Glipizide (Monograph)
Brand names: Glucotrol, Glucotrol XL
Drug class: Sulfonylureas
VA class: HS502
Chemical name: 1-cyclohexyl-3-[[p-[2-(5-methylpyrazine-carboxamido)ethyl]phenyl]sulfonyl]urea
Molecular formula: C21H27N5O4S
CAS number: 29094-61-9
Introduction
Antidiabetic agent; sulfonylurea.1 2 3
Uses for Glipizide
Type 2 Diabetes Mellitus
Used as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus.1 2 3 19 27 50 51 52 53 54 55 56 57 58 59 60 95
Used in combination with one or more other oral antidiabetic agents or insulin as an adjunct to diet and exercise in patients who do not achieve adequate glycemic control with diet, exercise, and oral antidiabetic agent monotherapy.120 127 128 129 130 139 153 154 155 157 158 161 159 160 161 162 164
Used in fixed combination with metformin as initial therapy in patients with type 2 diabetes mellitus whose hyperglycemia cannot be controlled by diet and exercise alone and as second-line therapy in patients with type 2 diabetes mellitus who have inadequate glycemic control with either sulfonylurea or metformin monotherapy.153
Current guidelines for the treatment of type 2 diabetes mellitus generally recommend metformin as first-line therapy in addition to lifestyle modifications in patients with recent-onset type 2 diabetes mellitus or mild hyperglycemia due to its well-established safety and efficacy (e.g., beneficial effects on glycosylated hemoglobin [hemoglobin A1c; HbA1c], weight, and cardiovascular mortality).698 704 705
In patients with metformin contraindications or intolerance (e.g., risk of lactic acidosis, GI intolerance) or in selected other patients, some experts suggest that initial therapy with a drug from another class of antidiabetic agents (e.g., a glucagon-like peptide-1 [GLP-1] receptor agonist, sodium-glucose cotransporter 2 [SGLT2] inhibitor, dipeptidyl peptidase-4 [DPP-4] inhibitor, sulfonylurea, thiazolidinedione, basal insulin) may be acceptable based on patient factors.698 704
May need to initiate therapy with 2 agents (e.g., metformin plus another drug) in patients with high initial HbA1c (>7.5% or ≥1.5% above target).698 704 In such patients with metformin intolerance, some experts suggest initiation of therapy with 2 drugs from other antidiabetic drug classes with complementary mechanisms of action.698 704
Consider early initiation of combination therapy for the treatment of type 2 diabetes mellitus to extend the time to treatment failure and more rapidly attain glycemic goals.704
For patients with inadequate glycemic control on metformin monotherapy, consider patient comorbidities (e.g., atherosclerotic cardiovascular disease [ASCVD], established kidney disease, heart failure), hypoglycemia risk, impact on weight, cost, risk of adverse effects, and patient preferences when selecting additional antidiabetic agents for combination therapy.698 699 704 705 706
Consider early introduction of insulin for severe hyperglycemia (e.g., blood glucose of ≥300 mg/dL or HbA1c >9–10%), especially if accompanied by catabolic manifestations (e.g., weight loss, hypertriglyceridemia, ketosis) or symptoms of hyperglycemia.698 704
Manufacturer states that glipizide is not recommended for use in patients with type 1 diabetes mellitus or diabetic ketoacidosis.95 707
Glipizide Dosage and Administration
General
-
Adjust dosage according to tolerance and urine and/or fasting blood glucose determinations.1 95 Monitor HbA1c to determine minimum effective dosage or detect primary or secondary failure.1 95 153
Administration
Oral Administration
Administer extended-release or conventional (immediate-release) tablets once daily, generally with breakfast or the first main meal of the day.1 95 1 Administer conventional tablets approximately 30 minutes before a meal.1 11 32
Administer the fixed combination of glipizide and metformin once daily with a meal.153
Some patients may have a more satisfactory response when conventional tablets are administered in 2 or 3 divided doses daily.1 2 11 44 50 51 52 53 54 57 58 59 60 When dosage exceeds 15 mg daily as conventional tablets, administer in divided doses before meals of sufficient caloric content.1 2 59
Extended-release tablets should be swallowed whole and should not be divided, chewed, or crushed.95
Administer glipizide at least 4 hours prior to colesevelam when drugs given concomitantly.1 95 (See Specific Drugs under Interactions.)
Dosage
Adults
Type 2 Diabetes Mellitus
Initial Dosage in Previously Untreated Patients
OralConventional or extended-release tablets: Initially, 5 mg daily.1 95 Titrate dosage of conventional tablets in increments of 2.5–5 mg daily at intervals of at least several days1 (usually 3–7 days).2 51 54 59 60 Maximum once daily dosage, 15 mg.1
For extended-release tablets, titrate dosage based on the patient's glycemic control.95
Initial Dosage in Patients Transferred from Conventional to Extended-release Glipizide Tablets
OralWhen transferring, administer the nearest equivalent total daily dosage of the extended-release tablets once daily.95
Initial Dosage in Patients Transferred from Other Oral Antidiabetic Agents
OralIndividualize initial dosage of glipizide; usually 5–10 mg daily.90 92 The other oral antidiabetic agent may be discontinued abruptly; no transition period generally required.1 95
It has been recommended that patients being transferred from a sulfonylurea agent with a longer half-life (e.g., chlorpropamide [no longer commercially available in the US]) be closely monitored during the initial 1–2 weeks due to potential for overlapping drug effects.1 A drug-free interval of 2–3 days has been advised before glipizide therapy is initiated as conventional tablets in patients being transferred from chlorpropamide, particularly if blood glucose concentration was adequately controlled with chlorpropamide.90 92
Initial Dosage in Patients Transferred from Insulin
OralInsulin requirement ≤20 units daily: Initially, 5 mg of glipizide once daily.1 May discontinue insulin abruptly.1
Insulin requirement >20 units daily: Initially, 5 mg of glipizide once daily and reduce insulin dosage by 50%.1 Withdraw insulin gradually and adjust daily glipizide dosage at intervals of at least several days according to tolerance and response.1
Maintenance Dosage
OralMaintenance dosage varies considerably, ranging from 2.5–40 mg daily.1 2 7 27 39 40 41 42 43 44 50 51 52 53 54 56 57 58 59 60
Conventional tablets: Generally, 5–25 mg daily.27 39 40 41 42 43 44 50 51 52 53 54 56 57 58 59 60
Extended-release tablets: Generally, 5–10 mg daily.7 25 95
Combination Therapy with Other Oral Antidiabetic Agents
OralWhen added to therapy with other antidiabetic agents, may initiate glipizide extended-release tablets at a dosage of 5 mg daily.95 May use lower initial dosages in patients at risk for hypoglycemia.95
May initiate fixed combination of 2.5 mg of glipizide and 250 mg of metformin hydrochloride once daily with a meal in treatment-naive patients.153
For more severe hyperglycemia (i.e., fasting plasma glucose concentrations of 280–320 mg/dL), consider 2.5 mg of glipizide and 500 mg of metformin hydrochloride as fixed combination twice daily.153 Efficacy of fixed combination in patients with fasting plasma glucose concentrations >320 mg/dL not established.153
May increase dosage of fixed combination in increments of one tablet153 (using the tablet strength at which therapy was initiated, either 2.5 mg glipizide/250 mg metformin hydrochloride or 2.5 mg glipizide/500 mg metformin hydrochloride)163 daily every 2 weeks until the minimum effective dosage required to achieve adequate glycemic control is reached.153
Maximum daily dosage of fixed combination in treatment-naive patients is 10 mg of glipizide and 2 g of metformin hydrochloride given in divided doses.153
In previously treated patients with inadequate glycemic control on sulfonylurea (e.g., glipizide) or metformin monotherapy, initiate fixed-combination therapy with 2.5 mg of glipizide and 500 mg of metformin hydrochloride or 5 mg of glipizide and 500 mg of metformin hydrochloride twice daily with the morning and evening meals.153
To minimize hypoglycemia risk, do not exceed the initial daily dosage of glipizide or metformin hydrochloride already being taken.153
Titrate dosage upward in increments not exceeding 5 mg of glipizide and 500 mg of metformin hydrochloride until adequate glycemic control or a maximum daily dosage of 20 mg of glipizide and 2 g of metformin hydrochloride is reached in patients on sulfonylurea or metformin monotherapy.153
For patients being switched from therapy with both glipizide (or another sulfonylurea antidiabetic agent) and metformin, the initial dosage of the fixed-combination preparation should not exceed the daily dosages of glipizide (or equivalent dosage of another sulfonylurea) and metformin hydrochloride currently being taken.153 158 Monitor for signs and symptoms of hypoglycemia following the switch.153 In the transfer, base decision on whether to switch to the nearest equivalent dosage or to titrate dosage on clinical judgment.153
Prescribing Limits
Adults
Type 2 Diabetes Mellitus
Oral
Maximum once-daily dosage as conventional tablets is 15 mg.1
Maximum total daily dosage is 40 mg as divided doses of conventional tablets or 20 mg as extended-release tablets.1 95
Maximum total daily dosage of fixed combination in treatment-naive patients is 10 mg of glipizide and 2 g of metformin hydrochloride in divided doses.153
Maximum total daily dosage of fixed combination in patients with inadequate glycemic control on sulfonylurea and/or metformin therapy is 20 mg of glipizide and 2 g of metformin hydrochloride in divided doses.153
Special Populations
Hepatic Impairment
Conventional tablets: Initially, 2.5 mg daily;1 conservative maintenance dosage.1
Extended-release tablets: Use conservative initial and maintenance dosage.1
Adjust dosage carefully.1 27 71 95
Generally, do not use in patients with severe hepatic impairment.2 65 72
Renal Impairment
Use conservative initial and maintenance dosage.1 95
Use generally not recommended in patients with severe renal impairment.2 65 72
Cautious dosing recommended.
Geriatric Patients
Conventional tablets: Initially, 2.5 mg daily.1
Initially, 5 mg (extended-release tablets) may be used.1 95
Use conservative initial and maintenance dosage of glipizide-containing formulations.1 95 153
Adjust dosage carefully.1 Any dosage adjustment of glipizide in fixed combination with metformin hydrochloride requires careful assessment of renal function.153
Dosage of glipizide and metformin hydrochloride in fixed combination should not be titrated to the maximum dosage.
Debilitated or Malnourished Patients
Conservative initial and maintenance dosage of conventional and extended-release tablets.1 95
Dosage of glipizide and metformin hydrochloride in fixed combination should not be titrated to the maximum dosage.153
Cautions for Glipizide
Contraindications
-
Known hypersensitivity to glipizide or any ingredient in the formulation.1 95
-
Hypersensitivity to sulfonamide derivatives.95
Warnings/Precautions
Hypoglycemia
Reported infrequently; usually mild.2 27 50 58 59 60
Possible severe and/or prolonged hypoglycemia, especially in geriatric or malnourished patients and those with adrenal, pituitary, hepatic, or renal insufficiency.1 27 70 71 Strenuous exercise, alcohol ingestion (see Interactions), insufficient caloric intake, or use in combination with other antidiabetic agents (see Interactions) may increase hypoglycemia risk.1 Severe hypoglycemia can lead to unconsciousness or seizures; may result in temporary or permanent impairment of brain function or death.95
Appropriate patient selection and careful attention to dosage are important to avoid glipizide-induced hypoglycemia.
Loss of Glycemic Control
Possible loss of glycemic control during periods of stress (e.g., fever of any cause, trauma, infection, surgery).1 2
Temporary discontinuance of glipizide and administration of insulin may be required.1
Hematologic Effects
Hemolytic anemia may develop in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency who receive sulfonylureas; consider a non-sulfonylurea antidiabetic agent in patients with G6PD deficiency.1
Cardiovascular Effects
Possible increased cardiovascular mortality reported with other sulfonylurea antidiabetic agents (i.e., tolbutamide or phenformin).1 75 However, the American Diabetes Association (ADA) has stated that the benefits of intensive glycemic control with insulin or sulfonylureas outweigh the risks overall.97 107 113
Macrovascular Outcomes
Manufacturer states that no clinical studies have conclusively established macrovascular risk reduction with glipizide or any other antidiabetic drug.95
GI Obstruction
Use extended-release tablets with caution in patients with severe preexisting GI narrowing, since obstruction may occur.95
Use of Fixed Combinations
When use in fixed combination with metformin hydrochloride, consider the cautions, precautions, contraindications, and interactions associated with metformin.153
Specific Populations
Pregnancy
Category C.1
Sulfonylureas cross the placenta and have been associated with neonatal adverse reactions (e.g., hypoglycemia); prolonged, severe hypoglycemia reported in some neonates born to women receiving sulfonylureas up to time of delivery.95 Observe neonates for symptoms of hypoglycemia and respiratory distress and manage accordingly.95
Many experts recommend that insulin be used during pregnancy.1 95
Lactation
Not known whether glipizide is distributed into milk;1 discontinue nursing or the drug.1
If glipizide used during breast-feeding, monitor infants for signs of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures).95
Pediatric Use
Safety and efficacy not established.1 95 153 However, ADA has stated that most pediatric diabetologists use oral antidiabetic agents in children with type 2 diabetes mellitus because of greater compliance and convenience and lack of evidence demonstrating better efficacy of insulin for type 2 diabetes mellitus.117
Geriatric Use
Increased risk of hypoglycemia.1 27 71 95 Cautious and conservative dosing recommended.1 27 71 95 (See Geriatric Patients under Dosage and Administration.)
Hepatic Impairment
Increased risk of hypoglycemia.1 27 71 95 Cautious and conservative dosing recommended.1 27 71 95 (See Hepatic Impairment under Dosage and Administration.)
Avoidance in severe impairment has been recommended.2 65 72
Renal Impairment
Increased risk of hypoglycemia.1 27 71 Cautious and conservative dosing recommended.1 27 71 (See Renal Impairment under Dosage and Administration.)
Avoidance in severe impairment has been recommended.2 65 72
Common Adverse Effects
Conventional tablets: Nausea,1 50 anorexia,50 vomiting,50 pyrosis,50 gastralgia,1 diarrhea,1 constipation.1 2 50
Extended-release tablets: Dizziness,95 diarrhea,95 nervousness,95 tremor,95 hypoglycemia,95 flatulence.95
Glipizide/metformin hydrochloride fixed combination: Upper respiratory tract infection,95 diarrhea,95 dizziness,95 hypertension,95 nausea/vomiting,95 musculoskeletal pain,95 headache,95 abdominal pain,95 urinary tract infection.95 153
Drug Interactions
Protein-bound Drugs
Potential pharmacokinetic interaction with other protein-bound drugs.1 2 47 72 80
Use with caution with protein-bound drugs.1
Specific Drugs
Drug |
Interaction |
Comments |
---|---|---|
ACE inhibitors |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Alcohol |
May either potentiate or weaken hypoglycemic effect95 Rarely, disulfiram-like reactions1 |
Increase frequency of monitoring with concomitant administration95 |
Angiotensin II receptor antagonists |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Antidiabetic agents |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Antifungals, azole (e.g, fluconazole, miconazole, voriconazole) |
Fluconazole increases plasma concentrations of glipizide1 95 |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
Antipsychotics, atypical (e.g., clozapine, olanzapine) |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
β-Adrenergic blocking agents |
Impaired glucose tolerance; increased frequency or severity of hypoglycemia and hypoglycemia-induced complications62 72 80 May either potentiate or weaken hypoglycemic effect95 Reduced or absent signs of hypoglycemia95 |
If concomitant therapy is necessary, a β1-selective adrenergic blocking agent may be preferred62 72 Increase frequency of monitoring with concomitant administration95 |
Calcium-channel blocking agents |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Chloramphenicol |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Clonidine |
May either potentiate or weaken hypoglycemic effect95 Reduced or absent signs of hypoglycemia95 |
Increase frequency of monitoring with concomitant administration95 |
Colesevelam |
Concomitant administration reduces glipizide AUC and peak plasma concentration by 12 and 13%, respectively1 95 |
|
Contraceptives, oral |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Corticosteroids |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Coumarins |
Glipizide could displace or be displaced by oral anticoagulants (e.g., coumarins) from plasma protein binding sites;2 47 72 80 95 153 does not displace dicumarol from plasma protein binding sites in vitro1 81 82 95 153 |
Observe closely when concurrent therapy is initiated or discontinued1 95 153 |
Danazol |
May exacerbate hyperglycemia95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Disopyramide |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Diuretics (e.g., thiazides) |
Increased antidiabetic requirements1 72 80 84 95 Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Estrogens |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Fibric acid derivatives |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Fluoxetine |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Glucagon |
May exacerbate hyperglycemia95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Guanethidine |
Reduced or absent signs of hypoglycemia95 |
Increase frequency of monitoring with concomitant administration95 |
H2-receptor antagonists (e.g., cimetidine) |
May increase hypoglycemic effect95 Cimetidine inhibits the hepatic metabolism of glipizide and potentiates hypoglycemic effect83 |
Observe closely when concurrent therapy is initiated or discontinued95 Glipizide dosage adjustment may be necessary when cimetidine is initiated or discontinued83 |
Hydantoins (e.g., phenytoin) |
Glipizide could displace or be displaced by hydantoins from plasma protein binding sites2 47 72 80 |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
Isoniazid |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
MAO inhibitors |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Niacin |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
NSAIAs |
May increase hypoglycemic effect95 Glipizide could displace or be displaced by NSAIAs from plasma protein binding sites1 2 47 72 80 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Pentoxifylline |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Phenothiazines |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Pramlintide |
Increases hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Probenecid |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Propoxyphene |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Protease inhibitors |
May exacerbate hyperglycemia95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Quinolones |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Reserpine |
May either potentiate or weaken hypoglycemic effect95 Reduced or absent signs of hypoglycemia95 |
Increase frequency of monitoring with concomitant administration95 |
Rifampin |
||
Salicylate |
May increase hypoglycemic effect95 Does not displace salicylate from plasma protein binding sites1 81 82 95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Somatostatin analogs (e.g., octreotide) |
May increase hypoglycemic effect95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Somatropin |
May exacerbate hyperglycemia95 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Sulfonamides |
May increase hypoglycemic effect95 Glipizide could displace or be displaced by sulfonamides from plasma protein binding sites1 2 47 72 80 |
Observe closely when concurrent therapy is initiated or discontinued95 |
Sympathomimetic agents (e.g., albuterol, epinephrine, terbutaline) |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
|
Thyroid hormones |
Observe closely when concurrent therapy is initiated or discontinued1 95 |
Glipizide Pharmacokinetics
Absorption
Bioavailability
Absorption is essentially complete; 1 30 31 32 33 34 35 36 37 38 80–100% of an oral dose may be absorbed.30 31 95
Onset
Conventional tablets: 15–30 minutes.6 32 33
Duration
Conventional tablets: In nonfasting diabetic patients, the hypoglycemic action may persist for up to 24 hours.1 39 40 41 42 43 44
Food
Glipizide conventional tablets: Food delays absorption but does not affect peak serum concentrations or extent of absorption.32 33 Peak serum concentrations following administration of conventional tablets generally are delayed 20–40 minutes in the nonfasting state compared with the fasting state.1 32 33
Fixed combination of glipizide and metformin: Food delays peak plasma glipizide concentration by 1 hour.153
Glipizide extended-release tablets: Food does not affect glycemic response or time to absorption.95 Peak blood concentration following administration of extended-release tablets with food increased.95
Distribution
Extent
Following IV administration in mice, distributed into the liver and blood, with lower concentrations in the lungs, kidneys, adrenals, myocardium, salivary glands, and retroscapular fat.45 In humans, small amounts of glipizide are apparently distributed into bile30 34 37 and very small amounts are distributed into erythrocytes and saliva.30
Not known if glipizide is distributed into milk.1
Plasma Protein Binding
Elimination
Metabolism
Appears to be almost completely metabolized, 30 34 35 36 37 mainly in the liver.1
Elimination Route
Glipizide and its metabolites are excreted principally in urine30 34 35 36 37 (60–90%) and to a lesser extent in feces (5–20%).30 34 35 37 95
Half-life
Terminal elimination half-life of glipizide averages 3–4.7 hours following oral administration in patients with normal renal and hepatic function.9 30 31 32 33 34 35 38 39 48
Terminal elimination half-life of total glipizide metabolites ranges from 2–6 hours.37
Special Populations
Renal or hepatic impairment may increase serum glipizide concentrations and reduce elimination.1 37 95
Severe renal impairment may decrease the renal excretion of and increase the terminal elimination half-life of glipizide metabolites.37 95
No differences in glipizide pharmacokinetics observed following single-dose administration to older diabetic patients compared with that in younger healthy individuals.95
Stability
Storage
Oral
Tablets (conventional)
Tight, light-resistant containers at 20–25°C.1 90
Tablets (extended-release)
20–25°C (may be exposed to 15–30°C); protect from moisture and humidity.95
Tablets (fixed-combination)
20–25°C (may be exposed to 15–30°C).153
Actions
-
Lowers blood glucose concentration in diabetic and nondiabetic individuals.2 3 5 6 7 8 9 10 11 12 13
-
Stimulates secretion of postprandial endogenous insulin from the beta cells of the pancreas.1 2 3 5 7 8 9 10 11 12 13
-
During prolonged administration, extrapancreatic effects such as enhanced peripheral sensitivity to insulin and reduction of basal hepatic glucose production contribute to the hypoglycemic action.3 5 7 8 10 12 13 14 16 17 23 24 95
Advice to Patients
-
Importance of regular clinical and laboratory evaluations, including blood and urine glucose determinations.1
-
Importance of adherence to diet and exercise regimen.1
-
Understanding of primary and secondary failure to oral sulfonylurea antidiabetic agents.1
-
Risks of hypoglycemia, the symptoms and treatment of hypoglycemic reactions, and conditions that predispose to the development of hypoglycemic reactions.1
-
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.1
-
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.1 95 Importance of advising breast-feeding women taking glipizide to monitor breast-fed infants for signs of hypoglycemia.95 (See Lactation under Cautions.)
-
Importance of informing patients of other important precautionary information. (See Cautions.)
Preparations
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Routes |
Dosage Forms |
Strengths |
Brand Names |
Manufacturer |
---|---|---|---|---|
Oral |
Tablets |
5 mg* |
glipiZIDE Tablets |
|
Glucotrol (scored) |
Pfizer |
|||
10 mg* |
glipiZIDE Tablets |
|||
Glucotrol (scored) |
Pfizer |
|||
Tablets, extended-release |
2.5 mg* |
glipiZIDE Tablets ER |
||
Glucotrol XL |
Pfizer |
|||
5 mg* |
glipiZIDE Tablets ER |
|||
Glucotrol XL |
Pfizer |
|||
10 mg* |
glipiZIDE Tablets ER |
|||
Glucotrol XL |
Pfizer |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Routes |
Dosage Forms |
Strengths |
Brand Names |
Manufacturer |
---|---|---|---|---|
Oral |
Tablets, film-coated |
2.5 mg with 250 mg Metformin Hydrochloride* |
Glipizide with Metformin Hydrochloride Tablets |
|
2.5 mg with 500 mg Meformin Hydrochloride* |
Glipizide with Metformin Hydrochloride Tablets |
|||
5 mg with 500 mg Metformin Hydrochloride* |
Glipizide with Metformin Hydrochloride Tablets |
AHFS DI Essentials™. © Copyright 2024, Selected Revisions June 21, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.
References
1. Pfizer. Glucotrol (glipizide) tablets prescribing information. New York, NY; 2016 Oct.
2. Brogden RN, Heel RC, Pakes GE et al. Glipizide: a review of its pharmacological properties and therapeutic use. Drugs. 1979; 18:329-53. http://www.ncbi.nlm.nih.gov/pubmed/389600?dopt=AbstractPlus
3. Jackson JE, Bressler R. Clinical pharmacology of sulphonylurea hypoglycaemic agents: part 1. Drugs. 1981; 22:211-45. http://www.ncbi.nlm.nih.gov/pubmed/7021124?dopt=AbstractPlus
4. Reynolds JEF, ed. Martindale: the extra pharmacopoeia. 28th ed. London: The Pharmaceutical Press; 1982:855.
5. Skillman TG, Feldman JM. The pharmacology of sulfonylureas. Am J Med. 1981; 70:361-72. http://www.ncbi.nlm.nih.gov/pubmed/6781341?dopt=AbstractPlus
6. Pisani Ceretti A, Losi S, Orsini G et al. A controlled study of the hypoglycemic and insulinopoietic effect of glipizide and glibenclamide in non-diabetic human subjects. Arzneimittelforschung. 1975; 25:675-6. http://www.ncbi.nlm.nih.gov/pubmed/808231?dopt=AbstractPlus
7. Greenfield MS, Doberne L, Rosenthal M et al. Effect of sulfonylurea treatment on in vivo insulin secretion and action in patients with non-insulin-dependent diabetes mellitus. Diabetes Care. 1982; 31:307-12.
8. Reaven GM. Effect of glipizide treatment on various aspects of glucose, insulin, and lipid metabolism in patients with noninsulin-dependent diabetes mellitus. Am J Med. 1983; 75(Suppl. 5B):8-14. http://www.ncbi.nlm.nih.gov/pubmed/6369970?dopt=AbstractPlus
9. Peterson CM, Sims RV, Jones RL et al. Bioavailability of glipizide and its effect on blood glucose and insulin levels in patients with non-insulin-dependent diabetes. Diabetes Care. 1982; 5:497-500. http://www.ncbi.nlm.nih.gov/pubmed/6765225?dopt=AbstractPlus
10. Lebovitz HE, Feinglos MN. Mechanism of action of the second-generation sulfonylurea glipizide. Am J Med. 1983; 75(Suppl. 5B):46-54. http://www.ncbi.nlm.nih.gov/pubmed/6369967?dopt=AbstractPlus
11. Sartor G, Scherstén B, Melander A. Effects of glipizide and food intake on the blood levels of glucose and insulin in diabetic patients. Acta Med Scand. 1978; 203:211-4. http://www.ncbi.nlm.nih.gov/pubmed/345754?dopt=AbstractPlus
12. Feinglos MN, Lebovitz HE. Sulfonylurea treatment of insulin-independent diabetes mellitus. Metabolism. 1980; 29:488-94. http://www.ncbi.nlm.nih.gov/pubmed/6990184?dopt=AbstractPlus
13. Lebovitz HE, Feinglos MN, Bucholtz HK et al. Potentiation of insulin action: a probable mechanism for the anti-diabetic action of sulfonylurea drugs. J Clin Endocrinol Metab. 1977; 45:601-4. http://www.ncbi.nlm.nih.gov/pubmed/903405?dopt=AbstractPlus
14. Kolterman OG, Gray RS, Shapiro G et al. The acute and chronic effects of sulfonylurea therapy in type II diabetic subjects. Diabetes. 1984; 33:346-54. http://www.ncbi.nlm.nih.gov/pubmed/6423429?dopt=AbstractPlus
15. Gurwich EL (The Upjohn Company, Kalamazoo, MI): Personal communication; 1984 Jun 25.
16. DeFronzo RA, Ferrannini E, Koivisto V. New concepts in the pathogenesis and treatment of noninsulin-dependent diabetes mellitus. Am J Med. 1983; 74(Suppl. 1A):52-81. http://www.ncbi.nlm.nih.gov/pubmed/6337486?dopt=AbstractPlus
17. Lockwood DH, Maloff BL, Nowak SM et al. Extrapancreatic effects of sulfonylureas: potentiation of insulin action through post-binding mechanisms. Am J Med. 1983; 74(Suppl. 1A):102-8. http://www.ncbi.nlm.nih.gov/pubmed/6401922?dopt=AbstractPlus
18. Larner J. Mediators of postreceptor action of insulin. Am J Med. 1983; 74(Suppl. 1A):38-51. http://www.ncbi.nlm.nih.gov/pubmed/6297300?dopt=AbstractPlus
19. Fineberg SE, Schneider SH. Glipizide versus tolbutamide, an open trial: effects on insulin secretory patterns and glucose concentrations. Diabetologia. 1980; 18:49-54. http://www.ncbi.nlm.nih.gov/pubmed/6988265?dopt=AbstractPlus
20. Marco J, Valverde I. Unaltered glucagon secretion after seven days of sulphonylurea administration in normal subjects. Diabetologia. 1973; 9(Suppl.):317-9.
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