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Glipizide - Wikipedia

From Wikipedia, the free encyclopedia

Chemical compound

Pharmaceutical compound

Glipizide Trade names Glucotrol, Glucotrol XL, others AHFS/Drugs.com Monograph MedlinePlus a684060 License data Pregnancy
category
Routes of
administration
By mouth Drug class Sulfonylurea ATC code Legal status Bioavailability 100% (regular formulation)
90% (extended release) Protein binding 98 to 99% Metabolism Liver hydroxylation Elimination half-life 2 to 5 hours Excretion Kidney and fecal IUPAC name CAS Number PubChem CID IUPHAR/BPS DrugBank ChemSpider UNII KEGG ChEBI ChEMBL CompTox Dashboard (EPA) ECHA InfoCard 100.044.919 Formula C21H27N5O4S Molar mass 445.54 g·mol−1 3D model (JSmol) Melting point 208 to 209 °C (406 to 408 °F) SMILES InChI  NY (what is this?)  (verify)

Glipizide, sold under the brand name Glucotrol among others, is an anti-diabetic medication of the sulfonylurea class used to treat type 2 diabetes.[1][2] It is used together with a diabetic diet and exercise.[1][2] It is not indicated for use by itself in type 1 diabetes.[1][2] It is taken by mouth.[1][2] Effects generally begin within half an hour and can last for up to a day.[1]

Common side effects include nausea, diarrhea, low blood sugar, and headache.[1] Other side effects include sleepiness, skin rash, and shakiness.[3] The dose may need to be adjusted in those with liver or kidney disease.[1] Use during pregnancy or breastfeeding is not recommended.[3] It works by stimulating the pancreas to release insulin and increases tissue sensitivity to insulin.[1]

Glipizide was approved for medical use in the United States in 1984.[1] It is available as a generic medication.[1] In 2022, it was the 42nd most commonly prescribed medication in the United States, with more than 14 million prescriptions.[4][5]

Mechanism of action[edit]

Glipizide sensitizes the beta cells of pancreatic islets of Langerhans insulin response, meaning that more insulin is released in response to glucose than would be without glipizide ingestion.[2] Glipizide acts by partially blocking potassium channels among beta cells of pancreatic islets of Langerhans. By blocking potassium channels, the cell depolarizes, which results in the opening of voltage-gated calcium channels. The resulting calcium influx encourages insulin release from beta cells.[6]

It was patented in 1969, and approved for medical use in 1971.[7] Glipizide was approved for medical use in the United States in 1984.[1]

Ion channel modulators Calcium VDCCsTooltip Voltage-dependent calcium channels Blockers Activators Potassium VGKCsTooltip Voltage-gated potassium channels Blockers Activators IRKsTooltip Inwardly rectifying potassium channel Blockers Activators KCaTooltip Calcium-activated potassium channel Blockers Activators K2PsTooltip Tandem pore domain potassium channel Blockers Activators Sodium VGSCsTooltip Voltage-gated sodium channels Blockers Activators ENaCTooltip Epithelial sodium channel Blockers Activators ASICsTooltip Acid-sensing ion channel Blockers Chloride CaCCsTooltip Calcium-activated chloride channel Blockers Activators CFTRTooltip Cystic fibrosis transmembrane conductance regulator Blockers Activators Unsorted Blockers Others TRPsTooltip Transient receptor potential channels LGICsTooltip Ligand gated ion channels See also: Receptor/signaling modulatorsTransient receptor potential channel modulators

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