Glipizide

Glipizide

Clinical data
Trade names	Glucotrol
AHFS/Drugs.com	Monograph
MedlinePlus	a684060
Pregnancy category	AU: C US: C (Risk not ruled out)
Routes of administration	Oral
ATC code	A10BB07 (WHO)
Legal status
Legal status	UK: POM (Prescription only) US: ℞-only
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
IUPAC name N-(4-[N-(cyclohexylcarbamoyl)sulfamoyl]phenethyl)-5-methylpyrazine-2-carboxamide
CAS Number	29094-61-9 Y
PubChem CID	3478
IUPHAR/BPS	6821
DrugBank	DB01067 Y
ChemSpider	3359 Y
UNII	X7WDT95N5C
KEGG	D00335 Y
ChEBI	CHEBI:5384 N
ChEMBL	CHEMBL1073 Y
ECHA InfoCard	100.044.919
Chemical and physical data
Formula	C21H27N5O4S
Molar mass	445.536 g/mol
3D model (Jmol)	Interactive image
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?)

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.

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.