Glibenclamide (Glyburide) is an antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.

Administered intravenously at a dose of 25 mg/kg, Glyburide increased sodium (Na) ion excretion by 350% one hour after treatment, without affecting potassium (K) ion excretion, glomerular filtration rate, mean arterial pressure, or heart rate. In awake rats subjected to a saline load, Glyburide dose-dependently increased urinary sodium excretion, while urinary potassium excretion remained largely unchanged.

Glyburide enhances the apparent affinity of scavenger receptor class B type I (SR-BI) for high-density lipoprotein (HDL) binding in insulin-secreting cells. It inhibits SR-BI-mediated selective lipid uptake and efflux, with potency similar to its inhibition of ABCA1 (IC50 approximately 275-300 mM). Regardless of the pre-existing relaxation level, Glyburide can also reverse the relaxation induced by pinacidil. At a concentration of 0.03 mM, Glyburide blocks ATP-modulated potassium channels in insulin-secreting cells. It causes a concentration-dependent increase in the IC50 values for BRL34915 and diazoxide, eliminating the relaxation response to minoxidil sulfate. Doses of Glyburide ranging from 10-500 nM proportionately inhibit the relaxation time brought about by potassium channel openers.