Glipizide

Not to be confused with gliclazide or glyburide.

Glipizide

File:Glipizide.svg
File: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	C (Au, U.S.)
Legal status	POM (UK), ℞-only (U.S.)
Routes of administration	Oral
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 Y
ATC code	A10BB07 (WHO)
PubChem	CID: 3478
IUPHAR/BPS	6821
DrugBank	DB01067 Y
ChemSpider	3359 Y
UNII	X7WDT95N5C Y
KEGG	D00335 Y
ChEBI	CHEBI:5384 N
ChEMBL	CHEMBL1073 Y
Chemical data
Formula	C21H27N5O4S
Molecular mass	445.536 g/mol
SMILES O=C(c1ncc(nc1)C)NCCc2ccc(cc2)S(=O)(=O)NC(=O)NC3CCCCC3
InChI 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) Y Key:ZJJXGWJIGJFDTL-UHFFFAOYSA-N Y
NY (what is this?)  (verify)

Glipizide is an oral rapid- and short-acting anti-diabetic drug 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

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. 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.

See also

• Glyburide
• Tolbutamide

External links

• Glucotrol XL Full U.S. Prescribing Information. Accessed on July 26, 2005.