Glipizide

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Not to be confused with gliclazide or glyburide.
Glipizide
Glipizide.svg
Glipizide ball-and-stick.png
Systematic (IUPAC) name
N-(4-[N-(cyclohexylcarbamoyl)sulfamoyl]phenethyl)-5-methylpyrazine-2-carboxamide
Clinical data
Trade names Glucotrol
AHFS/Drugs.com Monograph
MedlinePlus a684060
Pregnancy
category
Routes of
administration
Oral
Legal status
Legal status
  • POM (UK), ℞-only (U.S.)
Pharmacokinetic data
Bioavailability 100% (regular formulation)
90% (extended release)
Protein binding 98 to 99%
Metabolism Hepatic hydroxylation
Biological half-life 2 to 5 hours
Excretion Renal and fecal
Identifiers
CAS Number 29094-61-9 YesY
ATC code A10BB07 (WHO)
PubChem CID 3478
IUPHAR/BPS 6821
DrugBank DB01067 YesY
ChemSpider 3359 YesY
UNII X7WDT95N5C YesY
KEGG D00335 YesY
ChEBI CHEBI:5384 N
ChEMBL CHEMBL1073 YesY
Chemical data
Formula C21H27N5O4S
Molar mass 445.536 g/mol
 NYesY (what is this?)  (verify)

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 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.

Sulfonylureas may also cause the decrease of serum glucagon and potentiate the action of insulin at the extrapancreatic tissues.[citation needed] The mouse model of MODY diabetes suggested that the reduced glipizide clearance stands behind their therapeutic success in human MODY patients, but Urbanova et al. found that human MODY patients respond differently to the mouse model and that there was no consistent decrease in glipizide clearance in randomly selected HNF1A-MODY and HNF4A-MODY patients.[1]

See also[edit]

References[edit]

  1. ^ Urbanova, J.; et al. (2015). "Half-Life of Sulfonylureas in HNF1A and HNF4A Human MODY Patients is not Prolonged as Suggested by the Mouse Hnf1a-/- Model". Current Pharmaceutical Design. 21: 5736–5748. doi:10.2174/1381612821666151008124036. 

External links[edit]