Lorista pills 12.5mg, 30pcs

Composition

for 1 tablet 12.5 mg / 25 mg / 50 mg / 100 mg

Core:

Active ingredient:

Losartan Potassium 12.50 mg / 25.00 mg/50.00 mg/100.00 mg

Auxiliary substances:

Cellulose 801, pregelatinized starch, corn starch, microcrystalline cellulose, colloidal silicon dioxide, magnesium stearate

Film shell:

Hypromellose, talc, propylene glycol, quinoline yellow dye (E 104) (for tablets 12.5 mg and 25 mg), titanium dioxide (E 171)

1 Cellactose 80: lactose monohydrate, cellulose.

Pharmacological action

Angiotensin II receptor antagonist (ARA II)

Clinical pharmacology

Mechanism of action

Angiotensin II is a powerful vasoconstrictor, the main active hormone of the renin-angiotensin-aldosterone system (RAAS), and also a crucial pathophysiological link in the development of arterial hypertension (AH). Angiotensin II binds toAT1 receptors in many tissues (vascular smooth muscle, adrenal, kidney, and heart) and performs several important biological functions, including vasoconstriction and aldosterone release. In addition, angiotensin II stimulates the proliferation of smooth muscle cells.

_AT2receptors are the second type of receptors that angiotensin II binds to, but their role in regulating cardiovascular function is unknown.

Losartan is a selective angiotensin II AT1receptor antagonist that is highly effective when taken orally. Losartan and its pharmacologically active carboxylated metabolite (E-3174), both in vitroand in vivo, block all physiological effects of angiotensin II, regardless of its source or pathway of synthesis. Unlike some peptide antagonists of angiotensin II, losartan does not have agonist properties.

Losartan selectively binds to AT_-1receptors and does not bind or block the receptors of other hormones and ion channels that play an important role in regulating the function of the cardiovascular system. In addition, losartan does not inhibit the angiotensin-converting enzyme (ACE) kininase II, which is responsible for the destruction of bradykinin. Therefore, effects that are not directly related to AT1_{receptor blockade}, such as increased bradykinin-mediated effects or the development of edema (losartan 1.7%, placebo 1.9%), are not related to the effect

of losartan.

Losartan suppresses the increase in systolic and diastolic blood pressure (BP) during angiotensin II infusion. At the time of reaching the maximum concentration of losartan (cmax) in blood plasma after taking losartan at a dose of 100 mg, the above effect of angiotensin II is suppressed by approximately 85%, and 24 hours after single and multiple doses – by 26-39%.

When taking losartan, the elimination of negative feedback consisting in the suppression of renin secretion by angiotensin II leads to an increase in plasma renin activity (ARP). An increase in ARP leads to an increase in the concentration of angiotensin II in blood plasma.

Since losartan is a specific angiotensin_{II AT1}receptor antagonist, it does not inhibit ACE (kininase II), an enzyme that inactivates bradykinin. A study comparing the effects of losartan at 20 mg and 100 mg doses with those of an ACE inhibitor for the effects on angiotensin I, angiotensin II, and bradykinin showed that losartan blocked the effects of angiotensin I and angiotensin II without affecting the effects of bradykinin. This is due to the specific mechanism of action of losartan. The ACE inhibitor blocked the response to angiotensin I and increased the severity of bradykinin-related effects, without affecting the severity of the response to angiotensin II, which demonstrates the pharmacodynamic difference between losartan and ACE inhibitors.

The plasma concentrations of losartan and its active metabolite, as well as the antihypertensive effect of losartan, increase with increasing dose. Since losartan and its active metabolite are ARA II, they both contribute to the antihypertensive effect.

Losartan therapy in postmenopausal women with hypertension does not affect renal and systemic prostaglandin levels.

Losartan does not affect autonomic reflexes and does not have a long-term effect on the concentration of norepinephrine in blood plasma.

In patients with hypertension, losartan at doses up to 150 mg / day does not cause clinically significant changes in fasting serum concentrations of triglycerides, total cholesterol, and high-density lipoprotein cholesterol. At the same doses, losartan does not affect the fasting blood glucose concentration.

In patients with NYHA functional class II-IV chronic heart failure (CHF) and intolerance to ACE inhibitors, losartan 150 mg/day significantly reduces the risk of all-cause mortality or hospitalization for heart failure compared to a dose of 50 mg/day.

In patients with left ventricular insufficiency (NYHA functional class II-IV), most of whom are taking diuretics and/or cardiac glycosides, losartan at doses of 25 and 50 mg/day shows positive hemodynamic and neurohormonal effects. Hemodynamic effects include an increase in cardiac index and a decrease in pulmonary capillary jamming pressure, as well as a decrease in total peripheral vascular resistance( OPSS), mean systemic blood pressure, and heart rate (HR). The frequency of hypotension in these patients depends on the dose of losartan. Neurohormonal effects include decreased serum concentrations of aldosterone and norepinephrine.

Pharmacokinetics

Suction

When taken orally, losartan is well absorbed and undergoes metabolism during the “primary passage” through the liver with the formation of an active carboxylated metabolite and inactive metabolites. The systemic bioavailability of losartan in the dosage form of film-coated tablets is approximately 33%. Mean plasma concentrations of losartan and its active metabolite are reached in 1 hour and 3-4 hours, respectively. When losartan was taken during a normal meal, no clinically significant effect on the plasma losartan concentration profile was detected.

Distribution

Losartan and its active metabolite bind to plasma proteins (mainly albumin) by at least 99%. The volume of distribution of losartan is 34 liters. Studies in rats have shown that losartan practically does not penetrate the blood-brain barrier.

Metabolism

Approximately 14% of the dose of losartan is converted to its active metabolite by intravenous or oral use. After oral or intravenous use of radiolabeled losartan (14C losartan), the radioactivity of circulating blood plasma is primarily due to the presence of losartan and its active metabolite. Low conversion efficiency of losartan to its active metabolite was observed in approximately 1% of the patients who participated in the study. In addition to the active metabolite, biologically inactive metabolites are formed, including two main metabolites formed as a result of hydroxylation of the butyl side chain, and one minor – N-2-tetrazole-glucuronide.

Deduction

The plasma clearance of losartan and its active metabolite is approximately 600 ml / min and 50 ml / min, respectively. The renal clearance of losartan and its active metabolite is approximately 74 ml / min and 26 ml / min, respectively. When losartan is taken orally, about 4% of the dose is excreted unchanged by the kidneys and about 6% of the dose is excreted by the kidneys as an active metabolite. Losartan and its active metabolite have linear pharmacokinetics when taking losartan orally at doses up to 200 mg.

After oral use, plasma concentrations of losartan and its active metabolite decrease polyexponentially with a terminal half-life of approximately 2 and 6-9 hours, respectively. When the dosage regimen of the drug is 100 mg once a day, there is no significant accumulation in the blood plasma of either losartan or its active metabolite.

The elimination of losartan and its metabolites is carried out by the kidneys and through the intestines with bile. After ingestion of 14C losartan in men, about 35% of radioactivity is detected in the urine and 58% in the feces. After intravenous use of 14C losartan in men, approximately 43% of radioactivity is detected in the urine and 50% in the feces.

Pharmacokinetics in selected groups of patients

Elderly patients

The plasma concentrations of losartan and its active metabolite in elderly male patients with hypertension do not significantly differ from those in young male patients with hypertension.

Gender

The plasma concentrations of losartan in women with hypertension were 2 times higher than the corresponding values in men with hypertension. The concentrations of the active metabolite in the blood plasma did not differ between men and women. This clear pharmacokinetic difference, however, is not clinically relevant.

Patients with impaired liver function

When taking losartan orally in patients with mild and moderate alcoholic cirrhosis of the liver, the concentrations of losartan and its active metabolite in blood plasma were 5 and 1.7 times higher, respectively, than in young healthy male volunteers.

Patients withimpaired renal function

Plasma concentrations of losartan in patients with creatinine clearance (CC) above 10 ml / min did not differ from those in patients with unchanged renal function. The area under the concentration-time curve (AUC) of losartan in patients undergoing hemodialysis was approximately 2 times greater than the AUC of losartan in patients with normal renal function. Concentrations of the active metabolite in blood plasma did not change in patients with impaired renal function or patients on hemodialysis. Losartan and its active metabolite are not eliminated by hemodialysis.

Indications

• Arterial hypertension.
• Reduced risk of associated cardiovascular morbidity and mortality in patients with arterial hypertension and left ventricular hypertrophy, resulting in a combined reduction in the incidence of cardiovascular mortality, stroke, and myocardial infarction.
• Kidney protection in patients with type 2 diabetes mellitus with proteinuria – slowing the progression of renal failure, manifested by a decrease in the frequency of hypercreatininemia, the frequency of end-stage chronic renal failure requiring hemodialysis or kidney transplantation, mortality rates, and a decrease in proteinuria.
• Chronic heart failure with ineffective treatment with ACE inhibitors or intolerance to ACE inhibitors. It is not recommended to transfer patients with heart failure and stable hemodynamic parameters when taking ACE inhibitors to losartan therapy.

Use during pregnancy and lactation

Drugs that directly affect the RAAS can cause serious damage and death to the developing fetus, so when diagnosing pregnancy, Lorista® should be immediately discontinued and, if necessary, alternative antihypertensive therapy should be prescribed.

Lorista® therapy should not be initiated during pregnancy. If continuation of antihypertensive therapy with losartan is considered necessary in patients planning pregnancy, losartan should be replaced with alternative antihypertensive agents that have an established safety profile for use during pregnancy.

Although there is no experience with the use of losartan in pregnant women, preclinical animal studies have shown that taking losartan leads to the development of serious fetal and neonatal damage and death of the fetus or offspring. It is believed that the mechanism of these phenomena is due to the impact on the RAAS.

Renal perfusion in the fetus, which depends on the development of RAAS, occurs in the second trimester, so the risk to the fetus increases if Lorista® is used in the second or third trimester of pregnancy.

The use of drugs that affect the RAAS in the second and third trimester of pregnancy reduces fetal kidney function and increases the morbidity and mortality of the fetus and newborns. The development of oligohydramnios may be associated with fetal lung hypoplasia and skeletal deformities. Possible adverse events (AES) in newborns include cranial hypoplasia, anuria, hypotension, renal failure, and death.

The above-mentioned adverse outcomes are usually caused by the use of drugs that affect the RAAS in the second and third trimester of pregnancy. Most epidemiological studies on the development of fetal abnormalities after the use of antihypertensive drugs in the first trimester of pregnancy did not reveal differences between drugs that affect the RAAS and other antihypertensive drugs. When using antihypertensive therapy in pregnant women, it is important to optimize possible outcomes for the mother and fetus.

If it is not possible to choose an alternative therapy to replace therapy with drugs that affect the RAAS, it is necessary to inform the patient about the possible risk of therapy for the fetus. Periodic ultrasound examinations should be performed to assess the intra-amniotic space. If an oligohydramnion is detected, it is necessary to stop taking Lorista®, unless it is vital for the mother. Depending on the duration of pregnancy, appropriate tests should be performed in the fetus. Patients and doctors should be aware that oligohydramnion may not be detected until permanent fetal damage occurs. Careful monitoring of newborns whose mothers have taken Lorista® during pregnancy is necessary in order to control hypotension, oliguria and hyperkalemia.

It is not known whether losartan is excreted in breast milk. Since many medications are excreted in breast milk, and there is a risk of possible adverse effects in a breastfed child, a decision should be made to stop breastfeeding or to discontinue the drug, taking into account the need for its use for the mother.

Contraindications

• Hypersensitivity to any of the components of this drug.
• Severe hepatic impairment (no experience of use).
• Concomitant use with aliskiren and drugs containing aliskiren in patients with diabetes mellitus and/or moderate to severe renal impairment (glomerular filtration rate [GFR] less than 60 ml/min/1.73 m2 of body surface area) (see section “Interaction with other drugs”).
• Concomitant use with ACE inhibitors in patients with diabetic nephropathy.
• Hereditary problems of lactose intolerance, lactase deficiency, glucose-galactose malabsorption syndrome.
• Pregnancy and breast-feeding period.
• Age up to 18 years (efficacy and safety of use have not been established).

Interaction

Other antihypertensive drugs may enhance the antihypertensive effect of losartan. Concomitant use with other medications that may cause hypotension (such as tricyclic antidepressants, antipsychotics, baclofen, and amifostine) may increase the risk of hypotension.

No clinically significant interactions of losartan with hydrochlorothiazide, digoxin, warfarin, cimetidine, or phenobarbital have been identified in clinical studies of pharmacokinetic drug interactions. Rifampicin, being an inducer of drug metabolism, reduces the concentration of the active metabolite of losartan in blood plasma. Two inhibitors of the CYP3A4 isoenzyme, ketoconazole and erythromycin, were studied in clinical trials. Ketoconazole did not affect the metabolism of losartan to the active metabolite after intravenous use of losartan. Erythromycin did not have a clinically significant effect when taking losartan orally. Fluconazole, an inhibitor of the CYP2C9 isoenzyme, reduces the concentration of the active metabolite of losartan in blood plasma, but the pharmacodynamic significance of concomitant use of losartan and inhibitors of the CYP2C9 isoenzyme has not been studied. It has been shown that patients who do not metabolize losartan to the active metabolite have a very rare and specific defect of the CYP2C9 isoenzyme. These data suggest that the metabolism of losartan to the active metabolite is carried out by the CYP2C9 isoenzyme, and not by the CYP3A4 isoenzyme.

Concomitant use of losartan, as well as other drugs that block angiotensin II or its effects, with potassium-sparing diuretics (for example, spironolactone, eplerenone, triamterene, amiloride), potassium-containing supplements or potassium salts may lead to an increase in serum potassium.

As with other drugs that affect the elimination of sodium ions, losartan may reduce the elimination of lithium, so when lithium and ARA II preparations are used simultaneously, it is necessary to carefully monitor the content of lithium in the blood serum.

Nonsteroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 (COX-2) inhibitors, may reduce the effect of diuretics and other antihypertensive agents. As a result, the antihypertensive effect of ARA II or ACE inhibitors may be weakened when used concomitantly with NSAIDs, including selective COX-2 inhibitors.

In some patients with impaired renal function (for example, in elderly patients or patients with dehydration, including those taking diuretics), receiving NSAID therapy, including selective COX-2 inhibitors, the simultaneous use of ARA II or ACE inhibitors may cause further deterioration of renal function, including the development of acute renal failure. These effects are usually reversible. Concomitant use of these drugs should be carried out with caution in patients with impaired renal function.

Dual blockade of the RAAS with ARA II, ACE inhibitors, or aliskiren (a renin inhibitor) is associated with an increased risk of hypotension, syncope, hyperkalemia, and impaired renal function (including acute renal failure) compared to monotherapy.Regular monitoring of blood pressure, renal function, and plasma electrolytes is necessary in patients taking Lorista® concomitantly with other medications that affect the RAAS. Concomitant use of ARA II with drugs containing aliskiren is contraindicated in patients with diabetes mellitus and/or moderate to severe renal insufficiency (GFR less than 60 ml/min / 1.73 m2 of body surface area) and is not recommended in other patients. Concomitant use of ARA II with ACE inhibitors is contraindicated in patients with diabetic nephropathy and is not recommended in other patients.

How to take, course of use and dosage

Lorista® is taken orally regardless of the meal time. Lorista® can be taken in combination with other antihypertensive agents.

Arterial hypertension

The standard initial and maintenance dose for most patients is 50 mg of Lorista® once a day. The maximum antihypertensive effect is achieved after 3-6 weeks from the start of therapy. In some patients, to achieve a greater effect, the dose may be increased to a maximum dose of 100 mg of Lorista® once a day.

In patients with reduced BCC (for example, when taking large doses of diuretics), the initial dose of Lorista® should be reduced to 25 mg once a day (see the section “Special instructions”).

There is no need to select the initial dose of Lorista® for elderly patients and patients with impaired renal function, including patients on dialysis.

Patients with a history of liver disease are recommended to use lower doses of Lorista® (see section “Special instructions”).

Reduced risk of associated cardiovascular morbidity and mortality in patients with hypertension and left ventricular hypertrophy

The standard initial dose of Lorista® is 50 mg once a day. In the future, it is recommended to add low-dose hydrochlorothiazide to therapy or increase the dose of Lorista® to a maximum dose of 100 mg once a day, taking into account the degree of reduction in blood pressure.

Kidney protection in patients with type 2 diabetes mellitus and proteinuria

The standard initial dose of Lorista® is 50 mg once a day. In the future, the dose of Lorista® can be increased to a maximum dose of 100 mg once a day, taking into account the degree of reduction in blood pressure. Lorista® can be used in combination with other antihypertensive agents (for example, diuretics, slow calcium channel blockers, alpha – and beta-blockers, central antihypertensive agents), insulin and other hypoglycemic agents (for example, sulfonylureas, glitazones and glucosidase inhibitors).

Chronic heart failure

The initial dose of Lorista® for patients with CHF is 12.5 mg once a day. As a rule, the dose is selected at weekly intervals (i. e. 12.5 mg / day,25 mg / day,50 mg / day,100 mg / day up to the maximum dose [for this indication only] 150 mg 1 time per day), depending on individual tolerance.

Overdose

Information about overdose is limited.

Symptoms: the most likely manifestation of overdose is a marked decrease in blood pressure and tachycardia, bradycardia may occur due to parasympathetic (vagal) stimulation. If symptomatic hypotension develops, maintenance therapy is indicated.

Treatment: symptomatic therapy. Losartan and its active metabolite are not eliminated by hemodialysis.

Description

Tablets 12.5 mg: Oval, slightly biconvex tablets, film-coated from light yellow to yellow in color, with a chamfer.

View on the fracture: a rough mass of white color with a film shell from light yellow to yellow.

25 mg tablets: Oval, slightly biconvex tablets, yellow film-coated, with a risk on one side and a chamfer.

View at the break: a rough mass of white color with a yellow film shell.

50 mg tablets: Round, slightly biconvex tablets, film-coated in white, with a risk on one side and a chamfer.

View at the break: a rough mass of white color with a film shell of white color.

100 mg tablets: Oval, slightly biconvex tablets with a white film-coated surface.

View at the break: a rough mass of white color with a film shell of white color.

Special instructions

Bilateral renal artery stenosis or single kidney artery stenosis, hyperkalemia, post-kidney transplant condition (no experience), aortic or mitral stenosis, hypertrophic obstructive cardiomyopathy (HOCMP), heart failure with concomitant severe renal impairment, severe heart failure (NYHA Functional Class IV), heart failure with life-threatening arrhythmias, coronary heart disease (CHD), cerebrovascular diseases, primary hyperaldosteronism, a history of angioedema.

Patients with reduced circulating blood volume (BCC) (for example, patients treated with high doses of diuretics) may develop symptomatic hypotension.

Contraindicated in persons under 18 years of age (efficacy and safety of use have not been established).

There is no need to select the initial dose of Lorista® for elderly patients and patients with impaired renal function, including patients on dialysis.

It is contraindicated in patients with severe hepatic impairment (no experience of use).

Patients with a history of liver disease are recommended to use lower doses of Lorista® (see section “Special instructions”).

Hypersensitivity reactions

Patients with a history of angioedema (swelling of the face, lips, pharynx/larynx and / or tongue) when using Lorista® should be under strict medical supervision (see the section “Side effects”).

Embryotoxicity

The use of drugs that affect the RAAS in the second and third trimester of pregnancy reduces kidney function in the fetus and increases the morbidity and mortality of the fetus and newborns. The development of oligohydramnios may be associated with fetal lung hypoplasia and skeletal deformities. Possible neonatal AES include cranial hypoplasia, anuria, hypotension, renal failure, and death. If pregnancy is diagnosed, Lorista® should be discontinued immediately (see section “Use during pregnancy and lactation”).

Arterial hypotension and impaired water-electrolyte balance or decreased BCC

Patients with reduced BCC (for example, those treated with high doses of diuretics) may develop symptomatic hypotension. Correction of such conditions should be carried out before using Lorista® or start treatment with a lower dose of Lorista® (see the section “Dosage and use”). Impaired water-electrolyte balance is characteristic of patients with impaired renal function with or without diabetes mellitus, so careful monitoring of these patients is necessary. In clinical trials involving patients with type 2 diabetes mellitus with proteinuria, the incidence of hyperkalemia was higher in the losartan group than in the placebo group. Several patients discontinued therapy due to hyperkalemia (see the section “Side effects”, subsection “Laboratory and instrumental data”).

During treatment with Lorista®, it is not recommended to take potassium-sparing diuretics, potassium preparations or potassium-containing salt substitutes.

 

 

Aortic or mitral stenosis, HOCMP

Like all drugs with vasodilating effects, ARA II should be used with caution in patients with aortic or mitral stenosis or HOCMP.

CHD and cerebrovascular diseases

Like all drugs with vasodilating effects, ARA II should be used with caution in patients with CHD or cerebrovascular diseases, since a pronounced decrease in blood pressure in this group of patients can lead to the development of myocardial infarction or stroke.

CHF

As with other medications that affect the RAAS, patients with CHF and with or without impaired renal function are at risk of developing severe hypotension or acute renal impairment.

Since there is insufficient experience with Lorista® in patients with heart failure and concomitant severe renal impairment, in patients with severe heart failure (NYHA functional class IV), as well as in patients with heart failure and symptomatic life-threatening arrhythmias, Lorista® should be used with caution in patients of these groups.

Primary hyperaldosteronism

Since patients with primary hyperaldosteronism usually do not respond positively to antihypertensive agents that act by inhibiting RAAS, the use of Lorista® is not recommended in this group of patients.

Impaired liver function

Data from pharmacokinetic studies indicate that the concentration of losartan in the blood plasma in patients with cirrhosis of the liver is significantly increased, so patients with a history of impaired liver function should use Lorista® at a lower dose. There is no experience of using losartan in patients with severe hepatic impairment, so Lorista® should not be used in this group of patients (see the sections ” Pharmacological properties “[subsection “Pharmacokinetics”], “Contraindications”, “Method of use and doses”).

Impaired renal function

Due to RAAS inhibition, some predisposed patients experienced changes in renal function, including the development of renal failure. These changes in renal function may return to normal after discontinuation of treatment.

Some medications that affect the RAAS may increase serum urea and creatinine concentrations in patients with bilateral renal artery stenosis or stenosis of the renal artery of a single kidney. Similar effects have been reported with losartan. Such renal dysfunction may be reversible after discontinuation of therapy. Losartan should be used with caution in patients with bilateral renal artery stenosis or renal artery stenosis of a single kidney.

Special patient groups

Ethnic features

Analysis of data from the entire population of patients included in the clinical study on the effect of losartan on reducing the incidence of the main composite criterion for evaluating the study in patients with hypertension and left ventricular hypertrophy showed that the ability of losartan compared with atenolol to reduce the risk of stroke and myocardial infarction, as well as to reduce the cardiovascular mortality rate in patients with hypertension and left ventricular hypertrophy (by 13.0%) does not apply to black patients, although both treatment regimens effectively reduced blood pressure in these patients. In this study, losartan compared with atenolol reduced the rate of cardiovascular morbidity and mortality in patients with hypertension and left ventricular hypertrophy of all races except the black race. However, in this study, black patients treated with atenolol had a lower risk of developing the main composite criterion for evaluating the study (i. e., a lower combined incidence of cardiovascular mortality, stroke, and myocardial infarction) compared to patients of the same race taking losartan.

Children and teenagers

The efficacy and safety of losartan in children and adolescents under 18 years of age have not been established.

If newborns whose mothers took losartan during pregnancy develop oliguria or hypotension, it is necessary to conduct symptomatic therapy aimed at maintaining blood pressure and renal perfusion. Blood transfusions or dialysis may be required to prevent hypotension and / or maintain kidney function.

Elderly patients

Clinical studies have not revealed any specific features regarding the safety and efficacy of losartan in elderly patients (over 65 years of age).

No studies have been conducted to evaluate the effect of losartan on the ability to drive vehicles and operate mechanisms, but caution should be exercised when using antihypertensive therapy and driving vehicles or working with mechanisms, since dizziness and drowsiness may develop, especially at the beginning of therapy or with an increase in the dose of Lorista®.

Form of production

Film-coated tablets,12.5 mg,25 mg,50 mg,100 mg.

During production at KRKA-RUS LLC, Russia:

7,10 or 14 tablets in a contour cell package made of combined PVC material/PVDH and aluminum foil.

2 contour cell packages (7 tablets each); 3,6,9 contour cell packages (10 tablets each); 1 contour cell package (14 tablets each) together with the instructions for use are placed in a cardboard pack.

During production at JSC “KRKA, D. D., Novo Mesto”, Slovenia:

7,10 or 14 tablets in a blister of combined PVC material/PVDH and aluminum foil.

2 blisters (7 tablets each); 3,6,9 blisters (10 tablets each); 1 blister (14 tablets each) together with the instructions for use are placed in a cardboard pack.

Storage conditions

At a temperature not exceeding 25 ° C, in the original packaging.

Keep out of reach of children.

Shelf

life is 5 years.

Do not use the drug after the expiration date.

Active ingredient

Losartan

Conditions of release from pharmacies

By prescription

Dosage form

Tablets

Purpose

For adults as directed by your doctor

Indications

Prevention of heart attacks and strokes, Diabetic nephropathy, Hypertension, Heart failure