Main physicochemical properties: 5 mg tablets: white, round, biconvex, with a break line on one side.
Pharmacotherapeutic group
Angiotensin-converting enzyme (ACE) inhibitors are simple. ATC code C09A A03.
Pharmacological properties
Pharmacodynamics
Lisinopril is a peptidyl dipeptidase inhibitor. It inhibits ACE, which catalyzes the conversion of angiotensin I to the vasoconstrictor peptide, angiotensin II, which stimulates the secretion of aldosterone by the adrenal cortex. Inhibition of ACE leads to a decrease in the concentration of angiotensin II, which causes a decrease in vasoconstrictor activity and aldosterone secretion. A decrease in aldosterone secretion may lead to an increase in serum potassium. Lisinopril lowers blood pressure primarily by inhibiting the renin-angiotensin-aldosterone system (RAAS). At the same time, lisinopril has an antihypertensive effect even in patients with low renin levels. ACE is identical to kinase II, an enzyme that promotes the breakdown of bradykinin.
Against the background of the drug, there is a decrease in systolic and diastolic blood pressure. In addition, lisinopril reduces total peripheral resistance, renal vascular resistance and improves blood circulation in the kidneys. In most patients, the antihypertensive effect was manifested 1–2 hours after oral administration of lisinopril, the maximum - approximately 6–9 hours. Stabilization of the therapeutic effect was observed 3–4 weeks after the start of treatment. Withdrawal syndrome was not observed.
It has been demonstrated that the overall adverse reaction profile in patients receiving lisinopril at high or low doses was similar in nature and frequency.
Patients treated with lisinopril had a greater reduction in urinary albumin excretion, suggesting that the ACE inhibitory effect of lisinopril results in a reduction in microalbuminuria through a direct effect on renal tissue in addition to its blood pressure-lowering effect.
Lisinopril therapy did not affect blood glucose control, as evidenced by its negligible effect on glycosylated hemoglobin (HbA1c) levels.
It has been established that lisinopril plays a positive role in restoring the function of damaged endothelium in patients with hyperglycemia.
Pharmacokinetics
Lisinopril is an orally active, non-sulfhydryl ACE inhibitor.
Absorption
After oral administration of lisinopril, maximum serum concentrations (Cmax) are reached after 7 hours, although in patients with acute myocardial infarction there is a tendency for a slight delay in reaching peak concentrations. Based on urinary excretion, the mean extent of absorption of lisinopril in the range is approximately 25% with interpatient variability of 6–60% over all doses studied (5–80 mg). In patients with heart failure, absolute bioavailability is reduced by approximately 16%.
Food intake does not affect the absorption of the drug.
Distribution
Lisinopril does not bind to serum proteins, except for circulating ACE. Studies in rats have shown that lisinopril poorly crosses the blood-brain barrier.
Excretion from the body
Lisinopril is not metabolized and is excreted unchanged in the urine. The elimination half-life in patients receiving multiple doses is 12.6 hours. The clearance of lisinopril in healthy volunteers is 50 ml/min. In cases of renal impairment, the elimination of lisinopril is reduced in proportion to the degree of functional impairment. The decrease in serum concentrations demonstrates a prolonged terminal phase and is not related to drug accumulation. This terminal phase probably reflects extensive binding to ACE and is not dose-proportional.
Patients with liver dysfunction
In patients with cirrhosis, impaired liver function leads to a decrease in the absorption of lisinopril (approximately 30% as determined in the urine) and an increase in exposure (approximately 50%) compared to healthy volunteers due to a decrease in clearance.
Kidney dysfunction
Impaired renal function reduces the renal elimination of lisinopril, but this reduction is clinically significant only when the glomerular filtration rate (GFR) is below 30 ml/min. In moderate to mild renal impairment (creatinine clearance 30–80 ml/min), the mean area under the pharmacokinetic concentration-time curve (AUC) increases by only 13%, whereas in severe renal impairment (creatinine clearance 5–30 ml/min) the mean AUC increases by 4.5-fold. Lisinopril can be removed by dialysis. During 4 hours of hemodialysis, the plasma concentration of lisinopril is reduced by an average of 60% with a dialysis clearance between 40 and 55 ml/min.
Patients with heart failure have a much higher AUC of lisinopril compared to healthy volunteers (an increase in AUC of 125% on average), but based on the amount of lisinopril recovered in urine, the apparent reduction in absorption is approximately 16% compared to healthy volunteers.
Elderly patients
Elderly patients have higher blood levels of the drug and higher AUC values (an increase of approximately 60%) compared to younger patients.
Children
The pharmacokinetic profile of lisinopril was studied in 29 hypertensive children aged 6 to 16 years with a GFR greater than 30 mL/min/1.73 m2. Following administration of lisinopril at doses of 0.1–0.2 mg/kg, steady-state plasma concentrations were reached within 6 hours, and the extent of absorption based on urinary excretion was 28%. These data were similar to those previously observed in adults.
AUC and Cmax values in children were similar to those observed in adults.
Indication
Arterial hypertension.
Heart failure (symptomatic treatment).
Acute myocardial infarction (short-term treatment (6 weeks) of hemodynamically stable patients no later than 24 hours after acute myocardial infarction).
Renal complications in diabetes mellitus (treatment of kidney disease in hypertensive patients with type II diabetes mellitus and initial nephropathy).
Contraindication
Hypersensitivity to lisinopril, other excipients included in the composition of the medicinal product, or to other ACE inhibitors.
History of angioedema (including after use of ACE inhibitors, idiopathic and hereditary angioedema).
Aortic or mitral stenosis or hypertrophic cardiomyopathy with severe hemodynamic disturbances.
Bilateral renal artery stenosis or stenosis of the artery to a single kidney.
Acute myocardial infarction with unstable hemodynamics.
Cardiogenic shock.
Patients with serum creatinine levels ≥220 μmol/L.
Simultaneous use of the drug and high-flow polyacrylonitrile sodium-2-methylsulfonate membranes (e.g., AN69) in emergency dialysis.
Concomitant use of aliskiren-containing medicinal products in patients with diabetes mellitus or renal impairment (GFR <60 ml/min/1.73 m2).
Primary hyperaldosteronism.
Pregnant women or women planning to become pregnant (see section “Use during pregnancy or breastfeeding”).
Concomitant use with sacubitril/valsartan: Treatment with Lisinopril should only be initiated 36 hours after the last dose of sacubitril/valsartan (see sections 4.5 and 4.4).
Interaction with other medicinal products and other types of interactions
Medicinal products that increase the risk of angioedema. Concomitant use of ACE inhibitors with sacubitril/valsartan is contraindicated due to an increased risk of angioedema (see sections 4.3 and 4.4). Concomitant use of ACE inhibitors with racecadotril, mammalian target of rapamycin (mTOR) inhibitors (e.g. sirolimus, everolimus, temsirolimus) or vildagliptin may lead to an increased risk of angioedema (see section 4.4).
Diuretics. When diuretics are used concomitantly in patients already taking lisinopril, the antihypertensive effect is usually enhanced. At the beginning of the combination of lisinopril with diuretics, patients may experience an excessive decrease in blood pressure with lisinopril. The possibility of symptomatic hypotension with lisinopril may be reduced by discontinuing diuretic therapy before starting lisinopril therapy and by increasing volume or salt intake, and by initially treating with low doses of ACE inhibitors.
Potassium-containing dietary supplements, potassium-sparing diuretics or potassium-containing salt substitutes. Although serum potassium levels are usually within normal limits, hyperkalaemia may occur in some patients taking this medicine. Potassium-sparing diuretics (such as spironolactone, triamterene or amiloride), dietary supplements containing potassium or salt substitutes containing potassium may lead to significant increases in serum potassium. Caution should also be exercised when Lisinopril is used concomitantly with other medicinal products that increase serum potassium levels, such as trimethoprim and co-trimoxazole (trimethoprim/sulfamethoxazole), as trimethoprim is known to act as a potassium-sparing diuretic in the same way as amiloride. Therefore, the combination of Lisinopril with the above-mentioned medicinal products is not recommended. If concomitant use of such drugs is indicated, treatment should be carried out with caution and serum potassium levels should be monitored frequently (see section "Special warnings and precautions for use").
Heparin: Concomitant use of ACE inhibitors with heparin may lead to hyperkalemia. Monitoring of serum potassium is recommended.
Lithium preparations. Reversible increases in serum lithium concentrations and toxic reactions have been reported with concomitant use of lithium and ACE inhibitors. Concomitant use of thiazide diuretics may increase the risk of lithium toxicity and exacerbate existing toxicity. Concomitant use of lisinopril and lithium is not recommended, but if such a combination proves necessary, serum lithium levels should be closely monitored.
Nonsteroidal anti-inflammatory drugs (NSAIDs), including acetylsalicylic acid at a dose of ≥3 g/day. Long-term use of NSAIDs may reduce the antihypertensive effect of ACE inhibitors. NSAIDs and ACE inhibitors have an additive effect on serum potassium and may lead to impaired renal function. These effects are usually reversible. Acute renal failure may occur rarely, especially in patients at risk, such as the elderly and those with dehydration.
Other antihypertensive drugs (β-blockers, α-blockers, calcium antagonists). Concomitant use of these drugs may enhance the hypotensive effect of lisinopril. Concomitant use with nitroglycerin, other nitrates or other vasodilators may further reduce blood pressure.
Tricyclic antidepressants/antipsychotics/anesthetics: Concomitant use of some anesthetic drugs, tricyclic antidepressants, and neuroleptics with ACE inhibitors may lead to an increase in the hypotensive effect of the latter.
Sympathomimetic drugs: Sympathomimetic drugs may reduce the antihypertensive effect of ACE inhibitors. For this reason, the patient's blood pressure should be monitored more closely to determine whether the desired therapeutic effect has been achieved.
Antidiabetic medicinal products: Concomitant use of ACE inhibitors and antidiabetic medicinal products (insulin, oral hypoglycaemic agents) may lead to an increased blood glucose lowering effect with the risk of hypoglycaemia. This effect usually occurs during the first weeks of combination therapy and in patients with renal impairment.
Acetylsalicylic acid, thrombolytics, β-blockers, nitrates. Lisinopril can be used concomitantly with acetylsalicylic acid (in cardiological doses), thrombolytics, β-blockers and/or nitrates under medical supervision.
Gold preparations: Nitritoid reactions (symptoms of vasodilation including flushing, nausea, dizziness and hypotension, which may be very severe) following injections of gold preparations (e.g. sodium aurothiomalate) have been observed more frequently in patients treated with ACE inhibitors.
Dual blockade of the RAAS. It has been demonstrated that dual blockade of the RAAS with concomitant use of ACE inhibitors, angiotensin II receptor blockers or aliskiren is characterized by a higher incidence of adverse reactions such as arterial hypotension, hyperkalemia, renal dysfunction (including acute renal failure) compared with the use of monotherapy.
Allopurinol, cytostatics, immunosuppressants, corticosteroids, procainamide. When used simultaneously with lisinopril, they may cause leukopenia.
Drugs that suppress bone marrow function. When used simultaneously with lisinopril, the risk of neutropenia and/or agranulocytosis increases.
Estrogens. With simultaneous use, a decrease in the hypotensive effect of lisinopril is possible due to fluid retention in the body.
Other
Lisinopril should be administered with caution to patients with acute myocardial infarction within 6–12 hours after streptokinase administration (risk of hypotension).
Narcotics, anesthetics, alcoholic beverages, and sleeping pills in combination with lisinopril cause an increase in the hypotensive effect.
Application features
Symptomatic hypotension has been reported rarely in patients with uncomplicated hypertension. In hypertensive patients receiving lisinopril, symptomatic hypertension is more likely to occur in the setting of electrolyte and fluid imbalance, such as that caused by diuretic therapy, salt restriction, diarrhoea or vomiting, or in patients with severe renin-dependent hypertension. Symptomatic hypotension has been reported in patients with heart failure (with or without renal insufficiency).
If hypotension occurs, the patient should be placed on his back and, if necessary, an intravenous infusion of saline should be administered.
Transient hypotension is not a contraindication to further use of the drug, it can usually be administered without complications after blood pressure has increased following an increase in body fluid volume.
Some patients with heart failure who have normal or low blood pressure may experience an additional decrease in systemic blood pressure while receiving lisinopril. This effect is expected and usually does not require discontinuation of lisinopril therapy. If hypotension becomes symptomatic, it may be necessary to reduce the dose or discontinue lisinopril.
Hypotension in acute myocardial infarction. In acute myocardial infarction in hemodynamically stable patients, lisinopril should be administered within the first 24 hours to prevent left ventricular dysfunction and heart failure and to reduce mortality. In acute myocardial infarction, lisinopril should not be initiated if there is a risk of further serious hemodynamic deterioration following vasodilator treatment. This applies to patients with a systolic blood pressure of 100 mm Hg or less or patients who have developed cardiogenic shock. During the first 3 days after myocardial infarction, the dose should be reduced if the systolic blood pressure does not exceed 120 mm Hg. If the systolic blood pressure is equal to or below 100 mm Hg, the selected doses should be reduced to 5 mg or temporarily to 2.5 mg. If prolonged hypotension occurs after taking lisinopril (systolic blood pressure remains below 90 mm Hg for more than 1 hour), lisinopril treatment should be discontinued.
In patients with hypovolemia, sodium deficiency due to the use of diuretics, a salt-free diet, vomiting, diarrhea, after dialysis, sudden severe arterial hypotension, acute renal failure may develop. In such cases, it is advisable to compensate for fluid and salt losses before starting treatment with lisinopril and to ensure adequate medical supervision. With particular caution (taking into account the benefit/risk ratio) the drug should be prescribed to patients after kidney transplantation, as well as to patients with impaired renal function, liver, hematopoietic disorders, autoimmune diseases. All of the listed pathological conditions when using lisinopril require appropriate medical supervision and laboratory control.
Aortic and mitral valve stenosis/hypertrophic cardiomyopathy: As with other ACE inhibitors, lisinopril is not recommended for use in patients with mitral stenosis or obstruction in the outflow of blood from the left ventricle (as in aortic stenosis or hypertrophic cardiomyopathy).
Renal impairment: In patients with renal impairment (creatinine clearance <80 ml/min), the initial dose of lisinopril should be adjusted based on creatinine clearance and then according to the patient's response to treatment (see table). Creatinine and potassium levels should be monitored regularly in such patients.
In patients with heart failure, hypotension occurring at the beginning of treatment with ACE inhibitors may lead to deterioration of renal function. In such cases, acute renal failure, usually reversible, has been reported.
In some patients with bilateral renal artery stenosis or stenosis of the artery to a solitary kidney, ACE inhibitors have been shown to increase blood urea and serum creatinine, but these effects usually resolve after discontinuation of the drug. This is particularly likely in patients with renal insufficiency.
The presence of renovascular hypertension increases the risk of developing severe arterial hypotension and renal failure. Treatment of such patients should be initiated under the supervision of a physician, starting with low doses, carefully titrating them. Since diuretics can stimulate the development of the clinical dynamics described above, during the first weeks of treatment with lisinopril, their administration should be discontinued and renal function should be closely monitored.
In some hypertensive patients without overt renal vascular disease, the use of lisinopril, especially in combination with diuretics, has caused increases in blood urea and serum creatinine; these changes are usually minor and transient. They are more likely to occur in patients with impaired renal function. In such cases, it may be necessary to reduce the dose and/or discontinue the diuretic and/or lisinopril.
Hypersensitivity/angioedema. Angioedema of the face, extremities, lips, tongue, glottis and/or larynx has been reported very rarely in patients treated with ACE inhibitors, including lisinopril. Angioedema may occur at any time during treatment. In such cases, the drug should be discontinued immediately, appropriate therapy should be initiated, and the patient should be observed until symptoms resolve. Even in cases where the swelling is limited to the tongue and does not cause respiratory distress, the patient may require prolonged observation, as antihistamines and corticosteroids may be inadequate.
Isolated fatalities have been reported as a result of angioedema of the larynx or tongue. If the swelling extends to the tongue, glottis or larynx, obstructive respiratory failure may develop, particularly in patients who have previously undergone surgery on the respiratory tract. In such cases, emergency treatment should be initiated immediately, which may include the administration of adrenaline and/or the maintenance of a patent airway. The patient should be kept under close medical supervision until complete and sustained resolution of symptoms.
Patients with a history of angioedema unrelated to ACE inhibitor use may be at increased risk of developing angioedema in response to this class of drugs.
ACE inhibitors may cause more cases of angioedema in black patients than in white patients.
Concomitant use of ACE inhibitors with sacubitril/valsartan is contraindicated due to an increased risk of angioedema. Sacubitril/valsartan treatment should not be started until 36 hours after the last dose of Lisinopril. Lisinopril should not be started until 36 hours after the last dose of sacubitril/valsartan (see sections 4.3 and 4.5).
Concomitant use of ACE inhibitors with racecadotril, mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) or vildagliptin may lead to an increased risk of angioedema (e.g. swelling of the airways or tongue with or without respiratory distress) (see section 4.5). Caution should be exercised when initiating racecadotril, mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) and vildagliptin in patients already taking an ACE inhibitor.
Anaphylactoid reactions in patients undergoing hemodialysis. Anaphylactoid reactions have been reported in patients undergoing hemodialysis using high-flux membranes (e.g. AN69) and receiving concomitant ACE inhibitor therapy. These patients should be offered a change of dialysis membrane type or a different class of antihypertensive drug.
Desensitization: Patients receiving ACE inhibitors during desensitization therapy (e.g., to hymenoptera venom) have developed persistent anaphylactoid reactions. These reactions have been avoided in such patients by temporarily discontinuing ACE inhibitors, but the reactions have recurred after inadvertent rechallenge.
Hepatic failure. Very rarely, ACE inhibitors have been associated with a syndrome that begins with cholestatic jaundice and progresses rapidly to necrosis and (sometimes) death. The mechanism of this syndrome is not known. Patients who develop jaundice or significant elevations of liver enzymes while taking lisinopril should discontinue the drug and receive appropriate medical attention.
Neutropenia/agranulocytosis. Neutropenia/agranulocytosis, thrombocytopenia and anemia have been reported in patients receiving ACE inhibitors. Neutropenia is rare in patients with normal renal function and in the absence of other complicating factors. Neutropenia and agranulocytosis are reversible after discontinuation of the ACE inhibitor. Lisinopril should be used with extreme caution in patients with collagen vascular disease, immunosuppressive therapy, allopurinol or procainamide, or a combination of these complicating factors, especially in patients with impaired renal function. Some such patients develop serious infections that do not always respond to intensive antibiotic therapy. When using the drug in such patients, it is recommended to periodically monitor the number of white blood cells in the blood and instruct patients to report any signs of infection.
Surgery/Anesthesia: In patients undergoing surgery or anesthesia with agents that produce hypotension, lisinopril may block the formation of angiotensin II following compensatory renin secretion. If hypotension occurs due to this mechanism, volume expansion should be considered.
Serum potassium. There have been a few reports of increases in serum potassium in patients treated with ACE inhibitors, including lisinopril. Patients at high risk of developing hyperkalaemia include those with renal insufficiency, diabetes mellitus, and hypoaldosteronism. ACE inhibitors may cause hyperkalaemia because they inhibit the release of aldosterone. This effect is usually minor in patients with normal renal function. However, hyperkalaemia may occur in patients with impaired renal function and/or in patients taking potassium supplements (including salt substitutes), potassium-sparing diuretics, other medicinal products that increase serum potassium (e.g. heparin, trimethoprim or co-trimoxazole, also known as trimethoprim/sulfamethoxazole) and especially aldosterone antagonists or angiotensin receptor blockers. Potassium-sparing diuretics and angiotensin receptor blockers should be used with caution in patients receiving ACE inhibitors. Serum potassium and renal function should be monitored in such patients (see section 4.5).
If concomitant use of the above-mentioned drugs with lisinopril is considered appropriate, regular monitoring of serum potassium levels is recommended.
Diabetic patients: In diabetic patients receiving oral antidiabetic agents or insulin, close glycemic control is required during the first month of ACE inhibitor therapy.
Anaphylactoid reactions occurring during low-density lipoprotein (LDL) apheresis. During dextran sulfate apheresis, the use of ACE inhibitors may lead to anaphylactoid reactions that may be life-threatening. These symptoms can be avoided by temporarily stopping ACE inhibitor therapy before each apheresis or by replacing ACE inhibitors with other drugs.
Race: ACE inhibitors may cause a higher incidence of angioedema in black patients than in white patients. The antihypertensive effect of lisinopril is also less pronounced in this group of patients due to a higher prevalence of low-renin hypertension in black patients.
Lithium: The concomitant use of lithium and lisinopril is generally not recommended.
Dual blockade of the RAAS. Concomitant use of ACE inhibitors, angiotensin II receptor blockers or aliskiren has been reported to increase the risk of hypotension, hyperkalaemia and renal impairment (including acute renal failure). Therefore, dual blockade of the RAAS through concomitant use of ACE inhibitors, angiotensin II receptor blockers or aliskiren is not recommended.
If dual blockade therapy is absolutely necessary, it should be carried out under specialist supervision and regular monitoring of renal function, electrolytes and blood pressure should be performed. The concomitant use of ACE inhibitors and angiotensin II receptor blockers is not recommended in patients with diabetic nephropathy.
Proteinuria: Isolated cases of proteinuria have been reported in patients, particularly with impaired renal function or after high doses of lisinopril. In the presence of clinically significant proteinuria (>1 g/day), lisinopril should be used only after careful consideration of the therapeutic benefit and potential risk, with close monitoring of clinical and biochemical parameters.
Sodium: This medicinal product contains less than 1 mmol sodium (23 mg) per tablet, that is to say essentially “sodium-free”.
Ability to influence reaction speed when driving vehicles or other mechanisms
Due to the possibility of dizziness and fatigue, lisinopril may affect the ability to drive and use machines, especially at the beginning of treatment. Therefore, driving and using machines should be avoided until individual response to the drug is established.
Use during pregnancy or breastfeeding
Pregnancy. The drug is contraindicated for use in pregnant women and women planning pregnancy. If pregnancy is confirmed during the use of this drug, its use should be discontinued immediately and, if necessary, replaced with another drug approved for use in pregnant women.
Infants whose mothers have taken lisinopril should be closely monitored for hypotension, oliguria, and hyperkalemia.
Breast-feeding: Because no information is available regarding the use of lisinopril during breast-feeding, lisinopril is not recommended and alternative treatments with better established safety profiles during breast-feeding are preferable, especially while nursing a newborn or preterm infant.
Method of administration and doses
Lisinopril should be taken orally once daily. As with other once-daily medicinal products, lisinopril should be taken at approximately the same time each day. Food does not affect the absorption of lisinopril tablets. The dose should be individualised according to the patient's clinical status and blood pressure.
Arterial hypertension.
Lisinopril can be used as monotherapy or in combination with other classes of antihypertensive drugs.
Initial dose.
The usual starting dose for patients with hypertension is 10 mg. Patients with a very active RAAS (in particular, with renovascular hypertension, increased salt (sodium chloride) excretion from the body and/or reduced interstitial fluid volume, heart failure or severe arterial hypertension) may experience an excessive decrease in blood pressure after taking the initial dose. For such patients, the recommended starting dose is 2.5-5 mg, and treatment should be initiated under the direct supervision of a physician. A reduction in the starting dose is also recommended in the presence of renal insufficiency (see table).
Maintenance dose.
The usual recommended therapeutic dose is 20 mg once daily. If this dose does not provide sufficient therapeutic effect within 2–4 weeks of taking the drug at the indicated dosage, it can be increased. The maximum dose used in long-term controlled clinical trials was 80 mg daily.
Patients taking diuretics.
Symptomatic hypotension may occur after initiation of lisinopril therapy. This is more likely in patients receiving diuretics during treatment with lisinopril. Therefore, caution is advised in such patients due to the potential for increased salt (sodium chloride) excretion and/or volume depletion. If possible, diuretic therapy should be discontinued 2-3 days before initiating lisinopril therapy. In hypertensive patients who cannot discontinue diuretic therapy, lisinopril therapy should be initiated with an initial dose of 5 mg, and it is recommended that the patient be monitored closely after the first dose, as symptomatic hypotension may occur (maximum effect is seen 6 hours after administration). Renal function and serum potassium should be monitored. Subsequent doses of lisinopril should be titrated according to blood pressure response. If necessary, diuretic therapy can be resumed.
Dosage selection for patients with renal failure.
Dosage for patients with renal insufficiency should be based on creatinine clearance, the maintenance dose depends on the clinical response and is selected with regular measurement of renal function indicators, potassium and sodium concentrations in the serum, as shown in the table below.
Dosage selection for patients with renal failure
Creatinine clearance (ml/min)
Starting dose (mg/day)
Less than 10
Specifications
Characteristics
Active ingredient
Lisinopril
Adults
Can
ATC code
C MEDICINES AFFECTING THE CARDIOVASCULAR SYSTEM; C09 MEDICINES AFFECTING THE RENIN-ANGIOTENSIN SYSTEM; C09A ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS; C09A A ACE inhibitors, single-component; C09A A03 Lisinopril
Country of manufacture
Germany
Diabetics
With caution
Dosage
5 мг
Drivers
Contraindicated until individual reaction is detected
For allergies
With caution
For children
It is impossible.
Form
Tablets
Method of application
Inside, solid
Nursing
It is impossible.
Pregnant
It is impossible.
Primary packaging
blister
Producer
Teva
Quantity per package
30 pcs
Trade name
Lisinopril
Vacation conditions
By prescription
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