Glimepiride (Monograph)
Drug class: Sulfonylureas
Introduction
Antidiabetic agent; sulfonylurea.
Uses for Glimepiride
Type 2 Diabetes Mellitus
Used as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus.
Used as monotherapy or in combination with other antidiabetic agents.
Commercially available as a single entity preparation and in fixed combination with pioglitazone (Duetact).
Guidelines from the American Diabetes Association (ADA) and other experts generally recommend that use of sulfonylureas for the treatment of type 2 diabetes mellitus be limited or discontinued due to increased risk of weight gain and hypoglycemia. Sulfonylureas may be considered in patients with access or cost barriers to other antidiabetic agents. When used, these guidelines recommend the lowest possible dosage. When selecting a treatment regimen, consider factors such as cardiovascular and renal comorbidities, drug efficacy and adverse effects, hypoglycemic risk, presence of overweight or obesity, cost, access, and patient preferences. Weight management should be included as a distinct treatment goal and other healthy lifestyle behaviors should also be considered.
Not indicated for treatment of type 1 diabetes mellitus or diabetic ketoacidosis.
Glimepiride Dosage and Administration
General
Patient Monitoring
-
Monitor patients with regular laboratory evaluations (including fasting blood or plasma glucose determinations) to determine therapeutic response and minimum effective dosage of glimepiride.
-
Following initiation and at dosage titration, monitor HbA1c approximately every 3–6 months to determine patient’s continued response to therapy.
Dispensing and Administration Precautions
-
Based on the Institute for Safe Medication Practices (ISMP), glimepiride is a high-alert medication that has a heightened risk of causing significant patient harm when used in error.
Administration
Oral Administration
Glimepiride: Administer once daily with breakfast or first main meal of the day.
Fixed combination of glimepiride and pioglitazone: Administer once daily with the first main meal.
Adjust dosage according to tolerance and fasting glucose determinations.
Use lowest effective dosage (either as monotherapy or in combination regimens) to reduce both fasting glucose concentrations and HbA1c values to normal or near normal.
Dosage
Adults
Type 2 Diabetes Mellitus
Glimepiride Monotherapy
OralInitially, 1 or 2 mg of glimepiride once daily before breakfast or first main meal. In patients at risk for hypoglycemia, (e.g., geriatric patients), initial dosage should be 1 mg once daily.
In patients receiving 1 mg daily, increase dosage to 2 mg daily after 1–2 weeks if adequate glycemic control has not been achieved. After reaching 2 mg dosage, increase dosage in increments of no more than 1 or 2 mg daily at 1- to 2-week intervals up to a maximum of 8 mg once daily.
When transferring from most sulfonylurea antidiabetic agents to glimepiride, a transition period is generally not required. Since an exaggerated hypoglycemic response may occur during transition from a sulfonylurea with a prolonged half-life to glimepiride, monitor patients closely for hypoglycemia during the initial 1-2 weeks of the transition period.
Glimepiride/Pioglitazone Fixed-combination Therapy
OralSelect initial dosage based on patient’s current dosage of glimepiride (or another sulfonylurea agent) and/or pioglitazone.
Patients currently receiving glimepiride monotherapy: Usual initial dosage is 2 or 4 mg of glimepiride and 30 mg of pioglitazone once daily.
Patients currently receiving pioglitazone monotherapy: Usual initial dosage is 2 mg of glimepiride and 30 mg of pioglitazone once daily.
Patients switching from concurrent therapy with separate glimepiride and pioglitazone preparations: Initiate the fixed combination at doses that are as close as possible to the dose of glimepiride and pioglitazone already being taken; adjust subsequent dosage based on response.
Patients transferring from monotherapy with other sulfonylureas or from combination therapy with pioglitazone and a sulfonylurea other than glimepiride: Initially, 2 mg of glimepiride and 30 mg of pioglitazone once daily; adjust subsequent dosage based on response.
Special Populations
Hepatic Impairment
Glimepiride monotherapy: No specific population dosage recommendations at this time.
Fixed combination of glimepiride and pioglitazone: No specific population dosage recommendations at this time; use with caution in patients with liver disease.
Renal Impairment
Glimepiride monotherapy: Initially, 1 mg once daily. Titrate dosage upward based on fasting glucose concentrations; conservative titration scheme recommended.
Fixed combination of glimepiride and pioglitazone: No specific population dosage recommendations at this time. To minimize risk of hypoglycemia, initial dosage, dosage increments, and maintenance dosage should be conservative.
Geriatric Patients
Geriatric individuals may be particularly sensitive to the hypoglycemic effects of glimepiride.
Glimepiride monotherapy: Initially, 1 mg once daily. Titrate dosage upward with care. Conservative initial and maintenance dosages recommended.
Fixed combination of glimepiride and pioglitazone: No specific population dosage recommendations at this time; initial dosage, dosage increments, and maintenance dosage should be conservative.
Patients with Heart Failure
Fixed combination of glimepiride and pioglitazone: Initiate glimepiride/pioglitazone fixed-combination at lowest recommended dosage; use fixed-combination preparation only after patient has received pioglitazone 15 mg once daily as monotherapy and has safely tolerated dosage titration to 30 mg once daily. If subsequent dosage adjustment required, closely monitor for weight gain, edema, or other manifestations of heart failure exacerbation.
Cautions for Glimepiride
Contraindications
-
Known hypersensitivity to glimepiride or any ingredient in formulation.
-
Hypersensitivity to sulfonamide derivatives.
Warnings/Precautions
Hypoglycemia
Can cause severe hypoglycemia; ability to concentrate and react may be impaired as a result. These impairments may present risk in situations where these abilities are important, such as driving or operating machinery. Severe hypoglycemia can lead to unconsciousness or convulsions and may result in temporary or permanent impairment of brain function or death.
Appropriate patient selection and careful attention to dosage are important to avoid glimepiride-induced hypoglycemia. Geriatric patients, debilitated, or malnourished patients, or those with adrenal, pituitary, renal, or hepatic impairment may be particularly susceptible to hypoglycemia. Use caution when initiating and increasing dosage in patients predisposed to hypoglycemia. Hypoglycemia more likely to occur when caloric intake is deficient, after severe or prolonged exercise, and when alcohol is ingested. Hypoglycemia may be more difficult to recognize in geriatric patients, in patients with autonomic neuropathy, and in those receiving β-adrenergic blocking agents or other sympatholytic agents. In these situations, severe hypoglycemia may occur before patient is aware of hypoglycemia.
Inform patients and responsible family members of risks of hypoglycemia, symptoms and treatment of hypoglycemic reactions, and conditions that predispose to the development of such reactions.
Hypersensitivity Reactions
Postmarketing reports of hypersensitivity reactions, including anaphylaxis, angioedema, and Stevens-Johnson syndrome.
If hypersensitivity reaction suspected, promptly discontinue glimepiride, assess for other potential causes of reaction, and initiate alternate treatment for diabetes mellitus.
Hemolytic Anemia
Sulfonylureas, including glimepiride, can cause hemolytic anemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Hemolytic anemia reported in patients receiving glimepiride with no known history of G6PD deficiency.
Use caution in patients with G6PD deficiency and consider use of non-sulfonylurea alternative.
Increased Risk of Cardiovascular Mortality
Oral hypoglycemic drugs reported to be associated with increased cardiovascular mortality as compared to diet alone or diet plus insulin.
Inform patients of potential risk and advantages of glimepiride and of alternative therapy.
Macrovascular Outcomes
There have been no clinical studies establishing conclusive evidence of macrovascular risk reduction with glimepiride.
Use of Fixed Combinations
When used in fixed combination with pioglitazone or other drugs, consider the cautions, precautions, and contraindications associated with pioglitazone or other concomitant agent(s).
Specific Populations
Pregnancy
Available data from small number of published studies and decades of postmarketing experience have not identified any drug associated risk for major birth defects, miscarriage, or adverse maternal outcomes. Sulfonylureas (including glimepiride) cross the placenta and have been associated with neonatal adverse reactions such as hypoglycemia. Prolonged hypoglycemia (lasting 4—10 days) reported in neonates born to mothers receiving sulfonylureas at time of delivery and with use of agents with prolonged half-life.
Poorly controlled diabetes mellitus during pregnancy carries risks for mother and fetus. Due to risk of prolonged hypoglycemia in neonates born to mothers receiving a sulfonylurea at time of delivery, glimepiride should be discontinued at least 2 weeks before expected delivery. Observe newborns for symptoms of hypoglycemia and respiratory distress and manage accordingly.
Lactation
No information regarding presence in human milk or effect on milk production. Distributed into milk in rats. Developmental and health benefits of breastfeeding should be considered along with any potential adverse effects on breast-fed child from glimepiride or from underlying maternal condition. Breast-fed infants of lactating women using glimepiride should be monitored for symptoms of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures).
Pediatric Use
Use not recommended because of adverse effects on body weight and hypoglycemia.
Geriatric Use
No substantial differences in safety, efficacy, or pharmacokinetics relative to younger adults, but increased sensitivity cannot be ruled out.
Possible increased risk of adverse effects due to age-related decreases in renal function.
Increased risk of hypoglycemia; may be difficult to recognize in geriatric patients.
Use caution when initiating and increasing dosage of glimepiride in geriatric patients.
Hepatic Impairment
Pharmacokinetics of glimepiride not adequately evaluated in patients with hepatic impairment.
Renal Impairment
Increased risk of hypoglycemia; conservative dosing recommended.
Obesity
Lower maximum plasma concentration (Cmax) and AUC than patients with normal body weight with similar time to maximum plasma concentration (Tmax), clearance, and volume of distribution.
Common Adverse Effects
Most common adverse effects (≥5% and more common than placebo): Hypoglycemia, headache, nausea, dizziness.
Drug Interactions
Metabolized by CYP2C9.
Drugs Affecting Hepatic Microsomal Enzymes
Pharmacokinetic interactions likely with drugs that are inhibitors and inducers of CYP2C9; possible alteration in metabolism of glimepiride.
Protein-bound Drugs
Potential pharmacokinetic interaction (increased hypoglycemic effect).
Close observation recommended when initiating or discontinuing concomitant therapy with a highly protein-bound drug.
Drugs Affecting Glucose Metabolism
A number of medications affect glucose metabolism and may require glimepiride dosage adjustment and close monitoring for hypoglycemia or worsening glycemic control.
A number of medications reduce the glucose-lowering effect of glimepiride, leading to worsening glycemic control.
Signs of hypoglycemia may be reduced or absent in patients taking sympatholytic drugs such as β-adrenergic blocking agents and clonidine.
Close observation recommended when initiating or discontinuing concomitant therapy.
Specific Drugs
|
Drug |
Interaction |
Comments |
|---|---|---|
|
ACE inhibitors |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Alcohol (acute and chronic ingestion) |
May potentiate or weaken hypoglycemic effect |
|
|
Anabolic steroids and androgens |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Atypical antipsychotics (i.e., clozapine, olanzapine) |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Azole antifungals |
Miconazole (oral): Increased hypoglycemic effect; severe hypoglycemia reported Fluconazole: Increased plasma concentration of glimepiride; potential for increased hypoglycemic effect |
Miconazole: Not known whether interaction occurs with other antifungal dosage forms Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
β-Adrenergic blocking agents (e.g., propranolol) |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect Increased peak plasma concentrations and half-life and decreased clearance of glimepiride with concomitant propranolol |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy Signs of hypoglycemia may be reduced or absent |
|
Barbiturates |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Chloramphenicol |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Clarithromycin |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Colesevelam |
Reduced maximum plasma concentration and total exposure of glimepiride |
Administer glimepiride at least 4 hours prior to colesevelam |
|
Corticosteroids |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Coumarin anticoagulants (e.g., warfarin) |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect No change in warfarin protein binding with concomitant administration but slight decrease in pharmacodynamic response |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy No clinically important pharmacokinetic interaction with warfarin reported |
|
Cyclophosphamide |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Danazol |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Diazoxide |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Disopyramide |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Diuretics (e.g., thiazides) |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Estrogens |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Fibrates |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Fluoxetine |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Glucagon |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
H2-receptor antagonists (e.g., cimetidine, ranitidine) |
Absorption and disposition of glimepiride not altered |
|
|
Hormonal contraceptives |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Isoniazid |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Laxatives |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
MAO inhibitors |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Nicotinic acid |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
NSAIAs |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Pentoxifylline |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Phenothiazines |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Phenytoin |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Pramlintide acetate |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Probenecid |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Protease inhibitors |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Quinolones |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Rifampin |
Rifampin may induce metabolism of glimepiride, causing decreased plasma concentrations of glimepiride, which may lead to worsening glycemic control |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Salicylates (e.g., aspirin) |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect Possible decreased peak plasma concentrations and AUC of glimepiride |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Somatostatin analogs |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Somatropin |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Sulfonamides |
Highly protein-bound drugs may displace glimepiride from plasma proteins and potentiate hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Sympathomimetic agents |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
|
Tetracyclines |
Potential for increased hypoglycemic effect |
Observe carefully for hypoglycemic effects when initiating concomitant therapy or loss of glycemic control when discontinuing such therapy |
|
Thyroid hormones |
Potential for decreased hypoglycemic effect |
Observe carefully for loss of glycemic control when initiating concomitant therapy or hypoglycemic effects when discontinuing such therapy |
Glimepiride Pharmacokinetics
Absorption
Bioavailability
Peak blood concentrations attained within 2–3 hours.
Onset
Time to maximum effect about 2–3 hours.
Duration
Glucose-lowering effect persists for 24 hours.
Food
Food decreases mean peak blood concentrations and AUC by 8 and 9%, respectively.
Distribution
Extent
Not known if glimepiride is distributed into human milk.
Plasma Protein Binding
>99.5%.
Elimination
Metabolism
Metabolized by CYP2C9 and by cytosolic enzymes to active and inactive metabolites.
Elimination Route
Excreted in urine (60%) and feces (40%) predominantly as metabolites.
Special Populations
Renal impairment: Decreased serum drug concentrations and increased concentrations and half-lives of the metabolites.
Geriatric patients: At steady state, lower mean AUC (13%) and increased clearance (11%) compared with younger patients.
Obesity: lower maximum plasma concentration and AUC compared to normal body weight.
No difference in pharmacokinetics based on sex (when adjusted for body weight) or race.
No difference in pharmacokinetics between healthy subjects and patients with diabetes mellitus.
Stability
Storage
Oral
Tablets
Glimepiride: Well-closed containers with safety closures at 20–25°C.
Actions
-
Reduces both fasting and postprandial blood glucose concentrations and HbA1c in a dose-dependent manner.
-
Lowers blood glucose concentration principally by stimulating postprandial secretion of endogenous insulin from the beta cells of the pancreas. Also enhances peripheral sensitivity to insulin.
-
Provides overall glycemic control without appreciably increasing fasting insulin secretion.
-
Ineffective in the absence of functioning beta cells.
Advice to Patients
-
Inform patients of the potential risks and advantages of glimepiride therapy and of alternative forms of treatment.
-
Inform patients of the importance of taking glimepiride once daily with breakfast or with the first main meal.
-
Inform patients and caregivers of the risk of hypoglycemia. Inform patients of the symptoms and treatment of hypoglycemic reactions and identifying conditions that predispose to the development of such reactions. Inform patients that their ability to concentrate and react may be impaired as a result of hypoglycemia and that this may present a risk in situations where these abilities are especially important, such as driving or operating other machinery.
-
Inform patients that hypersensitivity reactions may occur with glimepiride and that if a reaction occurs to seek medical treatment and discontinue glimepiride.
-
Inform patients of the importance of regular monitoring of blood glucose (preferably self-monitoring) and of HbA1c.
-
Advise patients of the importance of informing clinicians if they are or plan to become pregnant or plan to breast-feed. Advise breast-feeding women taking glimepiride to monitor breast-fed infants for signs of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures).
-
Advise patients of the importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs and dietary or herbal supplements, as well as any concomitant illnesses.
-
Inform patients of other important precautionary information.
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer’s labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.
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, scored |
1 mg* |
Glimepiride Tablets |
|
|
2 mg* |
Glimepiride Tablets |
|||
|
4 mg* |
Glimepiride Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
|
Routes |
Dosage Forms |
Strengths |
Brand Names |
Manufacturer |
|---|---|---|---|---|
|
Oral |
Tablets |
2 mg with Pioglitazone Hydrochloride 30 mg (of pioglitazone)* |
Duetact |
Takeda |
|
Glimepiride with Pioglitazone Hydrochloride |
||||
|
4 mg with Pioglitazone Hydrochloride 30 mg (of pioglitazone)* |
Duetact |
Takeda |
||
|
Glimepiride with Pioglitazone Hydrochloride |
AHFS DI Essentials™. © Copyright 2025, Selected Revisions April 10, 2025. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.
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