Glipizide

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Glipizide
Glipizide.svg
Glipizide ball-and-stick.png
Clinical data
Trade namesGlucotrol
AHFS/Drugs.comMonograph
MedlinePlusa684060
Pregnancy
category
  • AU: C
  • US: C (Risk not ruled out)
Routes of
administration
Oral
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability100% (regular formulation)
90% (extended release)
Protein binding98 to 99%
MetabolismHepatic hydroxylation
Elimination half-life2 to 5 hours
ExcretionRenal and fecal
Identifiers
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
ECHA InfoCard100.044.919 Edit this at Wikidata
Chemical and physical data
FormulaC21H27N5O4S
Molar mass445.536 g/mol
3D model (JSmol)
Melting point208 to 209 °C (406 to 408 °F)
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Glipizide is an oral rapid- and short-acting anti-diabetic medication from the sulfonylurea class. It is classified as a second-generation sulfonylurea, which means that it undergoes enterohepatic circulation. Second-generation sulfonylureas are both more potent and have shorter half-lives than the first-generation sulfonylureas.

Originally available in 1984, it is marketed by Pfizer under the brand name Glucotrol in the USA, where Pfizer sells Glucotrol in doses of 5 and 10 milligrams and Glucotrol XL (an extended release form of glipizide) in doses of 2.5, 5, and 10 milligrams. Other companies also market glipizide, most commonly extended release tablets of 5 and 10 milligrams.

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[1]. 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. [2]

See also[edit]

References[edit]

  1. ^ Drugs@FDA (the official database of FDA-approved drugs) https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/020329s025lbl.pdf
  2. ^ 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

External links[edit]