As a Supplement to diet and exercise for patients with insulin-dependent type II diabetes: if monotherapy with sulfonylureas or Metformin does not provide an appropriate level of glycemic control; when replacing combined therapy with sulfonylureas and Metformin.
active ingredients: metformin hydrochloride, glimepiride;
1 tablet contains metformin hydrochloride (sustained release) 500 mg and glimepiride 1 mg metformin hydrochloride (sustained release) 500 mg and glimepiride 2 mg;
Duglimax excipients (tablets 500 mg / 2 mg): sodium carboxymethyl cellulose, hypromellose, microcrystalline cellulose, magnesium stearate, lactose, croscarmellose sodium, hydroxypropyl cellulose, Pigment Blend PO-51323 green.
Duglimax Dosage form
Basic physical and chemical properties:
Duglimax ® (500 mg / 2 mg): two-layer, capsule-like shape, biconvex green on one side, white on the other, smooth on both sides; marbling is allowed.
Antidiabetic drugs. A combination of oral hypoglycemic drugs.
ATX code А10В D02.
Glimepiride is a substance with hypoglycemic activity when administered orally and belongs to the group of sulfonylurea derivatives. It can be used for non-insulin dependent diabetes mellitus.
The effect of glimepiride is realized by stimulating the release of insulin from β-cells of the pancreas. Like other sulfonylurea derivatives, it increases the sensitivity of pancreatic β-cells to physiological glucose stimulation. In addition, glimepiride, like other sulfonylurea derivatives, is likely to have a pronounced popancreatic effect.
Sulfonylurea regulates insulin secretion by closing ATP-dependent potassium channels on the β-cell membrane. This closure leads to depolarization of the cell membrane, as a result of which calcium channels open and a large amount of calcium enters the cell.
It stimulates the release of insulin by exocytosis
Glimepiride binds with high affinity to a protein on the β-cell membrane associated with ATP-sensitive potassium channels, but not at the site to which sulfonylurea is usually attached.
Posapancreatic action consists, in particular, in increasing the sensitivity of peripheral tissues to insulin and decreasing the uptake of insulin by the liver.
The transfer of glucose from the blood to peripheral muscle and adipose tissue occurs through special transport proteins localized on the cell membrane. It is the transport of glucose to these tissues that is the stage that limits the rate of glucose uptake. Glimepiride very quickly increases the number of active glucose transporters on the plasma membrane of muscle and fat cells, thereby stimulating glucose uptake.
Glimepiride increases the activity of phospholipase C, specific to glycosyl-phosphatidylinositol, and this may be associated with an increase in lipogenesis and glycogenesis observed in isolated fat and muscle cells under the action of this agent.
Glimepiride inhibits the formation of glucose in the liver by increasing the intracellular concentration of fructose-2,6-diphosphate, which in turn inhibits gluconeogenesis.
As an adjunct to diet and exercise for people with insulin-dependent type II diabetes:
if monotherapy with sulfonylureas or metformin does not provide an adequate level of glycemic control;
when replacing combination therapy with sulfonylureas and metformin.
Insulin-dependent type I diabetes mellitus (eg, diabetes with a history of ketonemia), diabetic ketonemia, diabetic coma, and precoma.
Hypersensitivity to any of the excipients that make up this drug, or sulfonylurea derivatives, sulfonamides or biguanides.
Liver failure, severe liver dysfunction or hemodialysis patients. In severely impaired liver and kidney function, insulin should be switched to achieve proper control of the patient’s blood sugar level.
Renal impairment, kidney disease, or impaired renal function (as evidenced by, for example, an increase in plasma creatinine of ≥ 1.5 mg / dL in men and ≥ 1.4 mg / dL in women, or impaired creatinine clearance), which can also be caused by conditions such as cardiovascular collapse (shock), acute myocardial infarction, and septicemia.
Congestive heart failure, which requires medication; recent myocardial infarction, cardiovascular collapse or respiratory disorder.
Examination using radiological methods that use intravascular administration of iodine-containing contrast media (for example, intravenous urography, intravenous cholangiography, angiography, and computed tomography (CT) using intravascular contrast media). The use of examination methods with intravascular administration of iodine-containing contrast agents can lead to acute renal dysfunction and be accompanied by the development of lactic acidosis in patients receiving metformin. Therefore, the use of the drug Duglimax ® in patients who are planning any of these examinations should be temporarily canceled 48 hours before the procedure and the drug should be resumed no earlier than 48 hours after the procedure and only after a reassessment of renal function and confirmation that it is within norms.
Severe infections, conditions before and after surgery. The use of Duglimax ® must be temporarily canceled for the duration of any surgical procedure (with the exception of minor procedures that are not accompanied by restriction of food and fluid intake). Do not resume the use of the drug until the patient’s ability to receive is restored and until the results of the assessment of renal function demonstrate that it is within normal limits.
Malnutrition, starvation or exhaustion, also hypofunction of the pituitary or adrenal glands.
Liver dysfunction (since dysfunction of the liver is associated with isolated cases of lactic acidosis, the use of this drug should be avoided in patients with clinical or laboratory signs of liver disease), pulmonary infarction, severe pulmonary dysfunction and other conditions that are likely to be accompanied by the onset of hypoxemia ( such as heart or respiratory failure, recent myocardial infarction, shock), excessive alcohol consumption, dehydration, gastrointestinal disorders, including diarrhea and vomiting.