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For concomitant use with insulin for the treatment of noninsulin-dependent (type 2) diabetes mellitus.
The mechanism of action of glimepiride in lowering blood glucose appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells, and increasing sensitivity of peripheral tissues to insulin. Glimepiride likely binds to ATP-sensitive potassium channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Membrane depolarization stimulates calcium ion influx through voltage-sensitive calcium channels. This increase in intracellular calcium ion concentration induces the secretion of insulin.
Severe hypoglycemic reactions with coma, seizure, or other neurological impairment.
Completely (100%) absorbed following oral administration.
Approximately 5 hours following single dose.
* 21.8 ± 13.9 L [Volunteers] * 19.8 ± 12.7 L [Patients with Type 2 diabetes, Single Dose] * 37.1 ± 18.2 L [Patients with Type 2 diabetes, Multiple Dose]
* 52.1 +/- 16.0 mL/min [Normal subjects with single oral dose] * 48.5 +/- 29.3 mL/min [Patients with Type 2 diabetes, with single oral dose] * 52.7 +/- 40.3 mL/min [Patients with Type 2 diabetes, with multiple oral dose] * 47.8 mL/min [healthy after intravenous (IV) dosing]