Amaril (glimepiride) tablets 2 mg. №30

active ingredient: glimepiride;

1 tablet contains glimepiride 2 mg;

excipients: lactose, sodium starch (type A), povidone, microcrystalline cellulose, magnesium stearate, iron oxide yellow (E172), indigo aluminum lacquer (E 132)

Hypoglycemic agents, with the exception of insulins. Sulfonamides, urea derivatives. ATX code A10B B12.

Glimepiride is an orally active hypoglycemic agent that belongs to the sulfonylurea group. It can be used for non-insulin-dependent diabetes mellitus.

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

As with other sulfonylurea drugs, this effect is based on an increase in the sensitivity of pancreatic cells to physiological stimulation with glucose. In addition, glimepiride has a pronounced post-pancreatic effect, which is also characteristic of other sulfonylurea drugs.

Release of insulin. Sulfonylureas regulate insulin secretion by closing the ATP-dependent potassium channel located in the pancreatic beta cell membrane. Closing the potassium channel causes depolarization of the beta cell and, by opening calcium channels, leads to an increase in calcium influx 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 the location of its binding site differs from the usual binding site for sulfonylurea drugs.

Postpancreatic activity. Post-pancreatic effects include, for example, improved sensitivity of peripheral tissues to insulin and reduced utilization of insulin by the liver.

Utilization of blood glucose by peripheral tissues (muscle and fat) occurs with the help of special transport proteins located in the cell membrane. The transport of glucose into these tissues is limited by the rate of the glucose utilization step. Glimepiride very quickly increases the number of active glucose transport molecules on the plasma membranes of muscle and adipose tissue cells, which leads to stimulation of glucose uptake.

Glimepiride increases the activity of glycosylphosphatidylinositol-specific phospholipase C, with which drug-induced lipogenesis and glycogenesis can be correlated in isolated muscle and fat cells.

Glimepiride inhibits hepatic glucose production by increasing intracellular concentrations of fructose-2,6-bisphosphate, which in turn inhibits gluconeogenesis.

General characteristics. In healthy volunteers, the minimum effective oral dose was approximately 0.6 mg. The effect of glimepiride is dose-dependent and reproducible. The physiological response to acute physical exertion, that is, a decrease in insulin secretion, remains under the action of glimepiride.

There was no significant difference in the effect of glimepiride when taking the drug 30 minutes before a meal or immediately before a meal. In patients with diabetes mellitus, proper metabolic control within 24 hours can be achieved by taking the drug once a day.

Although the hydroxylated metabolite causes a slight but significant decrease in blood glucose levels in healthy individuals, this is only a minor component of the overall effect of the drug.

Use in combination with metformin. One study demonstrated improvement in metabolic control with concomitant therapy with glimepiride compared with metformin alone in patients whose diabetes is not adequately controlled by the highest doses of metformin.

Use in combination with insulin. Data on the use of the drug in combination with insulin are limited. In patients whose diabetes is not adequately controlled with maximum doses of glimepiride, concomitant insulin treatment may be initiated. In two studies, this combination achieved the same improvement in metabolic control as with insulin alone; however, combination therapy requires a lower average dose of insulin.

Special categories of patients. Children, including teenagers. In a 24-week clinical study with active control (glimepiride up to 8 mg per day or metformin at a dose up to 2000 mg per day), 285 children (aged 8-17 years) with type II diabetes participated.

Both glimepiride and metformin resulted in a significant reduction in HbA1c from baseline (glimepiride 0.95 (SD 0.41) metformin 1.39 (SD 0.40)). However, glimepiride has not been shown to be more effective than metformin in terms of mean change in HbA1c from baseline. The difference between the two treatments was 0.44% in favor of metformin. The upper limit (1.05) of the 95% confidence interval for this difference was no less than the 0.3% limit of non-inferiority.

No new safety concerns have been identified in pediatric patients compared with adult patients with type II diabetes mellitus in glimepiride treatment. There are no data on long-term efficacy and safety in children.

Type II diabetes mellitus in adults when blood sugar cannot be maintained by diet, exercise, and weight loss alone.

Amaryl is not intended for the treatment of insulin-dependent diabetes mellitus, diabetic ketoacidosis, diabetic coma. The use of the drug is contraindicated in patients with severely impaired renal or hepatic function. In case of severe impairment of kidney or liver function, the patient must be transferred to insulin.

Amaryl should not be taken by patients with hypersensitivity to glimepiride or to any auxiliary ingredient that is part of the drug, to other sulfonylurea derivatives or sulfanilamide drugs (risk of hypersensitivity reactions).