Equamer capsules 10mg + 20mg + 20mg №30

Release form, composition and packaging

Capsules solid gelatin, size No. 1, light pink color; the contents of the capsules are 1 round, white biconvex pill (contains lisinopril and amlodipine) and 1 round, biconvex pill coated with a yellow film shell (contains rosuvastatin).

Excipients: microcrystalline cellulose, type 12 - 60.41 mg, microcrystalline cellulose, type 101 - 45.27 mg, lactose monohydrate - 48.1 mg, sodium carboxymethyl starch - 9.5 mg, Magnesium hydroxide - 7.5 mg, magnesium stearate - 2 mg, Opadry II yellow - 2 mg ( polyvinyl alcohol 40%, titanium dioxide 23.5%, macrogol-3350 20.2%, talc 14.8%, iron dye yellow oxide 1.5%), hard gelatin capsule - 76 mg (dye blue patented 0.00022%, dye azorubine 0.03684%, dye sunset azure yellow 0.0204%, titanium dioxide 3.7037%, gelatin up to 100%).

Capsules solid gelatin, size No. 1, pink; the contents of the capsules - 1 round, white biconvex pill (contains lisinopril and amlodipine) and 2 round, biconvex tablets, film-coated yellow (contain rosuvastatin).

Excipients: microcrystalline cellulose, type 12 - 86.41 mg, microcrystalline cellulose, type 101 - 45.27 mg, lactose monohydrate - 96.2 mg, carboxymethyl starch sodium - 17.5 mg, magnesium hydroxide - 15 mg, magnesium stearate - 3 mg, Opadry II yellow - 4 mg ( polyvinyl alcohol 40%, titanium dioxide 23.5%, macrogol-3350 20.2%, talc 14.8%, iron dye yellow oxide 1.5%), hard gelatin capsule - 76 mg (azorubine dye 0.16%, titanium dioxide 1.8519%, gelatin up to 100%).

Capsules solid gelatin, size No. 1, purple; the contents of the capsules - 2 round, biconvex pills of white color (contain lisinopril and amlodipine) and 1 round, biconvex tablet, coated with a yellow film membrane (contains rosuvastatin).

Excipients: microcrystalline cellulose, type 12 - 94.82 mg, microcrystalline cellulose, type 101 - 90.54 mg, lactose monohydrate - 48.1 mg, carboxymethyl starch sodium - 11 mg, magnesium hydroxide - 7.5 mg, magnesium stearate - 3 mg, Opadry II yellow - 2 mg ( polyvinyl alcohol 40%, titanium dioxide 23.5%, macrogol-3350 20.2%, talc 14.8%, iron dye yellow oxide 1.5%), hard gelatin capsule - 76 mg (dye azorubine 0.0882%, indigo carmine 0.0284%, titanium dioxide 2.2056%, gelatin up to 100%).

Capsules solid gelatin, size No. 0, dark purple; the contents of the capsules - 2 round, biconvex pills of white color (contain lisinopril and amlodipine) and 2 round, biconvex tablets, film-coated yellow (contain rosuvastatin).

Excipients: microcrystalline cellulose, type 12 - 120.82 mg, microcrystalline cellulose, type 101 - 90.54 mg, lactose monohydrate - 96.2 mg, sodium carboxymethyl starch - 19 mg, magnesium hydroxide - 15 mg, magnesium stearate - 4 mg, Opadry II yellow - 4 mg ( polyvinyl alcohol 40%, titanium dioxide 23.5%, macrogol-3350 20.2%, talc 14.8%, iron dye yellow oxide 1.5%), hard gelatin capsule - 97 mg (dye blue patented 0.02933%, dye azorubine 0.3067%, dye sunflower yellow dye 0.02355%, titanium dioxide 3.7037%, gelatin up to 100%).

Mechanism of action

Combined antihypertensive and lipid-lowering drug. The composition of the drug Equamer^® There are three active ingredients - amlodipine, lisinopril and rosuvastatin. The mechanism of action of the drug Equamer^® based on the pharmacological properties of active substances.

Amlodipine

Derivative of dihydropyridine - a blocker of slow calcium channels (BMCC), has a hypotensive and antianginal effect. Blocks slow calcium channels, reduces transmembrane transition of calcium ions into the cell (to a greater extent in vascular smooth muscle cells than in cardiomyocytes).

Antianginal action due to the expansion of coronary and peripheral arteries and arterioles:

- with angina reduces the severity of myocardial ischemia; expanding peripheral arterioles, reduces round focal disease, reduces afterload on the heart, reduces myocardial oxygen demand;

- expanding the coronary arteries and arterioles in the unchanged and ischemic areas of the myocardium, increases the flow of oxygen into the myocardium (especially in vasospastic angina); prevents spasm of the coronary arteries (including caused by smoking).

In patients with stable angina, a single daily dose increases exercise tolerance, slows the development of strokes and ischemic depression of the ST segment, reduces the frequency of strokes and the consumption of Nitroglycerin and other nitrates.

It has a long dose-dependent antihypertensive effect. The antihypertensive effect is due to the direct vasodilating effect on vascular smooth muscle. In case of arterial hypertension, a single dose provides a clinically significant reduction in blood pressure for 24 hours (in the position of the patient lying and standing).

Orthostatic hypotension is quite rare with amlodipine. Amlodipine does not cause a decrease in exercise tolerance, left ventricular ejection fraction. Reduces the degree of hypertrophy of the left ventricular myocardium. Does not affect the contractility and conductivity of the myocardium, does not cause a reflex increase in heart rate, inhibits platelet aggregation, increases GFR, has a weak natriuretic effect. In diabetic nephropathy does not increase the severity of microalbuminuria. It does not have any adverse effect on the metabolism and plasma lipid concentration, it can be used in the treatment of patients with bronchial asthma, diabetes mellitus and gout. A significant decrease in blood pressure is observed after 6-10 hours, the duration of the effect is 24 hours.

In patients with diseases of the cardiovascular system (including coronary atherosclerosis with damage to one vessel and up to stenosis of 3 or more arteries, atherosclerosis of the carotid arteries) after myocardial infarction, percutaneous transluminal coronary angioplasty (PTCA) or in patients with angina pectoris, amlodipine. carotid intima-media complex, reduces mortality from myocardial infarction, stroke, PTCA,coronary artery bypass surgery; leads to a decrease in the number of hospitalizations for unstable angina and the progression of chronic heart failure (CHF); reduces the frequency of interventions aimed at restoring coronary blood flow.

It does not increase the risk of death or the development of complications and deaths in patients with CHF (III-IV functional class according to the NYHA classification) during therapy with Digoxin , diuretics and ACE inhibitors. In patients with CHF (III-IV functional class according to the NYHA classification) of non-ischemic etiology when using amlodipine, there is a likelihood of pulmonary edema.

Lisinopril

An ACE inhibitor, reduces the formation of angiotensin II from angiotensin I. A decrease in the concentration of angiotensin II leads to a direct decrease in the release of aldosterone. Reduces the degradation of bradykinin and increases prostaglandin synthesis. Reduces the OPSS, blood pressure, preload, pressure in the pulmonary capillaries, causes an increase in the minute volume of blood and an increase in myocardial tolerance to physical stress in patients with CHF. Expands arteries to a greater extent than veins. Some effects are due to effects on the tissue renin-angiotensin system. With prolonged use, hypertrophy of the myocardium and the walls of resistive arteries is reduced.

Improves blood supply to ischemic myocardium.

ACE inhibitors prolong life expectancy in patients with CHF, slow down the progression of left ventricular dysfunction in patients who have had a myocardial infarction without clinical manifestations of heart failure.

Onset of action - 1 hour after ingestion. The maximum hypotensive effect is determined after 6-7 hours and lasts for 24 hours. With arterial hypertension, the effect is observed in the first days after the start of treatment, a stable action develops after 1-2 months. With a sharp cancellation of lisinopril, no marked increase in blood pressure was observed. In addition to lowering blood pressure, lisinopril reduces albuminuria. In patients with hyperglycemia, it helps normalize the function of the damaged glomerular endothelium. Lisinopril does not affect the concentration of glucose in the blood in patients with diabetes mellitus and does not lead to an increase in hypoglycemia.

Rosuvastatin

Selective, competitive inhibitor of HMG-CoA reductase, an enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol. The main target of rosuvastatin is the liver, where cholesterol (Xc) is synthesized and LDL catabolism occurs.

Rosuvastatin increases the number of LDL receptors on the surface of hepatocytes, increasing the uptake and catabolism of LDL, which in turn leads to inhibition of the synthesis of VLDL, thereby reducing the total amount of LDL and VLDL.

Rosuvastatin reduces the elevated concentration of LDL cholesterol (Xc-LDL), total cholesterol (Xc) and triglycerides (TG) and increases the concentration of high-density lipoprotein cholesterol (Xc-HDL), and also decreases the concentration of apolipoprotein B (ApoV) Xc-neLPVP - VLDL, TG-VLDL and increases the concentration of apolipoprotein AI (ApoA-I) (see Tables 1 and 2), reduces the ratio of Xc-LDL / Xc-HDL, total Xs / Xc-HDL, Xs-non-LPVP / Xs- HDL and apoB / ApoA-I ratio.

The therapeutic effect appears within the first week after the start of rosuvastatin therapy and after 2 weeks of treatment reaches 90% of the maximum possible. The maximum therapeutic effect is usually achieved by week 4 and is maintained with regular use.

Table 1. Dose-dependent effect in patients with primary hypercholesterolemia (type IIa and IIb according to Fredrickson's classification) (average corrected percentage change compared with baseline)