Glibenclamide was discovered in 1969 and approved for medical use in the United States in 1984.[4][1] It is available as ageneric medication.[3] In 2021, it was the 214th most commonly prescribed medication in the United States, with more than 2million prescriptions.[5][6]
Frequently reported side effects include: nausea, heartburn, weight gain, and bloating.[8] The medication is also a major cause of medication-inducedhypoglycemia. The risk is greater than with othersulfonylureas.[9]
This results in an increase in intracellularcalcium in the pancreaticbeta cell and subsequent stimulation ofinsulin release.[13]
After a stroke, theblood–brain barrier is broken and glibenclamide can reach the central nervous system. Glibenclamide has been shown to bind more efficiently to the ischemic hemisphere.[14] Moreover, under ischemic conditions SUR1, the regulatory subunit of the KATP- and the NCCa-ATP-channels, is expressed in neurons,astrocytes,oligodendrocytes,endothelial cells[15] and by reactivemicroglia.[14]
According to the research, this and other sulphonylurea drugs also have extra hepatic effects. It works by inhibiting the enzyme Carnityl Acyl Transferase I (CAT-I) indirectly, which is present in the mitochondria. This prevents the transport of long chain fatty acids into the mitochondria for beta-oxidation. This prevents hyperglycemia for which it is prescribed.[16][17]
Glibenclamide is available as ageneric medication, is manufactured by many pharmaceutical companies and is sold under many brand names including Gliben-J, Daonil,[19] Diabeta,[20] Euglucon, Gilemal, Glidanil, Glybovin, Glynase, Maninil, Micronase and Semi-Daonil. It is also available in a fixed-dosecombination drug withmetformin that is sold under various trade names, e.g. Bagomet Plus, Benimet, Glibomet, Gluconorm, Glucored, Glucovance, Metglib and many others.[21]
^He Y, Chang Y, Peng Y, Zhu J, Liu K, Chen J, et al. (October 2022). "Glibenclamide Directly Prevents Neuroinflammation by Targeting SUR1-TRPM4-Mediated NLRP3 Inflammasome Activation In Microglia".Molecular Neurobiology.59 (10):6590–6607.doi:10.1007/s12035-022-02998-x.PMID35972671.S2CID242029244.
^"Glyburide".Lexicomp. Wolters Kluwer N.V.Archived from the original on 2 June 2023. Retrieved3 June 2023.
^abOrtega FJ, Gimeno-Bayon J, Espinosa-Parrilla JF, Carrasco JL, Batlle M, Pugliese M, et al. (May 2012). "ATP-dependent potassium channel blockade strengthens microglial neuroprotection after hypoxia-ischemia in rats".Experimental Neurology.235 (1):282–296.doi:10.1016/j.expneurol.2012.02.010.hdl:2445/34278.PMID22387180.S2CID4828181.
^Chen S, Ogawa A, Ohneda M, Unger RH, Foster DW, McGarry JD (July 1994). "More direct evidence for a malonyl-CoA-carnitine palmitoyltransferase I interaction as a key event in pancreatic beta-cell signaling".Diabetes.43 (7):878–883.doi:10.2337/diab.43.7.878.PMID8013751.S2CID25251669.
^Lehtihet M, Welsh N, Berggren PO, Cook GA, Sjoholm A (August 2003). "Glibenclamide inhibits islet carnitine palmitoyltransferase 1 activity, leading to PKC-dependent insulin exocytosis".American Journal of Physiology. Endocrinology and Metabolism.285 (2):E438 –E446.doi:10.1152/ajpendo.00057.2003.PMID12684219.S2CID175394.
