Glanil^®

Consumer | Pharmacists

GLANIL, Pharmacist Data Sheet

^{Data Sheets}

Presentation   30 and 100 tablets of 5mg   Dosage and Administration:   By mouth, adult, initially 5mg (elderly patients 2.5 mg) adjusted according to response; up to a max. 15-20mg daily; taken with breakfast

Description

Glanil^® Gilbenclamide is a potent, second-generation, oral sulfonylurea antidiabetic agent used as an adjunct to diet to lower blood glucose levels in patients with diabetes mellitus type II. Glanil® Gilbenclamide is 150 times more potent than tolbutamide on a molar basis. Glanil^® Gilbenclamide is also twice as potent as the related second-generation agent glipizide.

Although mechanisms are similar, there are quantitative differences in pharmacokinetic properties that distinguish one sulfonylurea from another. In vitro, acidic drugs such as warfarin and aspirin displace sulfonylureas with ionic binding (i.e., older agents) to a much greater extent than sulfonylureas with non-ionic binding (e.g., Gilbenclamide).

Mechanism of Action:

The hypoglycemic action of Glanil^® Gilbenclamide is due to stimulation of pancreatic islet cells, which results in an increase in insulin secretion. Sulfonylureas are believed to bind to ATP-sensitive potassium-channel receptors on the pancreatic cell surface, thereby reducing potassium conductance and causing depolarisation of the membrane. Depolarisations stimulate calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin. The drug is not effective in the absence of functioning beta-cells, as occurs in diabetes mellitus type I, or when the number of viable beta-cells is low, as occurs in severe cases of diabetes mellitus type II. 

Prolonged administration of Glanil^® Gilbenclamide also produces extrapancreatic effects that contribute to its hypoglycemic activity. These effects include reduction of basal hepatic glucose production and an enhanced peripheral sensitivity to insulin secondary to an increase in insulin receptors or to changes in the events that follow insulin-receptor binding. The relative importance of each of these actions to the overall therapeutic effect of the drug will vary among oral antidiabetic agents and from patient to patient, which may account for the variability in potency among these drugs. Like glipizide, Gilbenclamide exhibits mild diuretic actions but does not affect uric acid concentrations.

Pharmacokinetics:

Glanil^® Gilbenclamide is administered orally, and is rapidly and completely absorbed from the GI tract. The onset of action occurs within 2 hours, with a maximal decrease in serum glucose occurring within 3 to 4 hours. After repeated administration in diabetics, there is no significant correlation between dose and serum drug concentration. Glanil^® Gilbenclamide is highly protein-bound via non-ionic binding, which differs from the ionic protein binding observed with first generation sulfonylureas. Glanil^® Gilbenclamide is metabolised completely in the liver to 2 metabolites, which are only weakly active. Both unchanged drug and metabolites are excreted equally in the urine and faeces. The elimination half-life of the drug is 10 hours, and the duration of action is 24 hours in patients with normal renal function.