From Wikipedia, the free encyclopedia
Jump to navigation Jump to search
Glipizide ball-and-stick.png
Clinical data
Trade namesGlucotrol, others
  • AU: C
  • US: C (Risk not ruled out)
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
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.044.919 Edit this at Wikidata
Chemical and physical data
Molar mass445.536 g/mol g·mol−1
3D model (JSmol)
Melting point208 to 209 °C (406 to 408 °F)
 ☒N☑Y (what is this?)  (verify)

Glipizide, sold under the trade name Glucotrol among others, is an anti-diabetic medication of the sulfonylurea class used to treat type 2 diabetes.[1] It is used together with a diabetic diet.[1] It is not indicated for use by itself in type 1 diabetes.[1] It is taken by mouth.[1] 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.[2] The dose may need to be adjusted in those with liver or kidney disease.[1] Use during pregnancy or breastfeeding is not recommended.[2] 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 the United States the wholesale cost per dose is less than 0.05 USD as of 2018.[3] In the United Kingdom it costs the NHS less than 0.05 pounds per dose as of 2018.[2] In 2016 it was the 44th most prescribed medication in the United States with more than 17 million prescriptions.[4]

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.[5] 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]

See also[edit]


  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 British national formulary : BNF 76 (76 ed.). Pharmaceutical Press. 2018. p. 693. ISBN 9780857113382.
  3. ^ "NADAC as of 2018-12-19". Centers for Medicare and Medicaid Services. Retrieved 22 December 2018.
  4. ^ "The Top 300 of 2019". Retrieved 22 December 2018.
  5. ^ Drugs@FDA (the official database of FDA-approved drugs)
  6. ^ LH Bösenberg & DG van Zyl (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, 80-88, DOI: 10.1080/22201009.2008.1087217
  7. ^ Fischer, Jnos; Ganellin, C. Robin (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 449. ISBN 9783527607495.