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Clinical data
Trade namesGlucotrol, Glucotrol XL, others
License data
  • AU: C
Routes of
By mouth
Drug classSulfonylurea
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability100% (regular formulation)
90% (extended release)
Protein binding98 to 99%
MetabolismLiver hydroxylation
Elimination half-life2 to 5 hours
ExcretionKidney and fecal
  • N-(4-[N-(cyclohexylcarbamoyl)sulfamoyl]phenethyl)-5-methylpyrazine-2-carboxamide
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.044.919 Edit this at Wikidata
Chemical and physical data
Molar mass445.54 g·mol−1
3D model (JSmol)
Melting point208 to 209 °C (406 to 408 °F)
  • O=C(c1ncc(nc1)C)NCCc2ccc(cc2)S(=O)(=O)NC(=O)NC3CCCCC3
  • InChI=1S/C21H27N5O4S/c1-15-13-24-19(14-23-15)20(27)22-12-11-16-7-9-18(10-8-16)31(29,30)26-21(28)25-17-5-3-2-4-6-17/h7-10,13-14,17H,2-6,11-12H2,1H3,(H,22,27)(H2,25,26,28) checkY
 ☒NcheckY (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 2021, it was the 48th most commonly prescribed medication in the United States, with more than 13 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]


  1. ^ a b c d e f g h i j k "Glipizide Monograph for Professionals". AHFS. Retrieved 24 December 2018.
  2. ^ a b c d e "Glucotrol XL- glipizide tablet, extended release". DailyMed. 17 August 2018. Retrieved 31 July 2020.
  3. ^ a b British national formulary : BNF 76 (76 ed.). Pharmaceutical Press. 2018. p. 693. ISBN 9780857113382.
  4. ^ "The Top 300 of 2021". ClinCalc. Archived from the original on 15 January 2024. Retrieved 14 January 2024.
  5. ^ "Glipizide - Drug Usage Statistics". ClinCalc. Retrieved 14 January 2024.
  6. ^ Bösenberg LH, Van Zyl DG (December 2008). "The mechanism of action of oral antidiabetic drugs: a review of recent literature". Journal of Endocrinology, Metabolism and Diabetes of South Africa. 13 (3): 80–8. doi:10.1080/22201009.2008.10872177. hdl:2263/10139.
  7. ^ Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 449. ISBN 9783527607495.