Edarbiclor (azilsartan medoxomil, chlorthalidone) coated tablets 40 mg/25 mg. №28

Description

Edarbiclor Storage:

active substances: azilsartan medoxomil, chlorthalidone.

1 tablet of 40 mg / 12.5 mg contains 42.68 mg of azilsartan medoxomil potassium (equivalent to 40 mg of azilsartan medoxomil) and 12.5 mg of chlorthalidone;

1 tablet of 40 mg / 25 mg contains 42.68 mg of azilsartan medoxomil potassium (equivalent to 40 mg of azilsartan medoxomil) and 25 mg of chlorthalidone;

Edarbiclor Excipients:

mannitol (E 421), microcrystalline cellulose, fumaric acid, sodium hydroxide, hydroxypropylcellulose, crospovidone, magnesium stearate, hypromellose 2910, talc, titanium dioxide (E 171), iron oxide red (black) (E 172) F1.

Edarbiclor Dosage form.

Film-coated tablets.

Basic physical and chemical properties:

40 mg / 12.5 mg tablets: light pink, round, film-coated tablets marked “A / C” and “40 / 12.5” on one side;

40 mg / 25 mg tablets: Pink, round, film-coated tablets marked “A / C” and “40/25” on one side.

Pharmacotherapeutic group.

Angiotensin II antagonists and diuretics.

ATX code C09D A09.

Pharmacological properties.

Mechanism of action. The active substances in EdarbiClor® affect two separate mechanisms involved in the regulation of blood pressure.

Thiazide and thiazide-like diuretics act primarily on the distal part of the renal tubules (initial part of the convoluted tubule), inhibiting the reabsorption of NaCl ions (counteracting the co-transporter Na + Cl‒) and promoting the reabsorption of Ca ++ (by an unknown mechanism). Increased excretion of Na + and water to the cortical collecting tube and / or increased flow rate causes increased secretion and excretion of K + and H +.

Azilsartan medoxomil. Angiotensin II is formed from angiotensin I due to a reaction catalyzed by angiotensin-converting enzymes (ACE, kinase II). Angiotensin II is the major pressor agent of the renin-angiotensin system, which affects vasoconstriction, stimulation of aldosterone synthesis and release, cardiac stimulation and renal sodium reabsorption. Azilsartan medoxomil is an oral preparation that is rapidly converted by the esterase to the active substance azilsartan during absorption.

Azilsartan blocks the vasoconstrictor and aldosterone-secretory effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Thus, its action does not depend on the routes of synthesis of angiotensin II.

The AT2 receptor is also present in many tissues, but there is no evidence that this receptor is associated with cardiovascular homeostasis. Azilsartan has an affinity for the AT1 receptor that is 10,000 times higher than the AT2 receptor.

Blockade of the renin-angiotensin system by ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the breakdown of bradykinin, a reaction that is catalyzed by ACE inhibitors. Because azilsartan does not inhibit ACE inhibitors (kinase II), it should not affect bradykinin levels. It is still unknown whether this difference is clinically relevant. Azilsartan does not bind to or block other receptors or ion channels that are important for cardiovascular regulation.

Indication.

Treatment of hypertension to lower blood pressure:

– in patients whose blood pressure is not adequately controlled by monotherapy;

– as initial therapy for patients in need of combination antihypertensive therapy.

Contraindication.

– Hypersensitivity to the active substance or other components of the drug;

– anuria;

– therapy-resistant hypokalemia, hypercalcemia, hyponatremia;

– severe hepatic and renal impairment (creatinine clearance <30 ml / min);

– cholestasis, obstruction of the biliary tract;

– pregnancy and breastfeeding;

– do not use together with allyl-containing drugs in patients with diabetes mellitus;

– children’s age;

– Contraindicated for women who are planning a pregnancy.