blood plasma, as well as between the dose and the area under the concentration-time curve (AUC). When glimepiride is taken in, its absolute bioavailability is complete. Food intake nc has a significant effect on absorption, with the exception of a slight slowing of its speed.

    Glimepiride is characterized by a very low volume of distribution (about 8.8 liters), approximately equal to the volume of distribution of albumin, a high degree of binding to plasma proteins (more than 99%) and low clearance (about 48 ml / min).

    The average half-life is approximately 5-8 hours. After taking high doses, there is a slight increase in the half-life. Significant accumulation of the drug is absent.

    Metabolism and excretion

    After a single glmmeiride intake, 58% of the dose is excreted by the kidneys and 35% by the intestine. Unchanged glimespiride in the urine is not detected. In urine and feces, two metabolites, formed as a result of metabolism in the liver (mainly with the help of isoenzyme CYP2C9), one of them was a hydroxy derivative, and the other was a carboxy derivative. After glimepiride intake, the half-life of these metabolites was 3-5 hours and 5-6 hours, respectively.

    ChlImpyrid penetrates into breast milk and through the placental barrier.

    Pharmacokinetics in specific patient groups

    Pharmacokinetic parameters are similar in patients of different sex and different age groups. In patients with impaired renal function (with low creatinine clearance), there is a tendency to increase the clearance of glimepiride and to reduce its average concentrations in blood plasma, which is most likely due to a faster elimination of the drug due to its lower binding to the protein. Thus, in this category of patients there is no additional risk of cumulation of the drug.

    Indications:

    Diabetes mellitus type 2 (in monotherapy or as part of combination therapy with metformin or with insulin).

    Contraindications:
    • type 1 diabetes mellitus;
    • diabetic ketoacidosis, diabetic precoma and coma;
    • increased sensitivity to glimeppride or to any inactive component of the drug, to other derivatives of sulfonylureas or to sulfonamide preparations (risk of developing hypersensitivity reactions);
    • severe violations of liver function;
    • severe violations of kidney function, including in patients undergoing hemodialysis;
    • pregnancy and the period of breastfeeding;
    • childhood;
    • lactose intolerance; deficiency of lactase; glucose-galactose malabsorption.
    Carefully:
    • in the first weeks of treatment (increased risk of hypoglycemia);
    • if there are risk factors for the development of hypoglycemia;
    • at intercurrent illnesses during treatment or when changing the lifestyle of patients (changing diet and eating time, increasing or decreasing physical activity);
    • with insufficiency of glucose-6-phosphate dehydrogenase;
    • with violations of absorption of food and drugs in the gastrointestinal tract (intestinal obstruction, intestinal paresis).
    Pregnancy and lactation:

    Pregnancy

    Glimepiride contraindicated in pregnancy. In the case of a planned pregnancy or at the onset of pregnancy, a woman should be transferred to insulin therapy.

    Breastfeeding period

    Determined that glimepiride penetrates into breast milk. In the period of breastfeeding, a woman should be transferred to insulin therapy or to stop breastfeeding.

    Dosing and Administration:

    Inside.

    Glimepiride tablets are taken without chewing, squeezed with a sufficient amount of water (about 0.5 cup). If necessary, the drug tablets Glimepiride can be divided along the risks into equal parts.

    Initial dose and dose selection

    As a rule, the dose of glimepiride is determined by the target concentration of glucose in the blood. The lowest dose, sufficient to achieve the necessary metabolic control, should be used.

    The initial dose of glimepiride is 1 mg 1 time per day.

    If necessary, the daily dose can be gradually increased (at intervals of 1-2 weeks). It is recommended to increase the dose under regular control of blood glucose concentration and in accordance with the following step of increasing the dose: 1 mg - 2 mg - 3 mg - 4 mg - 6 mg (-8 mg).

    The range of doses of patients with well-controlled diabetes mellitus

    Typically, the daily dose in patients with well-controlled diabetes mellitus is 1-4 mg glimepiride. A daily dose of more than 6 mg (8 mg) is more effective only in a small number of patients.

    Dosing regimen

    Time of taking the drug Glimepiride and the distribution of doses during the day is set by the doctor depending on the lifestyle of the patient at a given time (meal time, amount of exercise).

    It is usually sufficient to take a single dose of the drug Glimepiride during the day. It is recommended that in this case the entire dose of the drug Glimepiride was taken immediately before a full breakfast or, if it was not accepted at this time, - just before the first main meal.

    It is very important after taking the drug Glimepiride do not skip meals.

    Since improvement in metabolic control is associated with an increase in insulin sensitivity, the need for glimepiride may decrease during treatment. In order to avoid the development of hypoglycemia, it is necessary to reduce doses in a timely manner or stop taking glimepiride.

    Conditions in which glimepiride dose adjustment may also be required:

    • weight loss in the patient;
    • changing the lifestyle of the patient (changing diet, meal time, amount of exercise);
    • the occurrence of other factors that lead to a predisposition to the development of hypoglycemia or hyperglycemia (see section "Special instructions").
    Duration of treatment

    Treatment with glimepiride is usually carried out for a long time.

    Transfer of the patient from taking another oral hypoglycemic agent to taking Glimepiride

    There is no precise correlation between doses glimepiride and other oral hypoglycemic agents. When another oral hypoglycemic agent is substituted for glimepirideIt is recommended that the procedure for its purpose was the same as the initial assignment of glimepiride, i.e. the treatment should begin with an initial dose of 1 mg (even if the patient is transferred to the drug Glimepiride with a maximum dose of another oral hypoglycemic agent).

    Any increase in the dose should be carried out in stages, taking into account the reaction to glimepiride, in accordance with the above recommendations.

    It is necessary to take into account the strength and duration of the effect of the previous oral hypoglycemic agent. An interruption in treatment may be required in order to avoid any summation of effects that may increase the risk of developing hypoglycemia.

    Use in combination with metformin

    In patients with insufficiently controlled diabetes mellitus, the combination of these two drugs can be started with maximum daily doses or glimepiride or metformin. In this case, the previous treatment with either glimepiride or metformin is continued at the same doses, and an additional intake of metformin or glimepiride begins with a low dose, which is then titrated, depending on the target level of metabolic control, up to the maximum daily dose. Combination therapy should begin under strict medical supervision.

    Use in combination with insulin

    Patients with insufficiently controlled diabetes mellitus at intake of the maximum daily doses of glimepiride can simultaneously be prescribed insulin administration.In this case, the last dose of glimepiride prescribed to the patient remains unchanged. In this case, treatment with insulin begins with low doses, which gradually increase under the control of the concentration of glucose in the blood. Combined treatment requires careful medical supervision.

    Use in patients with renal insufficiency

    There is a limited amount of information on the use of the drug Glimepiride in patients with renal insufficiency. Patients with impaired renal function may be more sensitive to the hypoglycemic effect of glimepiride.

    Use in patients with hepatic impairment

    There is a limited amount of information on the use of the drug Glimepiride with hepatic insufficiency.

    Use in children

    Dnepr on the use of the drug Glimepiride children are not enough.

    Side effects:

    Disorders from the metabolism and nutrition

    As a result of hypoglycemic action of glimepiride, hypoglycemia may develop, which, like with other sulfonylurea derivatives, can be prolonged.Symptoms of hypoglycemia are: headache, hunger, nausea, vomiting, fatigue, drowsiness, sleep disorders, anxiety, aggressiveness, impaired concentration, alertness and reaction speed, depression, confusion, speech disorders, aphasia, visual disorders, tremor, paresis, sensory disturbances, dizziness, loss of self-control, delirium, cerebral cramps, doubt or loss of consciousness right up to coma, shallow breathing, bradycardia. In addition, in response to hypoglycemia, adrenergic counterregulation such as the appearance of cold "sticky" sweat, anxiety, tachycardia, increased blood pressure, angina pectoris, palpitations and cardiac arrhythmias can occur.

    The clinical picture of severe hypoglycemia may be similar to a stroke. Symptoms of hypoglycemia almost always disappear after elimination.

    Disturbances on the part of the organ of sight

    During treatment (especially at the beginning), transient visual impairment may occur, due to changes in the concentration of glucose in the blood.Their cause is a temporary change in the swelling of the lens, depending on the concentration glucose in the blood, and due to this change in the refractive index of the lens.

    Disorders from the gastrointestinal tract

    In rare cases: nausea, vomiting, a feeling of heaviness or overflow in the epigastrium, abdominal pain, diarrhea. In some cases: hepatitis, increased activity of liver enzymes and / or cholestasis and jaundice, which can progress to life-threatening liver failure, but may undergo reverse development if the drug is withdrawn.

    Violations of the blood and lymphatic system

    Rarely: thrombocytopenia. In some cases: leukopenia, hemolytic anemia, erythrocytopenia, granulocytopenia, agranulocytosis and pancytopenia.

    Immune system disorders

    In rare cases, allergic and pseudo-allergic reactions, such as pruritus, urticaria, skin rash, are possible. Such reactions almost always have an easy form, but they can turn into severe reactions with shortness of breath, a sharp drop in blood pressure, which sometimes progresses down to anaphylactic shock.When symptoms of urticaria appear, consult a doctor immediately. In some cases, allergic vasculitis and photosensitivity may occur.

    Laboratory and instrumental data

    In some cases, a decrease in the concentration of sodium in the blood plasma is possible.

    Overdose:

    Overdose Symptoms

    Acute overdose, as well as long-term treatment with too high doses of glimepiride, can lead to the development of severe life-threatening hypoglycemia accompanied by symptoms such as headache, hunger, nausea, vomiting, fatigue, drowsiness, sleep disorders, anxiety, aggressiveness, , vigilance and speed of reactions, depression, confusion, speech disorders, aphasia, visual disorders, tremor, paresis, sensory disturbances, dizziness, loss of self-control, eliry, cerebral convulsions, somnolence and loss of consciousness up to coma, shallow breathing, bradycardia. In addition, in response to hypoglycemia, such manifestations of adrenergic counter-regulation as the appearance of cold "sticky" sweat, anxiety, tachycardia,increased blood pressure, angina pectoris, palpitations and heart rhythm disturbances.

    Treatment of overdose

    As soon as an overdose with glimepiride is discovered, the doctor must be informed immediately. Hypoglycemia can almost always be quickly stopped by the immediate intake of carbohydrates (glucose or a piece of sugar, sweet fruit juice or tea). In this regard, the patient should always have at least 20 grams of glucose (4 pieces of sugar). Sugary substitutes are ineffective in the treatment of hypoglycemia.

    Until the doctor decides that the patient is out of danger, the patient needs careful medical supervision. It should be remembered that hypoglycemia may resume after initial recovery of blood glucose. If a patient with diabetes is treated by different doctors (for example, during a hospital stay after an accident, with a disease on a weekend), he must necessarily inform them about his illness and about the previous treatment.

    Sometimes it may be necessary to hospitalize the patient, even as a precautionary measure.Significant overdose and severe reactions with such manifestations as loss of consciousness or other serious neurological disorders are urgent medical conditions and require immediate treatment and hospitalization.

    In the unconscious state of the patient, intravenous administration of a concentrated solution of dextrose (glucose) (in adults, starting with 40 ml of a 20% solution) is necessary. As an alternative to adults, intravenous, subcutaneous or intramuscular administration of glucagon in a dose of 0.5-1 mg is possible.

    In the treatment of hypoglycemia due to the occasional intake of glimepiride by infants or young children, the dose of dextrose administered should be carefully adjusted in terms of the possibility of dangerous hyperglycaemia, and the administration of dextrose should be performed under constant control of the glucose concentration in the blood.

    In case of glimepiride overdose, it may be necessary to perform gastric lavage and receive activated charcoal.

    After a rapid recovery of blood glucose concentration, it is necessary to conduct intravenous infusion of dextrose (glucose) solution at a lower concentration to prevent the resumption of hypoglycemia.The concentration of glucose in the blood in these patients should be constantly monitored within 24 hours. In severe cases with prolonged course of hypoglycemia, the risk of lowering blood glucose levels to the hypoglycemic level may persist for several days.

    Interaction:
    Glimepiride is megabolized by cytochrome P450 2C9 (CYP2C9), which should be taken into account when used concomitantly with inducers (eg rifampicin) or inhibitors of the CYP2C9 isoenzyme (eg, fluconazole).
    Potentiation of hypoglycemic action and in some cases associated with this possible development of hypoglycemia can be observed when combined with one of the following drugs: insulin and other oral hypoglycemic agents, angiotensin converting enzyme (DFT) inhibitors, anabolic steroids and male sex hormones, chloramppicol, coumarin derivatives, cyclophosphamide, disopyramide, fenfluramine, phenyramidol, fibrates, fluoxetine, guanethidine, ifosfamide, monoamine oxidase (MAO) inhibitors, fluconazole, para-aminosalicylic acid, pentoxifylline (high parenteral doses),phenylbutazone, azapropane, oxypepbutazone, probenecid, quinolones, salicylates, sulfinpyrazoi, clarithromycin, sulfonamides, tetracyclines, grossoclase, trophosphamide. The weakening of hypoglycemic action and the associated increase in blood glucose concentration can be observed when combined with one of the following drugs: acetazolamide, barbiturates, glucocorticosteroids, diazoxide, diuretics, epinephrine and other sympathomimetic agents, glucagon, laxatives (for prolonged use), nicotinic acid (in high doses), estrogens and progestogens, phenothiazines, phenytoids, rifampicia, iodine-containing hormones of the thyroid gland.
    Blockers H2-gistaminovyh receptors, beta-adrenoblockers, clonidine and reserpine are able both to intensify, and to weaken the hypoglycemic action of glimepiride.
    Prd influence of such sympatholytic agents, as beta-adrenoblockers, clonidine, guanstidine and reserpine, signs of adrenergic counterregulation in response to hypoglycaemia may be reduced or absent.
    Against the background of taking glimepiride, there may be an increase or decrease in the action of coumarin derivatives.
    A single or chronic use of alcohol can both enhance and weaken the hypoglycemic effect of glimepiride.
    The colosevels bind to glimepiride and reduce the absorption of glimepiride from the gastrointestinal tract. In the case of using glimepiride at least 4 hours prior to the intake of colesevelum, no interaction is observed. therefore glimepiride must be taken no less than 4 hours before the intake of Wheelsewell.
    Special instructions:

    In special clinical stressors such as trauma, surgery, infection with febrile temperature, metabolic control may worsen in patients with diabetes, which may require temporary transfer of patients to insulin therapy to maintain adequate metabolic control.

    In the first weeks of treatment, the risk of developing hypoglycemia may increase, and therefore at this time a particularly careful control of the concentration of glucose in the blood is required. In addition, regular monitoring of glycosylated hemoglobin is recommended.

    Factors that contribute to the risk of developing hypoglycemia include:

    • unwillingness or inability of the patient (most often observed in elderly patients) to cooperate with a doctor;
    • malnutrition, irregular eating or skipping meals;
    • an imbalance between exercise and carbohydrate intake;
    • changing diet;
    • alcohol consumption, especially when combined with meals;
    • severe renal dysfunction;
    • severe violations of liver function (in patients with severe impairment of liver function, a transfer to insulin therapy is indicated, at least until metabolic control is achieved);
    • an overdose of glimepiride;
    • some decompensated endocrine disorders that disrupt carbohydrate metabolism or adrenergic counterregulation in response to hypoglycemia (for example, certain disorders of the thyroid gland and anterior pituitary gland, insufficiency of the adrenal cortex);
    • simultaneous intake of certain medicines (see section "Interaction with other drugs");
    • reception glimepirida in the absence of indications for its reception.

    Treatment with derivatives of sulfonylurea, which includes glimepiride, can lead to the development of hemolytic anemia, therefore, patients with glucose-6-phosphate dehydrogenase deficiency should be especially careful in the appointment of glimepiride, and it is better to use hypoglycemic agents that are not derivatives of sulfonylurea.

    If these risk factors for hypoglycemia are present, then a correction of the dose of glimepiride or the whole therapy may be required. This also applies to the occurrence of intercurrent illnesses during treatment or a change in the lifestyle of patients.

    Those symptoms of hypoglycemia that reflect adrenergic counter-regulation of the body in response to hypoglycemia may be mild or absent with the gradual development of hypoglycemia in elderly patients, in patients with autonomic neuropathy or in patients receiving beta-blockers. Clopidine, reserpine, guanstidine and other sympatholytic agents.

    Hypoglycemia can be quickly eliminated by immediate intake of rapidly digestible carbohydrates (glucose or sucrose).

    As with the administration of other sulfonylureas, despite the initial successful reduction of hypoglycemia, hypoglycemia may resume. Therefore, patients should remain under constant supervision.

    In severe hypoglycemia, immediate treatment and supervision of the physician, and in some cases, hospitalization of the patient, are required.

    During treatment with glimepiride, regular monitoring of liver function and peripheral blood pattern (especially the number of leukocytes and platelets) is required.

    Since certain side effects, such as severe hypoglycemia, severe changes in the blood picture, severe allergic reactions, liver failure, can under certain circumstances pose a life threat, in the event of unwanted or severe reactions, the patient should immediately be notified of the treating doctor and neither In any case, do not continue taking the drug without his recommendation.

    Incorrect drug intake (eg, skipping the next dose) should never be replenished by the subsequent administration of a higher dose.The patient's actions in case of mistakes while taking the drug (in particular, if the next dose is skipped or when meals are skipped) or in situations where there is no possibility to take the drug, should be discussed by the patient and the doctor in advance.

    Effect on the ability to drive transp. cf. and fur:

    In the case of hypoglycemia or hyperglycaemia, especially at the beginning of treatment or after a change in treatment, or when the drug is taken regularly, there may be a decrease in attention and speed of psychomotor reactions. This can disrupt the patient's ability to drive vehicles or other mechanisms.

    Form release / dosage:

    Tablets 1 mg, 2 mg, 3 mg, 4 mg and 6 mg.

    Packaging:

    10, 15, 20 or 30 tablets in a planar cell pack of film polyvinylchloride and aluminum foil.

    30 or 60 tablets in a can of high-density polyethylene.

    3 or 6 contiguous cell packs of 10 tablets, 2 or 4 contour packs of 15 tablets, 3 contour packs of 20 tablets, 1 or 2 contour packs of 30 tablets, or one bank, along with instructions for use in a pack of cardboard.

    Storage conditions:

    Store in a dark place at a temperature of no higher than 25 ° C. Keep out of the reach of children.

    Shelf life:

    3 years.

    Not apply at the expiration date.

    Terms of leave from pharmacies:On prescription
    Registration number:LP-002219
    Date of registration:04.09.2013 / 07.08.2015
    Expiration Date:04.09.2018
    The owner of the registration certificate:VERTEKS, AO VERTEKS, AO Russia
    Manufacturer: & nbsp
    Representation: & nbspVERTEKS CJSC VERTEKS CJSC Russia
    Information update date: & nbsp30.04.2017
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