Glinova tablets 2 mg. №30

Description

Glinova Storage:

active substance: glimepiride;

1 tablet contains 1 mg or 2 mg, or 3 mg, or 4 mg of glimepiride,

Glinova excipients:

1 mg tablets: lactose monohydrate, sodium starch glycolate (type A), povidone, polysorbate 80, microcrystalline cellulose, magnesium stearate, iron oxide red (E 172);

2 mg tablets: lactose monohydrate, sodium starch glycolate (type A), povidone, polysorbate 80, microcrystalline cellulose, magnesium stearate, iron oxide yellow (E 172), indigo carmine aluminum varnish (E 132);

3 mg tablets: lactose monohydrate, sodium starch glycolate (type A), povidone, polysorbate 80, microcrystalline cellulose, magnesium stearate, iron oxide yellow (E 172);

4 mg tablets: lactose monohydrate, sodium starch glycolate (type A), povidone, polysorbate 80, microcrystalline cellulose, magnesium stearate, indigo carmine aluminum varnish (E 132).

Glinova Dosage form.

Tablets.

Basic physical and chemical properties:

1 mg tablets – capsule-shaped tablets with a flat surface, with beveled edges, with a line on both sides, light pink;

tablets of 2 mg – capsule-shaped tablets with a flat surface, with beveled edges, with a line on both sides, light green, the presence of inclusions is allowed;

3 mg tablets – capsule-shaped tablets with a flat surface, with beveled edges, with a line on both sides, light yellow;

4 mg tablets – capsule-shaped tablets with a flat surface, with beveled edges, with a line on both sides, light blue.

Pharmacotherapeutic group.

Antidiabetic drugs. Oral hypoglycemic agents, except insulins. Sulfonamides, urea derivatives. Glimepiride.

ATX code A10B B12.

Pharmacological properties.

Pharmacodynamics.

Glimepiride is an oral hypoglycaemic substance that belongs to the group of sulfonylureas. It can be used in non-insulin dependent diabetes mellitus.

Glimepiride acts primarily by stimulating the release of insulin from pancreatic beta cells.

As with other sulfonylureas, this effect is based on increasing the sensitivity of pancreatic cells to physiological glucose stimulation. In addition, glimepiride has a pronounced extrapancreatic effect, which is also characteristic of other sulfonylureas.

Insulin release

Sulfonylurea drugs regulate insulin secretion by closing the ATP-dependent potassium channel located in the membrane of the pancreatic beta cell. Closure of the potassium channel causes depolarization of the beta cell and, as a result of the opening of the calcium channels, leads to an increase in the influx of calcium into the cell, which in turn leads to the release of insulin by exocytosis.

Glimepiride binds at a high rate of substitution to the beta-cell membrane protein associated with the ATP-dependent potassium channel, but its location of binding differs from the usual binding site of sulfonylureas.

Non-pancreatic activity