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Home / Drugs / Starting with G / Glipizide

An oral hypoglycemic agent which is rapidly absorbed and completely metabolized. [PubChem]
Glipizide Extended-Release Tablets
Glucotrol XL
CategoriesHypoglycemic Agents
ManufacturersWatson laboratories inc
Pfizer inc
Alphapharm party ltd
Apotex inc
Caraco pharmaceutical laboratories ltd
Endo pharmaceuticals inc
Ivax pharmaceuticals inc sub teva pharmaceuticals usa
Mylan pharmaceuticals inc
Par pharmaceutical inc
Pliva inc
Sandoz inc
Teva pharmaceuticals usa inc
PackagersActavis Group
Advanced Pharmaceutical Services Inc.
Alphapharm Party Ltd.
Amerisource Health Services Corp.
Apotex Inc.
Apotheca Inc.
AQ Pharmaceuticals Inc.
A-S Medication Solutions LLC
Atlantic Biologicals Corporation
Bristol-Myers Squibb Co.
Bryant Ranch Prepack
Caraco Pharmaceutical Labs
Cardinal Health
Coupler Enterprises Inc.
Dept Health Central Pharmacy
Direct Dispensing Inc.
Dispensing Solutions
Diversified Healthcare Services Inc.
Goldline Laboratories Inc.
Greenstone LLC
Heartland Repack Services LLC
Ivax Pharmaceuticals
Kaiser Foundation Hospital
Lake Erie Medical and Surgical Supply
Legacy Pharmaceuticals Packaging LLC
Liberty Pharmaceuticals
Major Pharmaceuticals
Mckesson Corp.
Medisca Inc.
Medvantx Inc.
Murfreesboro Pharmaceutical Nursing Supply
Novopharm Ltd.
Nucare Pharmaceuticals Inc.
Palmetto Pharmaceuticals Inc.
Patheon Inc.
PD-Rx Pharmaceuticals Inc.
Pfizer Inc.
Pharmaceutical Utilization Management Program VA Inc.
Pharmacy Service Center
Physicians Total Care Inc.
Pratt Pharmaceuticals
Preferred Pharmaceuticals Inc.
Prepackage Specialists
Prepak Systems Inc.
Rebel Distributors Corp.
Remedy Repack
Resource Optimization and Innovation LLC
Sandhills Packaging Inc.
Southwood Pharmaceuticals
Stat Rx Usa
Stat Scripts LLC
Teva Pharmaceutical Industries Ltd.
Torpharm Inc.
UDL Laboratories
United Research Laboratories Inc.
US Pharmaceutical Group
Va Cmop Dallas
Vangard Labs Inc.
Watson Pharmaceuticals
SynonymsGlipizida [INN-Spanish]
Glipizidum [INN-Latin]


For use as an adjunct to diet for the control of hyperglycemia and its associated symptomatology in patients with non-insulin-dependent diabetes mellitus (NIDDM; type II), formerly known as maturity-onset diabetes, after an adequate trial of dietary therapy has proved unsatisfactory.


Glipizide, a second-generation sulfonylurea, is used with diet to lower blood glucose in patients with diabetes mellitus type II. The primary mode of action of glipizide in experimental animals appears to be the stimulation of insulin secretion from the beta cells of pancreatic islet tissue and is thus dependent on functioning beta cells in the pancreatic islets. In humans glipizide appears to lower the blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. In man, stimulation of insulin secretion by glipizide in response to a meal is undoubtedly of major importance. Fasting insulin levels are not elevated even on long-term glipizide administration, but the postprandial insulin response continues to be enhanced after at least 6 months of treatment. Some patients fail to respond initially, or gradually lose their responsiveness to sulfonylurea drugs, including glipizide.

mechanism of action

Sulfonylureas likely bind to ATP-sensitive potassium-channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin.


The acute oral toxicity was extremely low in all species tested (LD50 greater than 4 g/kg). Overdosage of sulfonylureas including glipizide can produce hypoglycemia.


Hepatic. The major metabolites of glipizide are products of aromatic hydroxylation and have no hypoglycemic activity. A minor metabolite which accounts for less than 2% of a dose, an acetylaminoethyl benzine derivatives, is reported to have 1/10 to 1/3 as much hypoglycemic activity as the parent compound.


Gastrointestinal absorption is uniform, rapid, and essentially complete.

half life

2-5 hours

route of elimination

The primary metabolites are inactive hydroxylation products and polar conjugates and are excreted mainly in the urine.

drug interactions

Acebutolol: Acebutolol may decrease symptoms of hypoglycemia and increase the time required for the body to compensate for hypoglycemia.

Acetylsalicylic acid: Acetylsalicylic acid increases the effect of the sulfonylurea, glipizide.

Atenolol: The beta-blocker, atenolol, may decrease symptoms of hypoglycemia.

Bisoprolol: The beta-blocker, bisoprolol, may decrease symptoms of hypoglycemia.

Carvedilol: The beta-blocker, carvedilol, may decrease symptoms of hypoglycemia.

Chloramphenicol: Chloramphenicol may increase the effect of sulfonylurea, glipizide.

Clofibrate: Clofibrate may increase the effect of sulfonylurea, glipizide.

Cyclosporine: The sulfonylurea, glipizide, may increase the effect of cyclosporine.

Esmolol: The beta-blocker, esmolol, may decrease symptoms of hypoglycemia.

Labetalol: The beta-blocker, labetalol, may decrease symptoms of hypoglycemia.

Metoprolol: The beta-blocker, metoprolol, may decrease symptoms of hypoglycemia.

Nadolol: The beta-blocker, nadolol, may decrease symptoms of hypoglycemia.

Oxprenolol: The beta-blocker, oxprenolol, may decrease symptoms of hypoglycemia.

Phenylbutazone: Phenylbutazone increases the effect of the hypoglycemic agent

Pindolol: The beta-blocker, pindolol, may decrease symptoms of hypoglycemia.

Propranolol: The beta-blocker, propranolol, may decrease symptoms of hypoglycemia.

Rifampin: Rifampin may decrease the effect of sulfonylurea, glipizide.

Somatropin recombinant: Somatropin may antagonize the hypoglycemic effect of glipizide. Monitor for changes in fasting and postprandial blood sugars.

Timolol: The beta-blocker, timolol, may decrease symptoms of hypoglycemia.

Tolbutamide: Tolbutamide, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Glipizide. Consider alternate therapy or monitor for changes in Glipizide therapeutic and adverse effects if Tolbutamide is initiated, discontinued or dose changed.