Amlodipine tablets 5 mg. №20

active substance: amlodipine;

1 tablet contains amlodipine besylate 6.935 mg, which is equivalent to amlodipine 5 mg;

excipients: microcrystalline cellulose, magnesium stearate, calcium hydrogen phosphate, sodium starch glycolate (type A).

Tablets.

The main physical and chemical properties: flat-cylindrical tablets with beveled edges and a line, white or almost white in color.

Selective calcium antagonists with a predominant effect on blood vessels. ATX code C08S A01.

Amlodipine is a calcium antagonist (dihydropyridine derivative) that blocks the influx of calcium ions to the myocardium and smooth muscle cells.

The mechanism of hypotensive action of amlodipine is caused by a direct relaxing effect on vascular smooth muscles. The exact mechanism of the antianginal effect of amlodipine is not well defined, but the following effects play a role.

1. Amlodipine dilates peripheral arterioles and thus reduces peripheral resistance (afterload). As the heart rate remains stable, the reduction in cardiac workload leads to a reduction in energy consumption and myocardial oxygen demand.
2. Dilation of the main coronary arteries and coronary arterioles (normal and ischemic) may also play a role in the mechanism of action of amlodipine. Such expansion increases myocardial oxygen saturation in patients with coronary artery spasm (Prinzmetal’s angina or variant angina).

In patients with arterial hypertension, the use of the drug 1 time per day provides a clinically significant decrease in blood pressure within 24 hours in both lying and standing positions. Because of the slow onset of action of amlodipine, acute arterial hypotension is usually not observed.

In patients with angina pectoris, using one daily dose of the drug increases the total time of physical exertion, the time to the onset of angina pectoris, and the time to 1 mm depression of the ST segment. The drug reduces the frequency of angina attacks and reduces the need to use nitroglycerin.

Amlodipine is not associated with any adverse metabolic effects or changes in plasma lipids and can be used in patients with asthma, diabetes and gout.

Absorption/distribution. After oral administration of therapeutic doses, amlodipine is gradually absorbed into the blood plasma. The absolute bioavailability of the unchanged molecule is approximately 64-80%. The maximum concentration in blood plasma is reached within 6-12 hours after application. The volume of distribution is approximately 21 l/kg; acid dissociation constant (pKa) of amlodipine is 8.6. In vitro studies have shown that the binding of amlodipine to blood plasma proteins is approximately 97.5%.

The simultaneous use of food does not affect the absorption of amlodipine.

Metabolism/excretion. The half-life from blood plasma is approximately 35-50 hours. Equilibrium concentration in blood plasma is reached after 7-8 days of continuous use of the drug. Amlodipine is mainly metabolized with the formation of inactive metabolites. About 60% of the administered dose is excreted in the urine, about 10% of which is unchanged amlodipine.

Elderly patients. The time to reach steady-state concentrations of amlodipine in blood plasma is similar in elderly patients and in adult patients. The clearance of amlodipine is usually slightly reduced, which in elderly patients leads to an increase in the area under the curve “concentration/time” (AUC) and the half-life of the drug.

Patients with impaired renal function. Amlodipine is extensively biotransformed to inactive metabolites. 10% of amlodipine is excreted unchanged in the urine. Changes in the concentration of amlodipine in the blood plasma do not correlate with the degree of renal dysfunction. In patients with impaired renal function, the usual doses of amlodipine can be used. Amlodipine is not removed by dialysis.

Patients with impaired liver function. Information on the use of amlodipine in patients with impaired liver function is very limited. In patients with hepatic insufficiency, the clearance of amlodipine is reduced, which leads to an increase in the duration of the half-life and an increase in AUC by approximately 40-60%.

Children. Typically, oral clearance in children aged 6 to 12 years and 13 to 17 years was 22.5 and 27.4 L/h, respectively, for boys and 16.4 and 21.3 L/h, respectively, for girls. There is considerable variability in exposure between patients. Information on patients under 6 years of age is limited.

• Arterial hypertension.
• Chronic stable angina pectoris.
• Vasospastic angina (Prinzmetal’s angina).