Gliclazide is an oral antihyperglycemic agent used for the treatment of Non-Insulin Dependent Diabetes Mellitus (NIDDM). It belongs to the sulfonylurea class of insulin secretagogues and acts by stimulating β cells of the pancreas to release insulin as well as increases both basal insulin secretion and meal-stimulated insulin release. Gliclazide stimulates the release of insulin from pancreatic β-cells by facilitating Ca⁺² transport across the β-cell membranes. It lowers blood glucose by stimulating the release of insulin from the pancreas, an effect dependent upon functioning β-cells in the pancreatic islets. In type 2 diabetics, gliclazide restores the first peak of insulin secretion in response to glucose and increases the second phase of insulin secretion. Extrapancreatic effects also may play a part in the mechanism of action of oral sulfonylurea hypoglycemic drugs. However, the mechanism of action regarding these effects is still poorly understood. Two extrapancreatic effects shown to be important in the action of Gliclazide are - an increase in insulin sensitivity and a decrease in hepatic glucose production. The anti-oxidant, platelet inhibiting and fibrinolytic actions of Gliclazide involve processes which have been implicated in the pathogenesis of vascular complications of type 2 diabetes. Gliclazide decreases microthrombosis by two mechanisms which may be involved in complications of diabetes:

- A partial inhibition of platelet aggregation and adhesion, with a decrease in the markers of platelet activation (beta thromboglobulin, thromboxane B₂);

- A restoration of the vascular endothelium brinolytic activity with an increase in t-PA activity.