Lopril bosnalek®

INSTRUCTIONS FOR MEDICAL USE OF THE MEDICINAL PRODUCT LOPRIL BOSNALIJE® (LOPRILBOSNALIJEK®)

Composition:

active substance: lisinopril;

1 tablet contains lisinopril (as dihydrate) 5 mg or 10 mg or 20 mg;

excipients: calcium hydrogen phosphate dihydrate, mannitol (E 421), maize starch, pregelatinized starch, magnesium stearate, talc, colloidal anhydrous silicon dioxide, yellow iron oxide E 172 (in Lopril Bosnaliek® 10 mg and 20 mg tablets), red iron oxide E 172 (in Lopril Bosnaliek® 20 mg tablets).

Pharmaceutical form. Tablets.

Main physicochemical characteristics: round tablets of white (5 mg), yellow (10 mg), or light pink or pink color (20 mg), with smooth surface, with a break line in the middle.

Pharmacotherapeutic group. Agents acting on the renin-angiotensin system.

ACE inhibitors. ATC code C09A A03.

Pharmacological properties.

Pharmacodynamics.

Lisinopril is an inhibitor of peptidyl dipeptidase. It blocks the angiotensin-converting enzyme (ACE), which catalyzes the conversion of angiotensin I into vasoconstrictive angiotensin II. Angiotensin II also stimulates the secretion of aldosterone in the adrenal cortex. Inhibition of ACE leads to a decrease in angiotensin II concentration in blood plasma, resulting in reduced vasoconstriction and decreased aldosterone secretion, as well as potentially causing an increase in serum potassium levels.

Although the primary mechanism by which lisinopril reduces blood pressure is believed to be through inhibition of the renin-angiotensin-aldosterone system (RAAS), lisinopril also lowers blood pressure in patients with low-renin hypertension. ACE is identical to kininase II, an enzyme that degrades bradykinin. It has not yet been established whether increased levels of the potent vasodilatory peptide bradykinin play a role in the therapeutic effect of lisinopril.

Pharmacokinetics.

Maximum plasma concentration (Cmax) of lisinopril is reached 7 hours after oral administration, although in patients with acute myocardial infarction a tendency toward a slight delay in time to reach Cmax has been observed. The mean absorption value is approximately 25%, and varies among individual patients from 6% to 60% within the studied dose range (5–80 mg). These data are based on urinary recovery of lisinopril. Bioavailability is reduced by approximately 16% in patients with heart failure. Food intake does not affect the absorption of lisinopril.

Lisinopril is minimally bound to plasma proteins, except for circulating ACE. It is not metabolized and is excreted unchanged in urine. With repeated dosing, the effective cumulative half-life of lisinopril is 12.6 hours. The clearance of lisinopril in healthy volunteers is approximately 50 ml/min. The decline in serum concentration shows a prolonged terminal phase, which does not lead to drug accumulation. This phase is likely due to saturation of binding to ACE and is not dose-proportional.

In patients with cirrhosis, impaired liver function leads to reduced absorption of lisinopril (by about 30%) and, due to decreased clearance, increased exposure (by about 50%) compared to healthy volunteers.

In renal impairment, elimination of lisinopril is reduced, but this is clinically significant only when glomerular filtration rate is below 30 ml/min. In moderate renal impairment (creatinine clearance 30–80 ml/min), the mean area under the plasma concentration-time curve (AUC) increases by only 13%, whereas in severe renal impairment (creatinine clearance 5–30 ml/min), AUC increases by 4.5-fold. Lisinopril is removed during hemodialysis. During 4 hours of hemodialysis, plasma concentration of lisinopril decreased on average by 60%, and clearance ranged between 40–55 ml/min.

Patients with heart failure have greater exposure to lisinopril (mean AUC increase of 125%) but reduced absorption (mean reduction of 16%) compared to healthy volunteers.

Elderly patients have higher blood levels of lisinopril and an approximately 60% higher AUC value compared to younger patients.

Clinical characteristics.

Indications.

Hypertension, heart failure (symptomatic treatment), acute myocardial infarction (short-term treatment (6 weeks) of patients with stable hemodynamics within 24 hours after acute myocardial infarction), initial diabetic nephropathy in patients with type 2 diabetes mellitus and arterial hypertension.

Contraindications.

• Hypersensitivity to lisinopril or to any component of the medicinal product, hypersensitivity to other ACE inhibitors;
• Angioedema associated with previous use of ACE inhibitors;
• Hereditary or idiopathic angioedema;
• Pregnancy and planned pregnancy (see section "Use in pregnancy or breast-feeding");
• Concomitant use with aliskiren-containing medicinal products in patients with diabetes mellitus or renal impairment (see sections "Interaction with other medicinal products and other forms of interaction" and "Special precautions for use").

Interaction with other medicinal products and other forms of interaction.

Other antihypertensive agents: concomitant use with glyceryl trinitrate, other nitrates, or other vasodilators may lead to further reduction in arterial blood pressure.

Dual blockade of the RAAS by combining ACE inhibitors, angiotensin II receptor blockers, or aliskiren is associated with a higher incidence of adverse reactions such as arterial hypotension, hyperkalemia, and reduced renal function (including acute renal failure), compared to using a single RAAS-acting agent (see sections "Contraindications" and "Special precautions for use").

Tissue plasminogen activators, immunosuppressants such as mTOR inhibitors (e.g., temsirolimus, sirolimus, everolimus): possible increased risk of angioedema.

Diuretics: adding diuretics to treatment in patients receiving lisinopril usually enhances the antihypertensive effect. In patients receiving diuretics, especially those recently initiated on diuretic therapy, adding lisinopril may result in a significant decrease in arterial blood pressure. The likelihood of symptomatic hypotension can be reduced by discontinuing diuretic therapy prior to starting lisinopril.

Dietary supplements containing potassium, potassium-sparing diuretics, or potassium-containing salt substitutes: although serum potassium levels generally remained within normal limits in clinical studies, hyperkalemia developed in some patients. Risk factors include renal impairment, diabetes mellitus, or concomitant use of potassium-sparing diuretics (e.g., spironolactone, triamterene, amiloride), potassium-containing dietary supplements, or potassium-containing salt substitutes. Concomitant use of potassium-containing dietary supplements, potassium-sparing diuretics, or potassium-containing salt substitutes may lead to significant increases in serum potassium levels, particularly in patients with impaired renal function. During lisinopril therapy initiated on a background of potassium-depleting diuretics, hypokalemia caused by such diuretics may be attenuated.

Lithium: concomitant use of lithium and lisinopril is not recommended due to the possibility of reversible increases in serum lithium concentrations with development of toxic effects. Concomitant use of thiazide diuretics increases the risk of lithium toxicity. If concomitant use of lithium and lisinopril is necessary, serum lithium levels should be monitored.

Nonsteroidal anti-inflammatory drugs (NSAIDs), including acetylsalicylic acid at doses ≥ 3 g/day: possible reduction in antihypertensive effect, impaired renal function (including acute renal failure), and increased potassium levels, particularly in elderly patients and those with impaired renal function. These effects are usually reversible. Such combinations should be used with caution, especially in elderly patients. Patients should receive adequate fluid intake, and monitoring of renal function should be considered immediately after starting combination therapy and periodically thereafter.

Gold: nitritoid reactions (vasodilatory symptoms including flushing, nausea, dizziness, hypotension, which may be severe) following injection of gold (sodium aurothiomalate) have been observed more frequently in patients receiving ACE inhibitors.

Tricyclic antidepressants, neuroleptics, anesthetics: possible further reduction in arterial blood pressure.

Sympathomimetics may reduce the antihypertensive effect of ACE inhibitors.

Antidiabetic agents: concomitant use of lisinopril and antidiabetic agents (insulin, oral antidiabetic agents) may lead to decreased blood glucose levels with risk of hypoglycemia. This effect is more commonly observed during the first weeks of combination therapy and in patients with impaired renal function.

Co-trimoxazole (trimethoprim/sulfamethoxazole): possible increased risk of hyperkalemia (see section "Special precautions for use").

Acetylsalicylic acid, thrombolytic agents, ß-blockers, nitrates: lisinopril may be used concomitantly with these agents.

Special precautions for use.

Symptomatic hypotension. Symptomatic hypotension is rare in patients with uncomplicated hypertension. Hypotension is more likely to occur in patients with dehydration, e.g. due to diuretic therapy, low-salt diets, dialysis, diarrhoea or vomiting, or in cases of severe renin-dependent hypertension. In patients with heart failure, including those with concomitant renal impairment, ACE inhibitors may cause symptomatic hypotension. The likelihood of its occurrence is higher in patients with severe forms of heart failure, due to high doses of loop diuretics, hyponatremia, or functional renal impairment. For patients at high risk of symptomatic hypotension, as well as for patients with ischaemic heart disease or cerebrovascular disorders, in whom excessive reduction in blood pressure may lead to myocardial infarction or stroke, initiation of therapy and dose titration should be performed under close medical supervision.

If hypotension occurs, the patient should be placed in a supine position and, if necessary, physiological saline should be administered by intravenous infusion. A transient hypotensive response is not a contraindication for further use of lisinopril. Once blood pressure has increased after restoration of fluid volume, the drug may be continued.

In some patients with heart failure who have normal or low blood pressure, additional reduction in blood pressure may occur during treatment with lisinopril. This effect is expected and usually does not require discontinuation of treatment. If signs of hypotension become clinically significant, the dose should be reduced or treatment discontinued.

Arterial hypotension in acute myocardial infarction. Treatment with lisinopril should not be initiated in patients with acute myocardial infarction who are at high risk of further haemodynamic disturbances following vasodilator therapy: systolic blood pressure of 100 mm Hg or lower, or cardiogenic shock.

During the first 3 days after infarction, the dose should be reduced if systolic blood pressure is 120 mm Hg or lower. If systolic blood pressure is 100 mm Hg or lower, the dose should be reduced to 5 mg or temporarily to 2.5 mg. If systolic blood pressure is below 90 mm Hg for more than 1 hour, lisinopril therapy should be discontinued.

Aortic and mitral valve stenosis/hypertrophic cardiomyopathy. The drug should be used with caution in such patients.

Renal function impairment. In cases of renal impairment (creatinine clearance <80 ml/min), the initial dose of lisinopril should be adjusted according to creatinine clearance (see Table 1), and subsequently according to the patient's response to treatment. Regular monitoring of serum potassium and creatinine levels is required for such patients.

In patients with heart failure, hypotension at the beginning of ACE inhibitor therapy may lead to further deterioration of renal function, even to acute renal failure, usually reversible. In individual patients with bilateral renal artery stenosis or stenosis of the artery of a solitary kidney, treatment with ACE inhibitors has been associated with increased serum urea and creatinine levels, usually reversible. In cases of renovascular hypertension, the risk of severe hypotension and renal failure increases. For such patients, treatment should be initiated under close medical supervision, starting with low doses and careful dose titration. Since diuretic use may precipitate these events, diuretics should be discontinued prior to starting lisinopril, and renal function should be monitored during the first weeks of lisinopril therapy.

In isolated cases, in patients with previously undiagnosed renal vascular disorders, administration of an ACE inhibitor, particularly in combination with a diuretic, has led to increased urea and creatinine levels. In such cases, dose reduction or discontinuation of the drug may be necessary.

In acute myocardial infarction, lisinopril therapy should not be initiated in patients with signs of renal dysfunction (serum creatinine >177 µmol/L and/or proteinuria >500 mg/24 h), or if renal failure develops during lisinopril treatment (serum creatinine >265 µmol/L or twice the level observed before treatment initiation), lisinopril should be discontinued.

Increased sensitivity/angioedema.

Rare cases of angioedema of the face, extremities, lips, tongue, glottis and/or larynx have been reported in patients taking ACE inhibitors, including Lopril Bosnaliek®. Angioedema may occur at any time during treatment. In such cases, lisinopril therapy should be discontinued immediately and appropriate treatment and monitoring should be provided until symptoms completely resolve. In cases where swelling is localized to the tongue and does not impair breathing, prolonged observation may be required, as antihistamine and corticosteroid therapy may be insufficient.

Very rare fatal cases due to angioedema have been reported. In patients with swelling of the tongue, glottis and/or larynx, airway obstruction may occur, particularly in those who have undergone airway surgery. In such cases, immediate emergency measures (adrenaline administration, airway maintenance) are required, and careful monitoring should be maintained until symptoms completely resolve. Patients with a history of angioedema unrelated to ACE inhibitor use are more prone to angioedema during ACE inhibitor therapy.

Anaphylactoid reactions in patients undergoing hemodialysis. Anaphylactoid reactions have been reported in patients undergoing hemodialysis with high-flux membranes (e.g., AN 69) while taking ACE inhibitors. In such cases, either the type of membrane or the class of antihypertensive agent should be changed.

Anaphylactoid reactions during low-density lipoprotein (LDL) apheresis. In patients receiving ACE inhibitors, life-threatening anaphylactoid reactions have occasionally occurred during LDL apheresis with dextran sulfate. To avoid this, temporary discontinuation of ACE inhibitors before apheresis may be considered.

Desensitization. In patients taking ACE inhibitors, anaphylactoid reactions may occur during desensitization therapy (e.g., to hymenoptera venom). Such reactions resolve upon temporary discontinuation of ACE inhibitors but may reappear upon accidental re-exposure to the drug.

Hepatic impairment. In rare cases, ACE inhibitor use has been associated with a syndrome beginning with cholestatic jaundice and progressing to necrosis, sometimes resulting in death. The mechanism of this syndrome is unknown. Patients taking ACE inhibitors who develop jaundice or elevated liver enzymes should discontinue lisinopril and seek appropriate medical care.

Neutropenia/agranulocytosis. ACE inhibitors may cause neutropenia/agranulocytosis, thrombocytopenia, and anaemia, which are reversible upon discontinuation of the ACE inhibitor. In patients with normal renal function and no other complicating factors, neutropenia is rare. Extreme caution is required when prescribing lisinopril to patients with autoimmune or collagen vascular diseases, those receiving immunosuppressive therapy, or those treated with allopurinol or procainamide, especially if renal impairment is present. Serious infections, resistant to intensive antibiotic therapy, may develop in such patients; therefore, periodic blood cell count monitoring is necessary, and patients should be informed to report any signs of infection.

Dual blockade of the RAAS. Dual blockade of the renin-angiotensin-aldosterone system (RAAS) with angiotensin II receptor blockers, ACE inhibitors, or aliskiren is associated with an increased risk of arterial hypotension, hyperkalaemia, and impaired renal function (including acute renal failure). Therefore, dual RAAS blockade by combining ACE inhibitors with angiotensin II receptor blockers or aliskiren is not recommended.

If dual blockade is absolutely necessary, it should be performed only under specialist supervision with continuous careful monitoring of renal function, electrolyte levels, and blood pressure. ACE inhibitors and angiotensin II receptor blockers should not be used concomitantly in patients with diabetic nephropathy.

Race. ACE inhibitors more frequently cause angioedema in patients of black race and may be less effective, possibly due to the more prevalent low-renin status in these patients.

Cough. Cases of persistent, non-productive cough associated with ACE inhibitor use have been reported, which rapidly resolves after discontinuation of therapy. The possibility of a link between cough and ACE inhibitor use should be considered in the differential diagnosis of cough.

Surgery/anesthesia. In patients undergoing general surgery or anesthesia with agents causing arterial hypotension, lisinopril may block angiotensin II formation following compensatory renin secretion. If arterial hypotension occurs and is considered due to this mechanism, circulating blood volume should be corrected.

Hyperkalaemia. Treatment with ACE inhibitors, including lisinopril, may increase serum potassium levels. Risk factors for hyperkalaemia include renal impairment, diabetes mellitus, use of potassium-containing dietary supplements, potassium-sparing diuretics (e.g., spironolactone, triamterene, or amiloride), potassium-containing salt substitutes, or other drugs that increase serum potassium (e.g., heparin, trimethoprim/sulfamethoxazole combination, also known as co-trimoxazole). If concomitant use of these agents is considered appropriate, regular monitoring of serum potassium levels is recommended.

Diabetes mellitus. Patients with diabetes mellitus receiving oral antidiabetic agents or insulin require closer glycaemic monitoring during the first month of ACE inhibitor therapy.

Lithium preparations. In general, the combination of lithium and lisinopril is not recommended.

Use during pregnancy or breastfeeding.

Pregnancy. The medicinal product is contraindicated in pregnant women or women planning pregnancy. If pregnancy is confirmed during treatment with this medicinal product, it should be discontinued immediately, and if necessary, replaced with another medicinal product approved for use during pregnancy.

It is known that prolonged exposure to ACE inhibitors during the second and third trimesters of pregnancy induces fetotoxicity (impaired renal function, oligohydramnios, delayed skull ossification) and neonatal toxicity (renal failure, arterial hypotension, hyperkalaemia). If exposure to ACE inhibitors occurs during the second trimester of pregnancy, monitoring of renal and skull bone function by ultrasound is recommended.

Infants born to mothers who took lisinopril should be closely monitored for arterial hypotension.

Breastfeeding period. Since information on the use of lisinopril during breastfeeding is lacking, lisinopril is not recommended. An alternative treatment with a better-established safety profile should be considered, especially if breastfeeding a newborn or preterm infant.

Ability to influence reaction speed when driving or operating machinery.

When driving vehicles or operating machinery, the possibility of dizziness and fatigue should be taken into account.

Method of administration and dosage.

Lopril Bosnaliek® tablets should be taken orally once daily, preferably at the same time each day. Absorption is not affected by food intake. Dosages are prescribed by a physician individually for each patient, depending on the patient's condition.

Hypertension: lisinopril may be used as monotherapy or in combination with other antihypertensive medicinal products.

Recommended usual initial dose – 10 mg once daily. In patients with renovascular hypertension, salt or fluid imbalance, cardiac decompensation, or severe hypertension, an excessive reduction in arterial pressure may occur after the first dose. Therefore, treatment of such patients should be initiated under medical supervision with a dose of 2.5–5 mg daily. In case of renal impairment, treatment should be initiated with a reduced initial dose (see table).

Usual effective maintenance dose – 20 mg once daily. If the therapeutic effect has not been achieved with the prescribed dose within 2–4 weeks, the dose may be increased. Maximum daily dose – 80 mg.

Patients taking diuretics: arterial hypotension may develop at the beginning of lisinopril therapy. This is most likely in patients receiving diuretics. Therefore, it is advisable to discontinue diuretic therapy 2–3 days before starting lisinopril. If this is not possible, treatment should be initiated with 5 mg of lisinopril daily; the subsequent regimen should be adjusted based on arterial pressure readings. Renal function and plasma potassium levels must be monitored. If necessary, the diuretic may be reintroduced.

Dosage in renal impairment depends on creatinine clearance (see table):

Further dose adjustment depends on the response of arterial pressure.

Maximum dose – 40 mg per day.

Heart failure: lisinopril is recommended as an additional therapy to diuretics, digitalis preparations, or β-blockers. Initial dose – 2.5 mg once daily under medical supervision to determine the drug's effect on arterial pressure. Subsequently, the dose should be increased by no more than 10 mg at intervals of not less than 2 weeks up to the maximum dose of 35 mg per day.

Dosage selection should be based on the individual clinical response of each patient. In patients at high risk of developing symptomatic hypotension (e.g., excessive salt depletion, hypovolemia, intensive diuretic therapy), it is advisable to correct these conditions before initiating lisinopril therapy. Renal function and serum potassium levels must be monitored.

Acute myocardial infarction: patients should receive standard therapy (antithrombotic agents, acetylsalicylic acid, β-blockers). Intravenous or transdermal nitroglycerin may be used concomitantly with lisinopril.

Initial dose (first 3 days after myocardial infarction)

Lisinopril therapy may be initiated within 24 hours after the onset of symptoms of acute myocardial infarction, provided systolic blood pressure is not below 100 mm Hg. The initial dose is 5 mg, followed by 5 mg after 24 hours, 5 mg after 48 hours, and thereafter 10 mg once daily. Patients with systolic blood pressure of 120 mm Hg or lower during the first 3 days after infarction should receive 2.5 mg daily.

In patients with impaired renal function (creatinine clearance < 80 mL/min), the initial dose should be adjusted according to the table.

Maintenance dose

The maintenance dose is 10 mg once daily. If systolic arterial pressure during treatment is 100 mm Hg or lower, the maintenance dose may be temporarily reduced to 5 mg or to 2.5 mg if necessary. If arterial hypotension persists (systolic pressure below 90 mm Hg for more than 1 hour), the drug should be discontinued.

Treatment lasts for 6 weeks, after which the patient's condition should be re-evaluated. In case of heart failure, treatment should be continued.

Early nephropathy in patients with diabetes mellitus

In patients with type II diabetes mellitus, hypertension, and early nephropathy, the dose of lisinopril is 10 mg once daily. If necessary, the dose may be increased to 20 mg per day to achieve diastolic blood pressure below 90 mm Hg when measured in the sitting position. In patients with impaired renal function (creatinine clearance < 80 mL/min), the initial dose should be adjusted according to the table.

Elderly patients

There is no evidence of age-related differences in efficacy and safety of the drug. However, as age increases and is associated with reduced renal function, the initial dose of lisinopril should be selected according to the recommendations in Table 1. Thereafter, the dose should be adjusted based on the patient's response and arterial pressure.

Use in patients with transplanted kidney

Lisinopril is not recommended for patients after kidney transplantation due to lack of sufficient experience.

Children

Experience with the safety and efficacy of the drug in children is limited. The drug should not be used for the treatment of children.

Overdose

Data on cases of human overdose are limited. Symptoms associated with overdose of ACE inhibitors may include arterial hypotension, vascular collapse, electrolyte imbalance, renal failure, hyperventilation, tachycardia, rapid heartbeat, bradycardia, dizziness, restlessness, and cough.

Treatment consists of intravenous infusion of physiological saline. In case of arterial hypotension, the patient should be placed in a supine position with low head elevation. If necessary, infuse angiotensin II and/or intravenous catecholamines. If the drug was recently ingested, measures should be taken to remove it from the body (gastric lavage, emesis, administration of adsorbents or sodium sulfate). Lisinopril may be removed from the blood by hemodialysis. In case of treatment-resistant bradycardia, cardiac pacing may be indicated. Vital functions, electrolyte levels, and creatinine should be monitored.

Adverse Reactions

Blood and lymphatic system disorders: decreased hematocrit and hemoglobin levels, bone marrow suppression, anemia, thrombocytopenia, leukopenia, neutropenia, agranulocytosis, hemolytic anemia, lymphadenopathy, autoimmune disorders.

Metabolic and nutritional disorders: hypoglycemia.

Nervous system disorders: dizziness, headache, mood changes, paresthesia, vertigo, taste and smell disturbances, sleep disorders, hallucinations, confusion, depression, loss of consciousness.

Cardiovascular disorders: orthostatic effects including arterial hypotension; myocardial infarction, stroke—likely due to significant hypotension in patients at high risk for these conditions, palpitations, tachycardia, Raynaud's syndrome.

Respiratory system disorders: cough, rhinitis, bronchospasm, sinusitis, allergic alveolitis, eosinophilic pneumonia.

Gastrointestinal disorders: diarrhea, vomiting, nausea, stomach pain, dyspepsia, dry mouth, pancreatitis, intestinal angioneurotic edema, hepatocellular or cholestatic hepatitis, jaundice, liver failure.

Skin and subcutaneous tissue disorders: rash, pruritus, urticaria, alopecia, psoriasis, hypersensitivity reactions/angioneurotic edema (facial, limb, lip, tongue, pharyngeal, laryngeal swelling); increased sweating, bullous dermatosis, toxic epidermal necrolysis, Stevens-Johnson syndrome, erythema multiforme, cutaneous pseudolymphoma.

A symptom complex has been reported that may include fever, vasculitis, myalgia, arthralgia/arthritis, positive antinuclear antibody test, elevated ESR, eosinophilia, leukocytosis, rash, photosensitivity, or other skin manifestations.

Renal and urinary disorders: renal dysfunction, uremia, acute renal failure, oliguria, anuria.

Endocrine disorders: syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Reproductive system disorders: impotence, gynecomastia.

General disorders: fatigue, asthenia.

Laboratory findings: increased blood levels of urea, creatinine, transaminases, potassium, bilirubin; hyponatremia.

Healthcare professionals, patients, and pharmacists are kindly requested to report any suspected adverse reactions or lack of therapeutic effect to the email address of Bosnalijek d.d. representative: [email protected].

Shelf life. 3 years.

Storage conditions.

Store in a place inaccessible to children, at a temperature not exceeding 30 °C.

Packaging.

20 tablets in a blister, 1 blister per cardboard box (Lopril Bosnalijek® 5 mg).

10 tablets in a blister, 2 blisters per cardboard box (Lopril Bosnalijek® 10 mg and 20 mg).

Prescription category. Prescription only.

Manufacturer/Marketing Authorization Holder.

Bosnalijek d.d.

Manufacturer’s address and place of business / Holder’s and/or representative’s address.

Yukicheva 53, 71000 Sarajevo, Bosnia and Herzegovina.