Glimepirid-TEVA tablets 3 mg. №30


Manufacturer: Israel

Type II diabetes in adults, if the blood sugar level can not be maintained only by diet, exercise and weight loss.



Glimepirid-TEVA 3 mg Composition
active substance: glimepiride;

1 tablet contains glimepiride 2 mg;

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

Glimepirid-TEVA 3 mg  Dosage form

Basic physical and chemical properties: round green tablets interspersed, with a break line on each side. On one side of the tablet – embossing “9” on one side and embossing “3” on the other side of the fracture line. On the other side of the tablet – embossing “72” on one side and embossing “55” on the other side of the fracture line.

Pharmacotherapeutic group
Oral hypoglycemic agents. Sulfonamides, urea derivatives. ATX code A10B B12.

Glimepiride-Teva is a hypoglycemic substance that is active when taken orally, belongs to the group of sulfonylurea derivatives and can be used in non-insulin-dependent diabetes mellitus.

The drug works mainly by stimulating the release of insulin from the beta cells of the pancreas. As in the case of other sulfonylurea derivatives, this effect is based on an increase in the response of the beta cells of the pancreas to physiological glucose stimulation. In addition, Glimepiride-Teva has a pronounced effect not only on the pancreas, which is also inherent in other sulfonylurea derivatives.

Release of insulin. Sulfonylurea derivatives regulate insulin secretion by closing the ATP-sensitive potassium channel in the beta cell membrane. Potassium channel closure induces beta cell depolarization and leads to the opening of calcium channels and increased calcium influx into the cell, which leads to the release of insulin by exocytosis.

Glimepiride-Teva binds with a high rate of substitution to a beta-cell membrane protein bound to ATP-sensitive potassium channels, but the location of the binding site differs from the usual binding site for sulfonylurea derivatives.

Posapancreatic activity. The action of the drug in places other than the pancreas is to improve the sensitivity of peripheral tissues to insulin and reduce the 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 on the cell membrane. The transport of glucose to these tissues is limited by the rate of the glucose utilization step. Glimepiride-Teva very quickly increases the number of active glucose transporting molecules on the plasma membranes of muscle and adipose tissue cells, which leads to the stimulation of glucose uptake.

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

Insulin-dependent diabetes;
diabetic coma;
diabetic ketoacidosis;
severe impairment of kidney or liver function;
hypersensitivity to the drug or to any component of the drug, other sulfonylurea derivatives or other sulfonamide drugs.
In case of severe impairment of kidney or liver function, it is necessary to transfer the patient to insulin.