Glyburide is used as an adjunct to diet and exercise to improve glycemic control in adult patients with type 2 diabetes mellitus.1, 3, 4, 49, 50, 51, 52, 53, 54, 55, 56, 57 Sulfonylureas, including glyburide, also may be used in combination with one or more other oral antidiabetic agents (e.g., metformin, thiazolidinedione) or insulin as an adjunct to diet and exercise for the management of type 2 diabetes mellitus in patients who do not achieve adequate glycemic control with diet, exercise, and oral antidiabetic agent monotherapy.1, 124, 158, 162, 165, 166, 169, 170, 195, 198, 200, 201, 202, 203
Glyburide is commercially available as a single entity preparation and in fixed combination with metformin hydrochloride.1, 124, 158 The fixed combination of glyburide and metformin hydrochloride is used as an adjunct to diet and exercise to improve glycemic control in adult patients with type 2 diabetes mellitus.158
The manufacturer states that glyburide should not be used in patients with type 1 diabetes mellitus or diabetic ketoacidosis; such use is contraindicated.1, 124
When given as monotherapy for the management of type 2 diabetes mellitus, glyburide improves glycemic control as evidenced by reductions in fasting blood glucose and glycosylated hemoglobin (hemoglobin A1c; HbA1c).158 Glyburide may be useful in some patients with type 2 diabetes mellitus who have primary3 or secondary1, 3, 4 failure to other sulfonylurea antidiabetic agents; however, primary or secondary failure to glyburide may also occur.1, 3, 4, 129 Primary failure to sulfonylurea drugs is characterized by lack of efficacy when the drug is first administered to a patient.1, 124 Secondary failure to sulfonylurea drugs is characterized by progressively decreasing diabetic control1, 60 following 1 month to several years of good control.60, 103, 129
Interim data from a substudy (UKPDS 26) of UKPDS in newly diagnosed type 2 diabetic patients receiving intensive antidiabetic therapy (maintenance of fasting plasma glucose below 108 mg/dL by increasing doses of glyburide or chlorpropamide [no longer commercially available in the US] to maximum recommended dosage) showed that secondary failure (defined as fasting plasma glucose exceeding 270 mg/dL or symptoms of hyperglycemia despite maximum recommended daily dosage of 20 mg of glyburide or 500 mg of chlorpropamide) occurred overall at about 7% per year.128, 129 The failure rate at 6 years was 48% among patients receiving glyburide and about 40% among patients receiving chlorpropamide.129 In the UKPD studies, stepwise addition of insulin or metformin to therapy with maximal dosage of a sulfonylurea was required periodically over time to improve glycemic control.127, 128, 129, 130, 136, 143, 146, 147 In another substudy (UKPDS 49), progressive deterioration in diabetes control was such that monotherapy was effective in only about 50% of patients after 3 years and in only about 25% of patients after 9 years; thus, most patients require multiple-drug antidiabetic therapy over time to maintain such target levels of disease control.147 At diagnosis, risk factors predisposing toward sulfonylurea failure included higher fasting plasma glucose concentrations, younger age, and lower pancreatic β-cell reserve.129, 147
Sulfonylureas, including glyburide, may be used in combination with one or more other oral antidiabetic agents (e.g., metformin, glucagon-like peptide 1 [GLP-1] receptor agonists, sodium-glucose cotransporter 2 (SGLT2) inhibitors, dipeptidyl peptidase-4 [DPP-4] inhibitors, thiazolidinedione derivatives) as an adjunct to diet and exercise for the management of type 2 diabetes mellitus in patients who do not achieve adequate glycemic control with diet, exercise, and oral antidiabetic agent monotherapy.158, 195, 198, 200, 201, 202, 209, 707, 708
Glyburide may be used concomitantly with metformin as initial therapy in the management of patients with type 2 diabetes mellitus whose hyperglycemia cannot be controlled by diet and exercise alone.1, 124, 158 In a 20-week, double-blind, randomized trial in drug-naïve patients with type 2 diabetes mellitus whose hyperglycemia was inadequately controlled (baseline HbA1c values between 7 and 11%) by diet and exercise, treatment was initiated with either placebo, glyburide 2.5 mg, metformin hydrochloride 500 mg, or the fixed combination of glyburide 1.25 mg/metformin hydrochloride 250 mg or glyburide 2.5 mg/metformin hydrochloride 500 mg daily.158 The dosage of each therapy was progressively increased during weeks 4-8 to achieve a target fasting plasma glucose concentration of 126 mg/dL or to a maximum of 4 tablets daily.158 Patients receiving the fixed combination of glyburide and metformin had greater reductions in HbA1c and fasting plasma glucose concentrations than those receiving glyburide, metformin, or placebo; at the end of the study, strict glycemic control (e.g., HbA1c values <7%) was achieved in 59.9, 50.4, 66.4, or 71.7% of patients receiving mean dosages of glyburide 5.3 mg, metformin hydrochloride 1.32 g, glyburide 2.78 mg/metformin hydrochloride 557 mg, or glyburide 4.1 mg/metformin hydrochloride 824 mg, respectively.158
Glyburide also may be used concomitantly with metformin in patients who do not achieve adequate control of hyperglycemia despite diet, exercise, and monotherapy with either glyburide (or another sulfonylurea antidiabetic agent) or metformin.1, 124, 158, 188, 189 In a double-blind, randomized study, patients with type 2 diabetes mellitus whose hyperglycemia was inadequately controlled (mean baseline HbA1c values: 9.5%, mean baseline fasting plasma glucose: 213 mg/dL) with oral sulfonylurea therapy at a dosage at least 50% of the maximum recommended daily dosage (e.g., glyburide 10 mg daily, glipizide 20 mg daily) received therapy with glyburide 20 mg (fixed dosage), metformin hydrochloride 500 mg, or the fixed combination of glyburide 2.5 mg/metformin hydrochloride 500 mg or glyburide 5 mg/metformin hydrochloride 500 mg daily.158 The dosages of metformin and the fixed-combination preparations were titrated to achieve a target fasting plasma glucose concentration of <140 mg/dL or to a maximum of 4 tablets daily.158 At 16 weeks, patients receiving the fixed combination of glyburide and metformin hydrochloride in daily dosages of up to 20 mg of glyburide and 2 g of metformin hydrochloride had lower HbA1c, fasting plasma glucose, and postprandial plasma glucose concentrations than patients receiving monotherapy with glyburide or metformin, who had no appreciable change in HbA1c values.158
Combined therapy with insulin and oral antidiabetic agents may be useful in some patients with type 2 diabetes mellitus whose blood glucose concentrations are not adequately controlled with maximal dosages of the oral agent and/or as a means of providing increased flexibility with respect to timing of meals and amount of food ingested.116, 117, 118, 119, 120, 162, 165, 166, 169, 170 Concomitant therapy with insulin (e.g., given as intermediate- or long-acting insulin at bedtime or rapid-acting insulin at meal times)165, 166, 167, 171, 172, 173 and one or more oral antidiabetic agents appears to improve glycemic control with lower dosages of insulin than would be required with insulin alone and may decrease the potential for body weight gain associated with insulin therapy.162, 165, 166, 167, 174, 171, 172, 175, 173, 176, 177 Oral antidiabetic therapy combined with insulin therapy may delay progression to either intensive insulin monotherapy or to a second daytime injection of insulin combined with oral antidiabetic therapy.171 However, such combined therapy may increase the risk of hypoglycemic reactions.166, 178, 171, 172
The American Diabetes Association (ADA) publishes an annual guideline on diabetes management, which provides clinical practice recommendations for glucose-lowering therapies in patients with type 2 diabetes mellitus.707 The current 2025 ADA guideline states that in adults with type 2 diabetes mellitus, pharmacologic strategies that provide sufficient effectiveness to achieve and maintain the intended treatment goals should be used and guided by a person-centered shared decision-making approach.707 In general, higher-efficacy approaches have a greater likelihood of achieving glycemic goals.707 Weight management should be included as a distinct treatment goal, and healthy lifestyle behaviors should also be considered.707 When selecting an appropriate treatment regimen, clinicians should be guided by factors such as cardiovascular and renal comorbidities, drug efficacy and adverse effects, hypoglycemic risk, presence of overweight or obesity, cost, access, and patient preferences.707 Sulfonylureas do not have additive beneficial effects on cardiovascular or renal outcomes and are associated with an increased risk of weight gain and hypoglycemia.707 Therefore, their use should be limited or discontinued; when used, these guidelines recommend the lowest possible dosage.707
The American Association of Clinical Endocrinology (AACE) also publishes guidelines for the management of type 2 diabetes.708 The principles of diabetes management outlined in these guidelines are similar to those recommended by the ADA.708 The AACE guidelines state that in adult patients with type 2 diabetes, sulfonylureas are associated with a higher risk of hypoglycemia and weight gain and therefore are not preferred; however, sulfonylureas may remain a treatment option in those patients with access or cost barriers to other antidiabetic agents.708
Dispensing and Administration Precautions
Glyburide is administered orally.1, 124 The drug (as conventional or micronized formulations) is usually administered as a single daily dose given each morning with breakfast, or with the first main meal.1, 3, 124 Once-daily dosing of glyburide provides adequate control of blood glucose concentration throughout the day in most patients with usual meal patterns;1, 91, 92, 93 however, some patients, particularly those who require more than 10 mg of the drug daily (as conventional formulations) or more than 6 mg daily (as micronized glyburide),124 may have a more satisfactory response when glyburide is administered in 2 divided doses daily.1, 124 There is some evidence that, when a divided-dosing regimen is used, blood glucose concentration following breakfast may be better controlled when the morning dose is administered 30 minutes before rather than with the meal; a similar tendency has been observed following the midday meal, but not the evening meal, when the remaining portions of the equally divided daily dose were administered 30 minutes before rather than with these meals.28
When given concomitantly with colesevelam, glyburide should be administered at least 4 hours prior to colesevelam.1, 124
Patients who do not adhere to their prescribed dietary and drug regimens are more likely to have an unsatisfactory response to therapy.1 In patients usually well controlled by dietary management alone, short-term therapy with glyburide may be sufficient during periods of transient loss of diabetic control.1
The fixed combination of glyburide and metformin hydrochloride should be taken once or twice daily with meals.158 See the full prescribing information for additional administration instructions for the combination product.158
Store glyburide tablets at 20—25°C in a tightly closed container.1, 124, 158 Dispense in well-closed containers with safety closures.1, 124
Dosage of glyburide must be based on periodic fasting blood glucose and glycosylated hemoglobin (hemoglobin A1c [HbA1c]) determinations and must be carefully individualized.1 If appropriate glyburide dosage regimens are not followed, hypoglycemia may be precipitated .1
Formulations of micronized glyburide (Glynase® PresTab® and other micronized tablets available by nonproprietary name) contain smaller particles of the drug than those contained in nonmicronized (conventional) formulations.124As a result, micronized formulations of glyburide are not bioequivalent with conventional formulations, and dosage should be retitrated when transferring patients from micronized to conventional formulations or vice versa.124The manufacturers' labeling should be consulted for additional information on the use of micronized glyburide, including associated precautions and detailed information on dosage titration.124
Initial Dosage in Previously Untreated Patients
For the management of type 2 diabetes mellitus in patients not previously receiving insulin or sulfonylurea antidiabetic agents, the usual initial adult dosage of glyburide is 2.5-5 mg orally daily, although it may be necessary to initiate therapy with 1.25 mg daily in patients who are sensitive to the hypoglycemic effects of sulfonylureas (e.g., geriatric, debilitated or malnourished patients).1 Subsequent dosage should be adjusted according to the patient's tolerance and therapeutic response; increases in dosage should be made in increments of no more than 2.5 mg at weekly intervals.1
In general, initial dosages of micronized glyburide range from 1.5-3 mg daily, although it may be necessary to initiate micronized therapy with 0.75 mg daily in patients who are sensitive to the hypoglycemic effects of sulfonylureas (e.g., geriatric, debilitated, or malnourished patients); the manufacturer recommends that the initial dosage not exceed 3 mg daily regardless of the dosage of other sulfonylurea employed at transfer.124 Subsequent dosage should be adjusted according to the patient's tolerance and therapeutic response; increases in dosage should be made in increments of no more than 1.5 mg at weekly intervals.124
Initial Dosage in Patients Transferred from Other Oral Antidiabetic Agents
A transition period generally is not required when transferring from most other antidiabetic agents to glyburide, and administration of the other agent may be abruptly discontinued.1, 3 An initial or loading dose of glyburide is not necessary when transferring from other antidiabetic agents to glyburide.1, 124 The transfer should be performed conservatively.1
For the management of type 2 diabetes mellitus in patients previously receiving other oral antidiabetic agents, the initial dosage of glyburide should be 2.5-5 mg daily.1 Although patients may be transferred from the maximum dosage of other antidiabetic agents, the initial dosage of glyburide should not exceed 5 mg daily.1 Subsequent dosage is adjusted according to the patient's tolerance and therapeutic response.1 Although an exact dosage relationship between glyburide and other sulfonylurea antidiabetic agents does not exist, approximate dosage equivalencies have been estimated.1
The manufacturer recommends an initial dosage of micronized glyburide of 1.5-3 mg daily in patients transferring from other oral antidiabetic agents; the initial dosage should not exceed 3 mg daily regardless of the dosage of other antidiabetic agent employed at transfer.124
Initial Dosage in Patients Transferred from Insulin
In general, patients who were previously maintained on insulin dosages not exceeding 40 units daily may be transferred directly to glyburide, and administration of insulin may be abruptly discontinued; the initial glyburide dosage is 2.5-5 mg daily in patients whose insulin dosage was less than 20 units daily and 5 mg daily in patients whose insulin dosage was 20-40 units daily.1 In patients requiring insulin dosages exceeding 40 units daily, an initial glyburide dosage of 5 mg daily should be started and insulin dosage reduced by 50%.1 Subsequently, insulin is withdrawn gradually and dosage of glyburide is increased in increments of 1.25-2.5 mg daily every 2-10 days, according to the patient's tolerance and therapeutic response.1
The initial dosage of micronized glyburide is 1.5—3 mg daily in patients whose insulin dosage was less than 20 units daily and 3 mg daily in patients whose insulin dosage was 20—40 units daily.124 In patients requiring insulin dosages exceeding 40 units daily, an initial micronized glyburide dosage of 3 mg daily should be started and insulin dosage reduced by 50%.124 Subsequently, insulin is withdrawn gradually and dosage of micronized glyburide is increased in increments of 0.75—1.5 mg every 2—10 days.124
During the period of insulin withdrawal, patients should test their blood for glucose60 and their urine for glucose and/or ketones at least 3 times daily,1, 124 and should be instructed to report the results to their physician so that appropriate adjustments in therapy may be made, if necessary.1, 3, 124 The presence of persistent ketonuria with glycosuria, ketosis, and/or inadequate lowering or persistent elevation of blood glucose concentration indicates that the patient requires insulin therapy.1 During the period of insulin withdrawal, hypoglycemia may rarely occur.1
The adult maintenance dosage of glyburide for the management of type 2 diabetes mellitus ranges from 1.25-20 mg daily.1 Most patients require 2.5-10 mg daily and some may require up to 15 mg daily; only a few patients will benefit from dosages exceeding 15 mg daily.3 Once daily dosing is usually satisfactory; some patients, particularly those receiving more than 10 mg daily, may have a more satisfactory response with twice daily dosing.1 The maximum recommended dosage is 20 mg daily.1
Maintenance dosage of the micronized formulation should be individualized according to glycemic control but usually ranges from 0.75-12 mg daily given as a single dose or in divided doses.124 Once daily dosing is usually satisfactory; some patients, particularly those receiving more than 6 mg daily, may have a more satisfactory response with twice daily dosing.124 The maximum recommended dosage is 12 mg daily.124
Glyburide/Metformin Hydrochloride Fixed-combination Therapy
Glyburide should be added gradually to the existing dosage regimen of patients not responding adequately to 4 weeks of metformin monotherapy at maximum dosage.1, 124 When glyburide and metformin are administered concomitantly, dosage of each drug should be adjusted upward until adequate glycemic control is achieved, and patients should be monitored periodically (e.g., determination of blood glucose concentrations) to determine the optimal effective dosage of each drug.1, 124 In patients receiving glyburide concomitantly with metformin, the risk of hypoglycemia may be increased, and appropriate precautions should be taken.1, 124
If the commercially available fixed-combination preparation of glyburide and metformin hydrochloride is used in patients not currently receiving either glyburide (or another sulfonylurea antidiabetic agent) or metformin hydrochloride, the recommended initial dosage is 1.25 mg of glyburide and 250 mg of metformin hydrochloride once or twice daily with meals.158
In patients with inadequate glycemic control on either glyburide (or another sulfonylurea antidiabetic agent) or metformin hydrochloride alone, the recommended initial dosage of the commercially available fixed-combination preparation is 2.5 or 5 mg of glyburide with 500 mg of metformin hydrochloride twice daily with meals.158
In patients previously treated with a combination of glyburide (or another sulfonylurea antidiabetic agent) and metformin hydrochloride, the initial dosage of glyburide and metformin hydrochloride in fixed combination should not exceed the daily dosages of glyburide (or another sulfonylurea antidiabetic agent) and metformin given separately.158
The dosage of the fixed combination of glyburide and metformin should be gradually titrated upward based on glycemic control and tolerability until a maximum daily dosage of 20 mg of glyburide and 2 g of metformin hydrochloride is reached.158
Conventional formulations: The initial recommended dosage is 1.25 mg daily.1 Initial and maintenance dosages of glyburide should be conservative in patients with hepatic impairment to avoid hypoglycemic reactions.1
Micronized formulations: The initial recommended dosage is 0.75 mg daily.124 Initial and maintenance dosages of glyburide should be conservative in patients with hepatic impairment to avoid hypoglycemic reactions.124
Glyburide/Metformin Hydrochloride Fixed-combination Therapy
Use of glyburide in fixed combination with metformin hydrochloride is not recommended in patients with hepatic impairment.158
Conventional formulations: The initial recommended dosage is 1.25 mg daily.1 Initial and maintenance dosages of glyburide should be conservative in patients with renal impairment to avoid hypoglycemic reactions.1
Micronized formulations: The initial recommended dosage is 0.75 mg daily.124 Initial and maintenance dosages of glyburide should be conservative in patients with renal impairment to avoid hypoglycemic reactions.124
Glyburide/Metformin Hydrochloride Fixed-combination Therapy
Glyburide in fixed combination with metformin hydrochloride should not be initiated in patients with an estimated glomerular filtration rate (eGFR) between 30—45 mL/minute per 1.73 m2.158 Use of the fixed combination is contraindicated in patients with an eGFR less than 30 mL/minute per 1.73 m2.158 In patients taking glyburide in fixed combination with metformin whose eGFR falls below 45 mL/minute per 1.73 m2, assess the benefits and risks of continuing therapy.158 Discontinue if the patient's eGFR falls below 30 mL/minute per 1.73 m2.158
Conventional formulations: The initial recommended dosage is 1.25 mg daily.1 Initial and maintenance dosages of glyburide should be conservative in geriatric patients to avoid hypoglycemic reactions.1, 124
Micronized formulations: The initial recommended dosage is 0.75 mg daily.124 Initial and maintenance dosages of glyburide should be conservative in geriatric patients to avoid hypoglycemic reactions.124
Glyburide/Metformin Hydrochloride Fixed-Combination Therapy
Glyburide alone or in fixed combination with metformin should be used with caution in geriatric patients, since aging is associated with reduced renal function.1 The initial and maintenance dosages of glyburide alone or in fixed combination with metformin should be conservative in geriatric patients.1, 124 Renal function should be assessed with initial dosage selection and with each dosage adjustment in geriatric patients.1, 124
Conventional formulations: In debilitated or malnourished patients, or in patients with adrenal or pituitary insufficiency, the initial dosage of glyburide should be 1.25 mg daily.1
Micronized formulations: In debilitated or malnourished patients, or in patients with adrenal or pituitary insufficiency, the initial dosage of glyburide should be 0.75 mg daily.124
Increased Risk of Cardiovascular Mortality
The administration of oral antidiabetic agents has been reported to be associated with increased cardiovascular mortality as compared to treatment with diet alone or diet with insulin therapy.1, 124, 158
Several large, long-term studies have evaluated the cardiovascular risks associated with the use of oral sulfonylurea antidiabetic agents.60, 61, 62, 63, 127, 128, 131, 144 In 1970, the University Group Diabetes Program (UGDP) reported that administration of oral antidiabetic agents (i.e., tolbutamide or phenformin) was associated with increased cardiovascular mortality as compared to treatment with dietary regulation alone or with dietary regulation and insulin.1, 63, 124 The UGDP reported that type 2 diabetic patients who were treated for 5-8 years with dietary regulation and a fixed dose of tolbutamide (1.5 g daily) had a cardiovascular mortality rate approximately 2.5 times that of patients treated with dietary regulation alone; although a substantial increase in total mortality was not observed, the use of tolbutamide was discontinued because of the increase in cardiovascular mortality, thereby limiting the ability of the study to show an increase in total mortality.1, 63, 124 The results of the UGDP study have been exhaustively analyzed, and there has been general disagreement in the scientific and medical communities regarding the study's validity and clinical importance.60, 61, 62, 63 However, results from the United Kingdom Prospective Diabetes Study (UKPDS), a large, long-term (over 10 years) study in newly diagnosed type 2 diabetic patients, did not confirm an increase in cardiovascular events or mortality in the group treated intensively with sulfonylureas, insulin, or combination therapy compared with that in the group treated with less intensive conventional antidiabetic therapy.127, 128, 130, 131
In the UKPDS study, the overall aggregate rates of death from macrovascular diseases such as myocardial infarction, sudden death, stroke, or peripheral vascular disease were not appreciably different among either intensive therapies (stepwise introduction of chlorpropamide [no longer commercially available in the US] or glyburide then insulin, or an oral sulfonylurea and insulin, or insulin alone to achieve fasting plasma glucose concentrations of 108 mg/dL) or less intensive conventional therapy (diet and oral antidiabetic agents or insulin to achieve fasting plasma glucose concentrations below 270 mg/dL without symptoms of hyperglycemia).127, 128 However, a trend in reduction in fatal and nonfatal myocardial infarction with intensive therapy was noted with sulfonylurea or insulin, and epidemiologic analysis of the data indicate that each 1% decrease in HbA1c was associated with an 18% reduction of fatal and nonfatal myocardial infarction.128, 131
Although one drug in the sulfonylurea class (tolbutamide) was included in the UGDP study, it is prudent from a safety standpoint to consider that this warning may also apply to other oral antidiabetic agents in this class, in view of their close similarities in mode of action and chemical structure.1, 124 Inform patients of the potential risks and advantages of glyburide and alternative therapies.1, 124
The manufacturer states that there are no clinical studies that conclusively establish macrovascular risk reduction with glyburide or any other antidiabetic drug.1, 124
Hypoglycemia, which may be severe1, 67, 68, 69, 74, 105 and has occasionally been fatal,67, 68, 74, 105 may occur in patients receiving glyburide alone or combined with other antidiabetic agents.66, 67, 68, 69, 73, 74, 77, 105, 158 In a controlled clinical trial in patients receiving initial therapy, symptoms of hypoglycemia (e.g., dizziness, shakiness, sweating, hunger) occurred in 21.3, 3.1, 11.4, or 37.7% of patients receiving glyburide (mean daily dosage: 5.3 mg), metformin hydrochloride (mean daily dosage: 1317 mg), glyburide in fixed combination with metformin hydrochloride (mean daily dosage: 2.78 mg of glyburide/557 mg of metformin hydrochloride), or glyburide in fixed combination with a higher dosage of metformin hydrochloride (mean daily dosage: 4.1 mg of glyburide/824 mg of metformin hydrochloride).158 Approximately 6.8% of patients experienced hypoglycemic symptoms while receiving the fixed combination of glyburide and metformin hydrochloride following inadequate control with sulfonylurea monotherapy.158 Appropriate patient selection and careful attention to dosage are important to avoid glyburide-induced hypoglycemia .1, 67
Although not clearly established, it has been suggested that glyburide may be more likely than other sulfonylurea antidiabetic agents to produce severe hypoglycemia.62, 66, 67, 69, 74, 77 In some clinical studies, hypoglycemia was the most frequent adverse effect of the drug.62 Hypoglycemia may occur as a result of excessive glyburide dosa 1, 68, 69 however, since the development of hypoglycemia is a function of many factors, including diet, or exercise without adequate caloric supplementation, this effect may occur in some patients receiving usual dosages of the drug.1, 49, 67, 68, 69, 73, 105, 124 Severe hypoglycemia, sometimes fatal, has occurred in some patients receiving as little as 2.5-5 mg of glyburide daily.49, 74, 105 The risk of hypoglycemia is increased during concurrent use of other antidiabetic agents, certain other agents, or alcohol.1, 124, 158 In patients receiving glyburide alone or in fixed combination with metformin, renal or hepatic insufficiency may increase the serum concentrations of both agents, and hepatic insufficiency may diminish gluconeogenic capacity; both of these conditions increase the risk of hypoglycemia.158 Debilitated, malnourished, or geriatric patients may be particularly susceptible to glyburide-induced hypoglycemia; this condition may be difficult to recognize in geriatric patients or in those receiving β-adrenergic blocking agents.1, 105, 158 Glyburide-induced hypoglycemia may also occur in nontherapeutic situations (e.g., inadvertent or intentional ingestion).70, 71, 72, 73, 76, 77, 78, 79
Management of glyburide-induced hypoglycemia depends on the severity of the reaction;1, 67, 69 patients with severe reactions require immediate hospitalization and treatment and observation until complete recovery is assured.1, 67, 69, 105 Hypoglycemia is usually, but not always, readily controlled by administration of glucose.1, 3, 67, 69, 105 If hypoglycemia occurs during therapy with the drug, immediate reevaluation and adjustment of glyburide dosage and/or the patient's meal pattern are necessary.1, 67, 69
The risks, symptoms. and treatment of hypoglycemia, as well as the conditions that predispose to its development, should be explained to patients and responsible family members.1, 124
When a patient stabilized on an antidiabetic agent is exposed to stress (e.g., fever, trauma, infection, surgery), a loss of glycemic control may occur.1, 124 During periods of stress, it may be necessary to discontinue glyburide and administer insulin.1, 124
The effectiveness of any antidiabetic agent, including glyburide, in lowering blood glucose to a desired level decreases in many patients over time which may be due to progression of disease severity or to diminished responsiveness to the drug.1, 124 Adequate dosage adjustment and adherence to dietary recommendations should be assessed before classifying a patient as experiencing secondary failure to glyburide.1, 124
Therapy with sulfonylurea agents in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency can lead to hemolytic anemia.1, 124, 158 Because glyburide is a sulfonylurea, it should be used with caution in patients with G6PD deficiency; use of a nonsulfonylurea antidiabetic drug should be considered.1, 124, 158 In postmarketing experience, hemolytic anemia also has been reported in patients receiving glyburide who did not have known G6PD deficiency.1, 124, 158
When glyburide is used in fixed combination with metformin, the cautions, precautions, and contraindications associated with metformin must be considered in addition to those associated with glyburide.158
There is insufficient evidence with glyburide in pregnant women to evaluate a drug-associated risk of adverse outcomes.1, 124 Reproduction studies in rats and rabbits at up to 500 times the human dose have revealed no evidence of harm to the fetus.1, 124 Since abnormal maternal blood glucose concentrations during pregnancy may be associated with a higher incidence of congenital abnormalities, many experts recommend that insulin be used during pregnancy to maintain optimum control of blood glucose concentration.1, 124 Use of glyburide in pregnant women is generally not recommended,1, 114, 124 and the drug should be used during pregnancy only when clearly necessary (e.g., when insulin therapy is infeasible).1, 124 Glyburide has been used in some pregnant women without unusual adverse effects.81, 186 In a prospective, comparative clinical trial in women with gestational diabetes, treatment with glyburide (mean daily dosage 9 mg, range 2.5-20 mg) initiated in the second trimester (11-33 weeks gestation) and continued until delivery resulted in similar degrees of glycemic control and perinatal outcomes as treatment with human insulin (mean daily dosage: 85 units).186 The incidence of hypoglycemia in neonates whose mothers received either insulin or glyburide therapy also was similar.186 In a retrospective study, hypoglycemia occurred and persisted for up to 2 days or longer in a few neonates whose mothers had received glyburide up to the time of delivery.81 Prolonged, severe hypoglycemia lasting 4-10 days has been reported in some neonates born to women who were receiving other sulfonylurea antidiabetic agents up to the time of delivery;124 this effect has been reported more frequently with the use of agents with prolonged elimination half-lives.1, 124 To minimize the risk of neonatal hypoglycemia if glyburide is used during pregnancy, the manufacturers recommend that the drug be discontinued at least 2 weeks before the expected delivery date.1, 124
Although it is not known whether glyburide is distributed into human milk, some sulfonylurea antidiabetic agents are distributed into human milk.1, 124 Because of the potential for hypoglycemia in nursing infants, a decision should be made whether to discontinue nursing or the drug, taking into account the importance of the drug to the woman.1, 124 If glyburide is discontinued, and if dietary management alone is inadequate for controlling blood glucose concentration, administration of insulin should be considered.1, 124
Females and Males of Reproductive Potential
Reproduction studies in rats and rabbits using glyburide doses up to 500 times the usual human dose have not revealed evidence of impaired fertility.124
Safety and efficacy of glyburide in pediatric patients have not been established.1, 124
Geriatric patients are particularly susceptible to the hypoglycemic action of glucose-lowering drugs.1, 124 Geriatric patients are prone to develop renal insufficiency, which may put them at risk for hypoglycemia; dosage selection should include assessment of renal function.1, 124 Hypoglycemia may be difficult to recognize in geriatric patients.1, 124 Initial and maintenance dosing should be conservative to avoid hypoglycemic reactions.1, 124
Hepatic insufficiency may cause elevated levels of glyburide and may diminish gluconeogenic capacity, which may increase the risk of serious hypoglycemic reactions.1, 124 Initial and maintenance dosing should be conservative to avoid hypoglycemic reactions.1, 124
Renal insufficiency may cause elevated levels of glyburide, which may increase the risk of serious hypoglycemic reactions.1, 124 Initial and maintenance dosing should be conservative to avoid hypoglycemic reactions.1, 124
The most common adverse effects of glyburide (conventional and micronized formulations) are GI disturbances (e.g., nausea, epigastric fullness, heartburn).1, 124
The most common adverse effects of glyburide in fixed combination with metformin hydrochloride (>5% of patients) include diarrhea, headache, nausea/vomiting, abdominal pain, and dizziness.158
Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes
Glyburide is metabolized principally by cytochrome P-450 (CYP) isoenzyme 2C9.711, 712 Potential interactions should be considered when glyburide is used concomitantly with inducers or inhibitors of CYP2C9.711, 712
Drugs That May Alter the Hypoglycemic Effect of Sulfonylureas
Drugs that may enhance the hypoglycemic effect of sulfonylurea antidiabetic agents, including glyburide, include chloramphenicol,1, 60, 62 coumarins,1, 124 monoamine oxidase inhibitors,1, 62, 124 nonsteroidal anti-inflammatory agents,1, 124 fluoroquinolone antibiotics (e.g., ciprofloxacin),1, 124 probenecid62, 124 , salicylates1, 124 and sulfonamides1, 124 When these drugs are administered or discontinued in patients receiving glyburide, the patient should be observed closely for hypoglycemia or loss of glycemic control, respectively.1
Drugs that may decrease the hypoglycemic effect of sulfonylurea antidiabetic agents (e.g., glyburide) include diuretics (e.g., furosemide),1, 62, 124 corticosteroids,1, 62, 124 phenothiazines,1, 62, 124 thyroid agents,1, 62, 124 estrogens,1, 62, 124 oral contraceptives,1, 62, 124 phenytoin,1, 62, 124 nicotinic acid,1, 62, 124 sympathomimetic agents,1, 62, 124 calcium-channel blocking agents,1, 90, 124 rifampin,62 and isoniazid.1, 124 When these drugs are administered or discontinued in patients receiving glyburide, the patient should be observed closely for loss of glycemic control or hypoglycemia, respectively.1
Because glyburide is highly protein bound, it theoretically could be displaced from binding sites by, or could displace from binding sites, other protein-bound drugs such as oral anticoagulants, hydantoins, salicylate and other nonsteroidal anti-inflammatory agents, angiotensin-converting enzyme (ACE) inhibitors, disopyramide, fluoxetine, clarithromycin, chloramphenicol, monoamine oxidase (MAO) inhibitors, probenecid, β-adrenergic blocking agents, and sulfonamides.1, 37, 38, 39, 40, 60, 62, 124 Glyburide may be less likely to be displaced from binding sites by, or displace from binding sites, other highly protein-bound drugs whose protein binding is ionic in nature.37, 40 Patients receiving highly protein-bound drugs should be observed for adverse effects when glyburide therapy is initiated or discontinued and vice versa.1, 124
Disulfiram-like reactions have occurred very rarely following the concomitant use of alcohol and glyburide.87
Concomitant use of certain azole antifungals (i.e., miconazole, fluconazole) and oral antidiabetic agents has resulted in increased plasma concentrations of the oral antidiabetic agent and/or hypoglycemia.1, 124 A potential interaction between oral miconazole leading to severe hypoglycemia has been reported; whether this interaction occurs with intravenous, topical, or vaginal preparations is not known.1, 124 Clinically important hypoglycemia may be precipitated by concomitant use of oral hypoglycemic agents and fluconazole, and at least one fatality has been reported from hypoglycemia in a patient receiving glyburide and fluconazole concomitantly.211
Beta-Adrenergic Blocking Agents
Several potential interactions between β-adrenergic blocking agents and sulfonylurea antidiabetic agents exist.60, 62β-Adrenergic blocking agents may impair glucose tolerance;60, 62 increase the frequency or severity of hypoglycemia;60, 62 block hypoglycemia-induced tachycardia, but not hypoglycemic sweating which may actually be increased;62 delay the rate of recovery of blood glucose concentration following drug-induced hypoglycemia;60, 62 alter the hemodynamic response to hypoglycemia, possibly resulting in an exaggerated hypertensive response;60 and possibly impair peripheral circulation.60 There is some evidence that many of these effects may be minimized by use of a β1-selective adrenergic blocking agent rather than a nonselective β-adrenergic blocking agent.60, 62 Acebutolol and propranolol have been shown to decrease the hypoglycemic action of glyburide in type 2 diabetic patients, presumably by decreasing insulin secretion.88 In another study in type 2 diabetic patients, insulin secretion during short-term atenolol therapy was reduced, but the hypoglycemic action of glyburide was not altered during short- or long-term atenolol administration.89 It generally is recommended that concomitant use of β-adrenergic blocking agents and sulfonylurea antidiabetic agents be avoided when possible; if concomitant therapy is necessary, use of a β1-selective adrenergic blocking agent may be preferred.62
An increased risk of elevated serum aminotransferase concentrations has been observed in patients receiving glyburide and bosentan concomitantly.1, 124, 233 Therefore, concomitant use of glyburide and bosentan is contraindicated.1, 124, 233
Concomitant administration of colesevelam and glyburide resulted in reductions in glyburide area under the concentration-time curve (AUC) and peak plasma concentration of 32 and 47%, respectively.1, 124 The reductions in glyburide AUC and peak plasma concentration were 20 and 15%, respectively, when the drug was administered 1 hour before colesevelam, and were not substantially changed (decrease of 7% and increase of 4%, respectively) when glyburide was administered 4 hours before colesevelam.1, 124 Therefore, glyburide should be given at least 4 hours prior to colesevelam.1, 124
Concomitant administration of metformin hydrochloride (single dose) resulted in highly variable decreases in AUC and peak plasma concentrations of glyburide (certain preparations) in patients with type 2 diabetes mellitus; no changes in metformin pharmacokinetics or pharmacodynamics were noted.1, 124 The clinical importance of these effects is uncertain.1, 124
Thiazide diuretics may exacerbate diabetes mellitus, resulting in increased requirements of sulfonylurea antidiabetic agents, temporary loss of glycemic control, or secondary failure to the antidiabetic agent.1, 62, 124 When thiazide diuretics are administered concomitantly with sulfonylurea antidiabetic agents, caution should be used.62
In a pharmacokinetic study in patients with type 2 diabetes mellitus, concomitant administration of glyburide (5 mg daily) and topiramate (150 mg daily) resulted in a 22% reduction in glyburide peak plasma concentration and a 25% reduction in glyburide AUC.1, 124 Systemic exposure (AUC) of the active metabolites, 4- trans -hydroxyglyburide (M1) and 3- cis -hydroxyglyburide (M2), was also reduced by 13 and 15%, respectively, and peak plasma concentration was reduced by 18 and 25%, respectively.1, 124 The steady-state pharmacokinetics of topiramate were unaffected by concomitant administration of glyburide.1, 124
The precise mechanism(s) of hypoglycemic action of sulfonylurea antidiabetic agents has not been clearly established, but the drugs, including glyburide, initially appear to lower blood glucose concentration principally by stimulating secretion of endogenous insulin from the beta cells of the pancreas.1, 3, 4, 8, 9, 10, 11, 12, 124 Sulfonylureas bind to the sulfonylurea receptor in the pancreatic β-cell plasma membrane, leading to closure of the ATP-sensitive potassium channel, thereby stimulating the release of insulin.158 Other mechanisms of the hypoglycemic action associated with short-term glyburide therapy appear to include reduction of basal hepatic glucose production9, 12, 121 and enhancement of peripheral insulin action at postreceptor (probably intracellular) site(s).9, 12, 13, 16, 48, 121 Following short-term administration of glyburide, an increase in insulin binding has been demonstrated in monocytes obtained from healthy individuals,17 but not in adipocytes obtained from diabetic patients.9 Like other sulfonylureas, glyburide alone is ineffective in the absence of functioning beta cells.1, 4, 124 On a weight basis, glyburide is one of the most potent of the sulfonylurea antidiabetic agents;4, 8 although an exact dosage relationship does not exist, a daily glyburide dosage of 5 mg controls blood glucose concentration to approximately the same degree as daily dosages of glipizide 5-10 mg.8, 14
The mechanism(s) of action of glyburide during prolonged administration has not been fully established.1, 4, 8, 9, 10, 11, 12, 15, 16, 17, 124 Glyburide-induced improvement in glucose tolerance during long-term therapy persists despite a gradual decline in glucose- or meal-stimulated secretion of endogenous insulin towards pretreatment levels.1, 4, 8, 9, 10, 11, 12, 124 During prolonged administration of sulfonylureas, including glyburide, extrapancreatic effects appear to substantially contribute to the hypoglycemic action of the drugs.4, 8, 9, 10, 11, 12, 15, 16, 17, 110, 111, 112, 121 Many extrapancreatic effects of the drugs have been proposed and/or studied, but the principal effects appear to include enhanced peripheral sensitivity to insulin and reduction of basal hepatic glucose production;4, 8, 9, 12, 110, 111, 112, 121 however, the nature of the long-term hypoglycemic effect and the mechanism(s) involved remain to be fully elucidated.4, 8, 9, 10, 11, 12, 15, 16, 17, 110, 111, 112 There is evidence that glyburide enhances the peripheral action of insulin at postreceptor (probably intracellular) site(s)9, 12, 48, 112, 121 and reduces basal hepatic glucose production9, 12, 112, 121 during long-term administration. An increase in insulin binding and/or number of insulin receptors has also been demonstrated in monocytes16 and adipocytes9 obtained from diabetic patients receiving long-term therapy with the drug.
Glyburide produces a mild diuresis by enhancing renal free water clearance.1, 18, 19, 20, 45, 46, 124 The diuretic effect has been demonstrated in healthy individuals,18, 19, 45 diabetic patients,18 and patients with neurohypophyseal diabetes insipidus;19, 20, 46 the drug apparently has no diuretic effect in patients with nephrogenic diabetes insipidus.19 The exact mechanism by which glyburide enhances renal free water clearance is not known.18, 19, 20, 45, 46 The diuretic action apparently is not mediated through an effect on the release of vasopressin (antidiuretic hormone) from the posterior pituitary or on the action of vasopressin at the renal collecting ducts.18, 19, 20 It has been suggested that glyburide inhibits reabsorption of sodium in the proximal renal tubule18 or nonvasopressin-dependent reabsorption of water in the distal renal tubule.19, 20
Currently available tablet formulations of glyburide appear to be reliably and almost completely absorbed following oral administration.4, 23, 24 Bioavailability studies have demonstrated that micronized glyburide and nonmicronized (conventional) glyburide tablets are not bioequivalent; therefore, patients switching from micronized to nonmicronized tablets or vice versa should have their dosage retitrated.124 Food apparently does not affect the rate or extent of absorption of glyburide.27, 28 Following oral administration of a single 5-mg dose of glyburide, the drug appears in plasma or serum within 15-60 minutes and peak plasma concentrations are attained within 2-4 hours (range: 2-8 hours).1, 24, 25, 26, 27, 29, 30, 31, 32, 47 The AUC for glyburide increases in proportion to increasing doses.1, 32, 124 Substantial interindividual variations in steady-state serum concentration have been reported in diabetic patients receiving the same dosage of glyburide.27, 95 Following single oral doses of glyburide in nonfasting diabetic or healthy individuals, plasma insulin concentration generally begins to increase within 15-60 minutes4, 27, 28, 29, 33, 34 and is maximal within 1-2 hours;4, 27, 28, 29, 34 in diabetic patients, increases in plasma insulin concentration may persist for up to 24 hours.4, 33, 49 Following single oral doses of the drug in fasting healthy individuals, the degree and duration of lowering of blood glucose concentration are proportional to the dose administered and the AUC;1, 32, 124 the hypoglycemic action generally begins within 45-60 minutes and is maximal within 1.5-3 hours.4, 27, 32, 49 In nonfasting diabetic patients, the hypoglycemic action of a single morning dose of glyburide may persist for up to 24 hours.1, 33, 124
Distribution of glyburide into human body tissues and fluids has not been fully characterized.30, 34, 36 Following oral or IV administration in animals, highest concentrations of the drug are attained in the liver, kidneys, and small and large intestines, with lower concentrations in the stomach, pancreas, spleen, mesenteric lymph nodes, mesenteric and retroperitoneal fat, heart, lungs, gonads, skeletal muscle, and brain.3, 36 In humans, glyburide is distributed in substantial amounts into bile.1, 3, 25, 26, 36, 124 Glyburide appears to cross the placenta,81 since prolonged hypoglycemia has occurred in neonates born to women who received the drug up to the time of delivery.81 It is not known if the drug is distributed into human milk.1, 124 Glyburide is more than 99% bound to serum proteins7, 25, 37 and its major metabolite, 4- trans -hydroxyglyburide, is more than 97% bound to serum proteins.25 Glyburide has a higher affinity for binding to serum albumin than does glipizide.37, 38 The protein binding of glyburide is principally nonionic;1, 37, 38, 39, 40, 124 consequently, glyburide may be less likely to be displaced from binding sites by, or displace from binding sites, other highly protein-bound drugs whose protein binding is ionic in nature.37, 40
Serum concentrations of glyburide appear to decline in a biphasic manner.1, 25, 32, 124 In studies in healthy adults using assays relatively specific for unchanged glyburide, the terminal elimination half-life has reportedly averaged 1.4-1.8 hours (range: 0.7-3 hours);24, 27, 29, 41, 97 when assays that also measured metabolites of the drug were used, the terminal elimination half-life has averaged about 10 hours (range: 5-26 hours).25, 30, 31, 32, 124 Serum glyburide concentrations may be increased in patients with renal1, 27, 124 or hepatic1, 124 insufficiency.124 Data are limited, but the half-life may be prolonged in patients with severe renal impairment.42, 43 In one study in patients with normal hepatic function and impaired renal function given a single oral dose of radiolabeled glyburide, the plasma half-life of total radioactivity was 2-5 hours in those with creatinine clearances of 29-131 mL/minute per 1.73 m2 and 11 hours in one patient with a creatinine clearance of 5 mL/minute per 1.73 m2; in those patients with creatinine clearances of 29-131 mL/minute per 1.73 m2, no relationship between plasma half-life and creatinine clearance was observed.42
Glyburide appears to be completely metabolized,25, 26, 31, 36 probably in the liver.31 The drug is metabolized at the cyclohexyl ring principally to-hydroxyglyburide trans 4-;1, 25, 26, 31, 36, 124 the 4- trans -hydroxy metabolite has only 0.25% of the hypoglycemic activity of glyburide following oral administration in rabbits,1, 36, 124 but has about 15% of the hypoglycemic activity of the parent compound following intraperitoneal administration in rats.44, 98 Glyburide is also metabolized to the 3- cis -hydroxy derivative and to another unidentified metabolite;25, 26, 31 the 3- cis -hydroxy metabolite has 2.5% of the hypoglycemic activity of glyburide following oral administration in rabbits.1, 36 The hypoglycemic activity of glyburide metabolites is generally considered clinically unimportant;1, 36, 124 however, results of studies in rats indicate that retention of the 4- trans -hydroxy metabolite in the presence of renal insufficiency may enhance and prolong the hypoglycemic effect of the drug.98, 99
Unlike other currently available sulfonylurea antidiabetic agents which are excreted principally in urine,1, 8, 124 glyburide is excreted as metabolites in urine and feces in approximately equal proportions.1, 23, 25, 26, 30, 31, 47, 124 Fecal excretion appears to occur almost completely via biliary elimination;25, 26, 30 only small amounts may be excreted in feces as unabsorbed drug following oral administration.30 Most urinary excretion occurs within the first 6-24 hours after oral administration of the drug.25, 26, 30, 31, 47 Following oral administration of a single 5-mg dose of glyburide in healthy individuals, approximately 30-50% of the dose is excreted in urine as metabolites within 24 hours;30, 31 about 80% of the urinary excretion occurs as the 4- trans -hydroxy metabolite, 15% as the 3- cis -hydroxy metabolite, and 5% as an unidentified metabolite.25, 26 Fecal excretion occurs more slowly, but a single oral dose of the drug is completely excreted in urine and feces within 3-5 days in healthy individuals.25, 30
The effects of renal impairment on the elimination of glyburide and its metabolites have not been fully evaluated.42, 43, 98 Limited data indicate that renal excretion of glyburide metabolites98 and plasma clearance of glyburide42, 43 may be substantially decreased in patients with severe renal impairment. Glyburide appears to be only minimally removed by hemodialysis.42
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.
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.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets | 1.25 mg * | glyBURIDE Tablets | |
2.5 mg* | glyBURIDE Tablets | |||
5 mg* | glyBURIDE Tablets | |||
Tablets (micronized) | 1.5 mg* | glyBURIDE Micronized Tablets | ||
Glynase® PresTab® (scored) | ||||
3 mg* | glyBURIDE Micronized Tablets | |||
Glynase® PresTab® (scored) | Pfizer | |||
6 mg* | glyBURIDE Micronized Tablets | |||
Glynase® PresTab® (scored) | 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 | 1.25 mg with Metformin Hydrochloride 250 mg* | Glyburide with Metformin Hydrochloride Tablets | |
2.5 mg with Metformin Hydrochloride 500 mg* | Glyburide with Metformin Hydrochloride Tablets | |||
5 mg with Metformin Hydrochloride 500 mg* | Glyburide with Metformin Hydrochloride Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
AHFS® Drug Information. © Copyright, 1959-2025, Selected Revisions May 10, 2025. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
Only references cited for selected revisions after 1984 are available electronically.
1. Avet Pharmaceuticals Inc. Glyburide tablets prescribing information. East Brunswick, NJ; 2024 Jul.
3. Anon. Glibenclamide: a review. Drugs . 1971; 1:116-40. [PubMed 5004340]
4. Jackson JE, Bressler R. Clinical pharmacology of sulphonylurea hypoglycaemic agents: part 1. Drugs . 1981; 22:211-45. [PubMed 7021124]
7. Hadju VP, Kohler KF, Schmidt FH et al. Physikalisch-chemische und analytische Unter suchungen an HB 419. (German; with English abstract) Arzneim-Forsch . 1969; 19:1381-6.
8. Skillman TG, Feldman JM. The pharmacology of sulfonylureas. Am J Med . 1981; 70:361-72. [PubMed 6781341]
9. 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. [PubMed 6423429]
10. Duckworth WC, Solomon SS, Kitabchi AE. Effect of chronic sulfonylurea therapy on plasma insulin and proinsulin levels. J Clin Endocrinol Metab . 1972; 35:585-91. [PubMed 5052977]
11. Feldman JM, Lebovitz HE. Endocrine and metabolic effects of glybenclamide: evidence for an extrapancreatic mechanism of action. Diabetes . 1971; 20:745-55.
12. 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. [PubMed 6337486]
13. 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. [PubMed 6401922]
14. Brogden RN, Heel RC, Pakes GE et al. Glipizide: a review of its pharmacological properties and therapeutic use. Drugs . 1979; 18:329-53. [PubMed 389600]
15. Kolterman OG, Prince MJ, Olefsky JM. Insulin resistance in noninsulin-dependent diabetes mellitus: impact of sulfonylurea agents in vivo and in vitro. Am J Med . 1983; 74(Suppl 1A):82-101. [PubMed 6401923]
16. Beck-Nielsen H, Pedersen O, Lindskov HO. Increased insulin sensitivity and cellular insulin binding in obese diabetics following treatment with glibenclamide. Acta Endocrinol . 1979; 90:451-62. [PubMed 106617]
17. Hjollund E, Richelsen B, Beck-Nielsen H et al. The effect of glibenclamide on insulin receptors in normal man: comparative studies of insulin binding to monocytes and erythrocytes. J Clin Endocrinol Metab . 1983; 57:1257-62. [PubMed 6415086]
18. Moses AM, Howanitz J, Miller M. Diuretic action of three sulfonylurea drugs. Ann Intern Med . 1973; 78:541-4. [PubMed 4632790]
19. Rado JP, Borbély L, Szende L et al. Investigation of the diuretic effect of glibenclamide in healthy subjects and in patients with pituitary and nephrogenic diabetes insipidus. Horm Metab Res . 1974; 6:289-92. [PubMed 4213198]
20. Rado JP, Szende L. Inhibition of clofibrate-induced antidiuresis by glybenclamide in patients with pituitary diabetes insipidus. J Clin Pharmacol . 1974; 14:290-5. [PubMed 4208361]
23. Rupp W, Christ O, Fulberth W. Untersuchungen zur Bioavailability von Glibenclamid. (German; with English abstract) Arzneim-Forsch . 1972; 22:471-3.
24. Ings RMJ, Lawrence JR, McDonald A et al. Glibenclamide pharmacokinetics in healthy volunteers: evidence for zero-order drug absorption. Br J Clin Pharmacol . 1982; 13:264-5P.
25. Christ OE, Heptner W, Rupp W. Investigations on absorption, excretion and metabolism in man after administration of14C-labelled HB 419. Horm Metab Res Suppl Ser . 1969; 1:51-4.
26. Rupp VW, Christ O, Heptner W. Resorption, Ausscheidung and Metabolismus nach intravenoser und oraler Gabe von HB 419-14C an Menschen. (German; with English abstract) Arzneim-Forsch . 1969; 19:1428-34.
27. Sartor G, Melander A, Scherstén B et al. Serum glibenclamide in diabetic patients, and influence of food on the kinetics and effects of glibenclamide. Diabetologia . 1980; 18:17-22. [PubMed 6767639]
28. Sartor G, Lundquist I, Melander A et al. Improved effect of glibenclamide on administration before breakfast. Eur J Clin Pharmacol . 1982; 21:403-8. [PubMed 6804245]
29. Sartor G, Melander A, Scherstén B et al. Comparative single-dose kinetics and effects of four sulfonylureas in healthy volunteers. Acta Med Scand . 1980; 208:301-7. [PubMed 6778079]
30. Fucella LM, Tamassia V, Valzelli G. Metabolism and kinetics of the hypoglycemic agent glipizide in man—comparison with glibenclamide. J Clin Pharmacol . 1973; 13:68-75.
31. Balant L, Fabre J, Zahnd GR. Comparison of the pharmacokinetics of glipizide and glibenclamide in man. Eur J Clin Pharmacol . 1975; 8:63-9. [PubMed 823030]
32. Ko H, Royer ME, Molony BA. Relationships between circulating glyburide/metabolite concentrations, serum glucose lowering, and dose of glyburide in man. In: Rifkin H, ed. Micronase® (glyburide): pharmacological and clinical evaluation. Amsterdam: Excerpta Medica; 1975:20-30.
33. Groop L, Harno K. Diurnal pattern of plasma insulin and blood glucose during glibenclamide and glipizide therapy in elderly diabetics. Acta Endocrinol Suppl . 1980; 239:44-52.
34. Balant L, Zahnd GR, Weber F et al. Behaviour of glibenclamide on repeated administration to diabetic patients. Eur J Clin Pharmacol . 1977; 11:19-25. [PubMed 401739]
35. Schmidt FH, Hrstka VE. Radio-immunoassay of glibenclamide: minimum effective dose levels and pharmacodynamics. XIIe Congrès International de Thérapeutique, Genève, 1973.
36. Kaiser DG, Forist AA. A review of glyburide metabolism in man and laboratory animals. In: Rifkin H, ed. Micronase® (glyburide): pharmacological and clinical evaluation. Amsterdam: Excerpta Medica; 1975:31-43.
37. Crooks MJ, Brown KF. The binding of sulphonylureas to serum albumin. J Pharm Pharmacol . 1974; 26:304-11. [PubMed 4153105]
38. Hsu P, Ma JKH, Luzzi LA. Interactions of sulfonylureas with plasma proteins. J Pharm Sci . 1974; 63:570-3. [PubMed 4208196]
39. Brown KF, Crooks MJ. Binding of sulfonylureas to serum albumin. II. The influence of salt and buffer compositions on tolbutamide and glyburide. Can J Pharm Sci . 1974; 9:75-7.
40. Brown KF, Crooks MJ. Displacement of tolbutamide, glibenclamide and chlorpropramide from serum albumin by anionic drugs. Biochem Pharmacol . 1976; 25:1175-8. [PubMed 820348]
41. Morrison PJ, Rogers HJ, Spector RG et al. Effect of pirprofen on glibenclamide kinetics and response. Br J Clin Pharmacol . 1982; 14:123-6. [PubMed 6809024]
42. Raehl CL, Goersch WA, Craig WA et al. The pharmacokinetics of14C-glyburide (Micronase®) in patients with reduced renal function. In: Official Program and Abstracts of Papers presented before the APhA Academy of Pharmaceutical Sciences. Washington, DC: American Pharmaceutical Association; 1983; 13(2):205. Abstract.
43. Balant L, Zahnd G, Petitpierre B et al. Influence of renal failure on the pharmacokinetics and hypoglycemic effect of sulfonylureas. Diabetologia . 1973; 9:59.
44. Balant L, Fabre J, Loutan L et al. Does 4-trans-hydroxy-glibenclamide show hypoglycemic activity? Arzneim-Forsch . 1979; 29:162-3.
45. Rado JP, Borbély L. Inhibition of the antidiuretic effect of 1-deamino-8d-arginine vasopressin (DDAVP) by glibenclamide in water-loaded healthy subjects. Endokrinologie . 1975; 66:88-93. [PubMed 817889]
46. Rado JP, Szende L, Marosi J. Influence of glyburide on the antidiuretic response induced by 1-deamino-8-d-arginine vasopressin (DDAVP) in patients with pituitary diabetes insipidus. Metabolism . 1974; 23:1057-63. [PubMed 4214480]
47. Anderson J, Stephenson RJ, Tomlinson RWS et al. Studies with14C-labelled glibenclamide. Postguard Med J . 1970; 46(Dec Suppl):42-5.
48. Larner J. Mediators of postreceptor action of insulin. Am J Med . 1983; 74(Suppl 1A):38-51. [PubMed 6297300]
49. Davidson M, Lewis AAG, de Mowbray RR. Metabolic and clinical effects of glibenclamide. Lancet . 1970; 1:57-61. [PubMed 4188623]
50. Johnson BF, Bhatia CK, Rzeszotarski WJ et al. Preliminary clinical evaluation of glybenclamide in treatment of diabetes mellitus. Diabetes . 1970; 19:579-84. [PubMed 4915447]
51. Clarke BF, Campbell IW. Long-term comparative trial of glibenclamide and chlorpropamide in diet-failed, maturity-onset diabetics. Lancet . 1975; 1:246-8. [PubMed 8667857]
52. Hamblin JJ, Ismay G, Good MS et al. A comparative study of glibenclamide and chlorpropamide (preliminary report). Postgrad Med J . 1970; 46(Dec Suppl):92-4. [PubMed 5416512]
53. Mogensen EF, Worm J, Mikkelsen BO. Clinical comparison between glibornuride (Glutril®) and glibenclamide in maturity-onset diabetes: a controlled double-blind trial. Curr Ther Res . 1976; 19:599-64.
54. Blohmé G, Waldenstrom J. Glibenclamide and glipizide in maturity onset diabetes. Acta Med Scand . 1979; 206:263-7. [PubMed 116480]
55. Frederiksen PK, Mogensen EF. A clinical comparison between glipizide (Glibenese®) and glibenclamide (Daonil®) in the treatment of maturity onset diabetes: a controlled doudle-blind cross-over study. Curr Ther Res . 1982; 32:1-7.
56. Allen GS. The comparative effectiveness of glyburide and tolazamide in patients with mild diabetes. In: Rifkin H, ed. Micronase® (glyburide): pharmacological and clinical evaluation. Amsterdam: Excerpta Medica; 1975:150-6.
57. Bryan JB, Inchaustegui HJ. Clinical impressions of Micronase® (glyburide) in a private practice. In: Rifkin H, ed. Micronase® (glyburide): pharmacological and clinical evaluation. Amsterdam: Excerpta Medica; 1975:225-34.
58. Murphey AT, Peskin H. Glyburide compared to previous therapy or tolbutamide. In: Rifkin H, ed. Micronase® (glyburide): pharmacological and clinical evaluation. Amsterdam: Excerpta Medica; 1975:204-10.
60. Carlisle BA, Kroon LA, Koda-Kimble MA,. Diabetes mellitus. In: Koda-Kimble MA, Young LY, eds. Applied therapeutics: the clinical use of drugs. 8th ed.Philadelphia, PA: Lippincott Williams & Wilkins, Inc; 2005: 50-1-50-86.
61. Scientific Advisory Panel of the Executive Committee, American Diabetes Association. Policy statement: the UGDP controversy. Diabetes . 1979; 28:168-70.
62. Jackson JE, Bressler R. Clinical pharmacology of sulphonylurea hypoglycaemic agents: part 2. Drugs . 1981; 22:295-320. [PubMed 7030708]
63. Food and Drug Administration. Labeling for oral hypoglycemic drugs of the sulfonylurea class. [Docket No. 75N-0062] Fed Regist . 1984; 49:14303-31.
66. Krans HMJ. Insulin, glucagon and oral hypoglycaemic drugs. In: Dukes MNG, ed. Side effects of drugs. Annual 2. New York: Elsevier/North Holland Inc; 1978:345.
67. Seltzer HS. Severe drug-induced hypoglycemia: a review. Compr Ther . 1979; 5(4):21-9. [PubMed 445986]
68. Gottesburen H, Gerdes H, Littman KP et al. Severe hypoglycemia after glibenclamide. Lancet . 1970; 2:576.
69. Howard FM. Hypoglycemia in diabetics treated with Micronase® (glyburide). In: Rifkin H, ed. Micronase® (glyburide): pharmacological and clinical evaluation. Amsterdam: Excerpta Medica: 1975:164-71.
70. Krans HMJ. Insulin, glucagon and oral hypoglycaemic drugs. In: Dukes MNG, ed. Side effects of drugs. Annual 1. New York: Elsevier/North Holland Inc; 1977:319.
71. Sillence DO, Court JM. Glibenclamide-induced hypoglycaemia. Br Med J . 1975; 3:490-1. [PubMed 808247]
72. Kullavanijaya P. Recovery from overdose with glibenclamide. Br Med J . 1970; 4:53-4. [PubMed 5470446]
73. Krans HMJ. Insulin, glucagon and oral hypoglycaemic drugs. In: Dukes MNG, ed. Side effects of drugs. Annual 3. New York: Elsevier/North Holland Inc; 1979:347.
74. Krans HMJ. Insulin, glucagon and oral hypoglycaemic drugs. In: Dukes MNG, ed. Side effects of drugs. Annual 4. New York: Elsevier/North Holland Inc; 1980:303.
76. Krans HMJ. Insulin, glucagon and oral hypoglycaemic drugs. In: Dukes MNG, ed. Side effects of drugs. Annual 7. New York: Elsevier/North Holland Inc.; 1983:409.
77. Pannekoek JH. Insulin, glucagon and oral hypoglycaemic drugs. In: Dukes MNG, ed. Meyler's side effects of drugs. 8th ed. Amsterdam: Excerpta Medica; 1975:914-5.
78. Sketris I, Wheeler D, York S. Hypoglycemic coma induced by inadvertent administration of glyburide. Drug Intell Clin Pharm . 1984; 18:142-3. [PubMed 6421558]
79. Walfish PG, Kashyap RP, Greenstein S. Sulfonylurea-induced factitious hypoglycemia in a nondiabetic nurse. Can Med Assoc J . 1975; 112:71-2. [PubMed 803250]
81. Coetzee EJ, Jackson WPU. Pregnancy in established non-insulin-dependent diabetics: a five-and-a-half year study at Groote Schuur Hospital. S Afr Med J . 1980; 58:795-802. [PubMed 6777880]
87. Wardle EN, Richardson GO. Alcohol and glibenclamide. Br Med J . 1971; 3:309.
88. Zaman R, Kendall MJ, Biggs PI. The effect of acebutolol and propranolol on the hypoglycaemic action of glibenclamide. Br J Clin Pharmacol . 1982; 13:507-12. [PubMed 6802160]
89. Hausmann L, Goebel KM. Atenolol in orally treated diabetic patients. Drugs . 1983; 25(Suppl 2):71-3.
90. De Marinis L, Barbarino A. Calcium antagonists and hormone release. I. Effects of verapamil on insulin release in normal subjects and patients with islet-cell tumor. Metabolism . 1980; 29:599-604. [PubMed 6247604]
91. O'sullivan DJ, Cashman WF. Blood glucose variations and clinical experience with glibenclamide in diabetes mellitus. Br Med J . 1970; 2:572-4. [PubMed 5526612]
92. Molony BA, Crim JA, Hearron AE Jr. Micronase® (glyburide): a comparison of single and divided daily dose treatment schedules. In: Rifkin H, ed. Micronase® (glyburide): pharmacological and clinical evaluation. Amsterdam: Excerpta Medica; 1975:248-53.
93. Owens DR, Wragg KG, Shetty KT et al. Glibenclamide, acute-long-term response in m.o. diabetics. Horm Metab Res . 1979; 11:411-2. [PubMed 112018]
95. Huupponen R, Viikari J, Saarimaa H. Chlorpropamide and glibenclamide serum concentrations in hospitalized patients. Ann Clin Res . 1982; 14:119-22. [PubMed 6814340]
97. Rogers HJ, Spector RG, Morrison PJ et al. Pharmacokinetics of intravenous glibenclamide investigated by a high performance liquid chromatographic assay. Diabetologia . 1982; 23:37-40. [PubMed 6811355]
98. Fabre J, Balant L, Loutan L et al. Hypoglycemic activity of the main metabolite of glibenclamide: influence of renal insufficiency. Kidney Int . 1978; 13:435.
99. Loutan L, Samimi H, Balant L et al. Metabolites of hypoglycemic sulfonylureas in renal insufficiency. Experiences with glibenclamide. (German) Schweiz Med Wochenschr . 1978; 108:1782-6.
103. Lebovitz HE. Clinical utility of oral hypoglycemic agents in the management of patients with noninsulin-dependent diabetes mellitus. Am J Med . 1983; 75(Suppl 5B):94-9. [PubMed 6369972]
105. Asplund K, Wiholm BE, Lithner F. Glibenclamide-associated hypoglycemia: a report on 57 cases. Diabetologia . 1983; 24:412-7. [PubMed 6411511]
109. Kritz H, Najemnik C, Irsigler K. Sulfinpyrazone and glibenclamide study of interaction in diabetics of type II. Wien Med Wochenschr . 1983; 133:237-43. [PubMed 6408808]
110. Best JD, Judzewitsch RG, Pfeifer MA et al. The effect of chronic sulfonylurea therapy on hepatic glucose production in non-insulin-dependent diabetes. Diabetes . 1982; 31:333-8. [PubMed 6759249]
111. Pfeifer MA, Halter JB, Judzewitsch RG et al. Acute and chronic effects of sulfonylurea drugs on pancreatic islet function in man. Diabetes Care . 1984; 7(Suppl 1):25-34. [PubMed 6376026]
112. DeFronzo RA, Simonson DC. Oral sulfonylurea agents suppress hepatic glucose production in non-insulin-dependent diabetic individuals. Diabetes Care . 1984; 7(Suppl 1):72-80. [PubMed 6428844]
114. Asmal AC, Marble A. Oral hypoglycaemic agents: an update. Drugs . 1984; 28:62-78. [PubMed 6378583]
116. Lotz N, Lacher F, Bachmann W. Combination of sulfonylureas (SU) and insulin (I) in the treatment of type-II-diabetes with “secondary failure” of SU-therapy (DSF). Diabetes . 1984; 33(Suppl 1):24A.
117. Simonson DC, Castellino P, Delprato S. Effect of glyburide on glucose control and metabolism in insulin treated diabetics. Diabetes . 1984; 33(Suppl 1):38A.
118. Rost CR, Brown JL. Combined insulin-sulfonylurea therapy in noninsulin-dependent diabetes mellitus (NIDDM). Diabetes . 1984; 33(Suppl 1):87A.
119. Groop L, Harno K, Nikkila EA et al. The combination of insulin and sulfonylurea (glibenclamide) in the treatment of non-insulin dependent diabetes poorly controlled with insulin alone: evaluation of its metabolic effects. Acta Endocrinol Suppl . 1983; 257:20.
120. Bachmann W, Sieger C, Haslbeck M et al. Combination of insulin and glibenclamide (gl) in the treatment of adult-onset diabetes (Type 2). Diabetologia . 1981; 21:245.
121. Simonson DC, Ferrannini E, Bevilacqua S et al. Mechanism of improvement in glucose metabolism after chronic glyburide therapy. Diabetes . 1984; 33:838-45. [PubMed 6432610]
124. Pharmacia & Upjohn Company LLC. Glynase® PresTab® (micronized glyburide) tablets prescribing information. New York, NY; 2023 Aug.
127. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet . 1998; 352:837-53. [PubMed 9742976]
128. American Diabetes Association. Implications of the United Kingdom Prospective Diabetes Study. Diabetes Care . 1999; 22(Suppl 1):S27-31.
129. Matthews DR, Cull CA, Stratton RR et al. UKPDS 26: sulphonylurea failure in non-insulin-dependent diabetic patients over 6 years. Diabet Med . 1998; 15:297-303. [PubMed 9585394]
130. Genuth P. United Kingdom prospective diabetes study results are in. J Fam Pract . 1998; 47:(Suppl 5):S27.
131. Bretzel RG, Voit K, Schatz H et al. The United Kingdom Prospective Diabetes Study (UKPDS): implications for the pharmacotherapy of type 2 diabetes mellitus. Exp Clin Endocrinol Diabetes . 1998; 106:369-72. [PubMed 9831300]
132. Schmitt JK, Moore JR. Hypertension secondary to chlorpropamide with amelioration by changing to insulin. Am J Hypertens . 1993; 6:317-9. [PubMed 8507452]
133. Genuth S, Brownless MA, Kuller LH et al. Consensus development conference on insulin resistance: Novermber 5-6 1997. Diabetes Care . 1998; 21:310-4. [PubMed 9540000]
134. Henry RR. Glucose control and insulin resistance in non-insulin-dependent diabetes mellitus. Ann Intern Med . 1996; 124:97-103. [PubMed 8554221]
136. Nathan DM. Some answers, more controversy, from UKDS. Lancet . 1998; 352:832-3. [PubMed 9742972]
143. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metfromin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet . 1998; 352:854-65. [PubMed 9742977]
144. American Diabetes Association. The United Kingdom Prosepective Diabetes Study (UKPDS) for type 2 diabetes: what you need to know about the results of a long-term study. Washington, DC; September 15, 1998. From American Diabetes Association web site. [Web]
146. Watkins PJ. UKPDS: a message of hope and a need for change. Diabet Med . 1998; 15:895-6. [PubMed 9827842]
147. Turner RC, Cull CA, Frighi V et al. Glycemic control with diet, sulfonlyurea, metformin, or insulin in patients with type 2 diabetes mellitus: progressive requirements for multiple therapies (UKPDS 49). JAMA . 1999; 281:2005-12. [PubMed 10359389]
158. Avet Pharmaceuticals Inc. Glyburide and metformin hydrochloride tablets prescribing information. East Brunswick, NJ; 2024 Feb.
162. Williams G. Management of non-insulin-dependent diabetes mellitus. Lancet . 1994; 343:95-100. [PubMed 7903785]
165. Chow CC, Sorensen JP, Tsang LWW et al. Comparison of insulin with or without continuation of oral hypoglycemic agents in the treatment of secondary failure in NIDDM patients. Diabetes Care . 1995; 18:307-14. [PubMed 7555472]
166. Zimmerman B, Espenshade J, Fujimoto W et al. The pharmacological treatment of hyperglycemia in NIDDM. Diabetes Care . 1996; 19:1510-18.
167. Landstedt-Hallin L, Bolinder J, Adamson U et al. Comparison of bedtime NPH or preprandial regular insulin combined with glibenclamide in secondary sulfonylurea failure. Diabetes Care . 1995; 18:1183-6. [PubMed 7587856]
169. Raskin P. Combination therapy in NIDDM N Engl J Med . 1992; 327:1453-4. Editorial.
170. Pugh JA, Ramirez G, Wagner ML et al. Is combination sulfonylurea and insulin therapy useful in NIDDM patients? A metaanalysis. Diabetes Care . 1992; 15:953-9. [PubMed 1387073]
171. Buse J. Combining insulin and oral agents. Am J Med . 2000; 108(Suppl 6A):23S-32S. [PubMed 10764847]
172. Johnson JL, Wolf SL, Kabadi UM. Efficacy of insulin and sulfonylurea combination therapy in type II diabetes: a meta-analysis of the randomized placebo-controlled trials. Arch Intern Med . 1996; 156:259-64. [PubMed 8572835]
173. Yki-Jarvinen H, Dressler A, Ziemen M et al. Less nocturnal hypoglycemia and better post-dinner glucose control with bedtime insulin glargine compared with bedtime HPH insulin during insulin combination therapy in type 2 diabetes. Diabetes Care . 2000; 23:1130-6 (IDIS 451244)
174. Trischitta V, Italia S, Mazzarino S et al. Comparison of combined therapies in treatment of secon dary failure to glyburide. Diabetes Care . 1992; 15:539-42. [PubMed 1499473]
175. Florence JA, Yeager BF. Treatment of type 2 diabetes mellitus. Am Fam Physician . 1999; 59:2835-44. [PubMed 10348076]
176. Bastyr EJ, Johnson ME, Trautman ME et al. Insulin lispro in the treatment of patients with type 2 diabetes mellitus after oral agent failure. Clin Ther . 1999; 21:1703-4. [PubMed 10566566]
177. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med . 1999; 131:281-303. [PubMed 10454950]
178. Krentz AJ, Ferner RE, Bailey CJ. Comparative tolerability profiles of oral antidiabetic agents. Drug Safety . 1994; 11:223-41. [PubMed 7848543]
186. Langer O, Conway DL, Berkus MD et al. A comparison of glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med . 2000; 343:1134-8. [PubMed 11036118]
188. Hermann LS, Scherstén B, Bitzén PO et al. Therapeutic comparison of metformin and sulfonylurea, alone and in various combinations. Diabetes Care . 1994; 17:1100-9. [PubMed 7821128]
189. Hermann L. Biguanides and sulfonylureas as combination therapy in NIDDM. Diabetes Care . 1990; 13:37-41. [PubMed 2209342]
195. Wolffenbuttel BHR, Gomist R, Squatrito S et al. Addition of low-dose rosiglitazone to sulphonylurea therapy improves glycaemic control in type 2 diabetic patients. Diabet Med . 2000; 17:40-7. [PubMed 10691158]
198. Kipnes MS, Krosnick a, Rendell MS et al. Pioglitazone hydrochloride in combination with sulfonylurea therapy improves glycemic control in patients with type 2 diabetes mellitus: a randomized, placebo-controlled study. Am J Med . 2001; 111:10-7. [PubMed 11448655]
200. Chiasson J, Josse R, Hunt J et al. The efficacy of acarbose in the treatment of patients with non-insulin-dependent diabetes mellitus. Ann Intern Med . 1994; 121:929-935.
201. Coniff RF, Shapiro JA, Seaton TB et al. Multicenter, placebo-controlled trial comparing acarbose (BAY g 5421) with placebo, tolbutamide, and tolbutamide-plus-acarbose in non-insulin-dependent diabetes mellitus. Am J Med . 1995; 98:443-51. [PubMed 7733122]
202. Calle-Pascual AL, Garcia-Honduvilla J, Martin-Alvarez PJ et al. Comparison between acarbose, metformin, and insulin treatment in type 2 diabetic patients with secondary failure to sulfonylurea treatment. Diabetes Metab . 1995; 21:256-60.
203. Klein W. Sulfonylurea-metformin-combination versus sulfonylurea-insulin-combination in secondary failures of sulfonylurea monotherapy. Diab Metab. 1991; 17(Suppl 1):235-40.
209. Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus. JAMA . 2002; 287:2563-9. [PubMed 12020338]
211. Pfizer. Diflucan® (fluconazole) tablets and powderfor oral suspension prescribing information. New York, NY; 2024 Feb.
233. Actelion Pharmaceuticals US. Tracleer® (bosentan) tablets prescribing information. Titusville, NJ; 2024 Feb.
707. American Diabetes Association Professional Practice Committee. 9. Pharmacologic approaches to glycemic treatment: standards of care in diabetes-2025. Diabetes Care . 2025; 48(Suppl 1):S181-206.
708. Samson SL, Vellanki P, Blonde L et al. American Association of Clinical Endocrinology consensus statement: comprehensive type 2 diabetes management algorithm-2023 update. Endocr Pract . 2023; 28:305-340.
709. Institute for Safe Medication Practices (ISMP). ISMP list of high-alert medications in acute care settings (2024). http://www.ismp.org/system/files/resources/2024-01/ISMP_HighAlert_AcuteCare_List_010924_MS5760.pdf (accessed 2025 Mar 17).
710. Institute for Safe Medication Practices (ISMP). ISMP list of confused drug names (2024). http://online.ecri.org/hubfs/ISMP/Resources/ISMP_ConfusedDrugNames.pdf (accessed 2025 Mar 17).
711. Tirkkonen T, Heikkilä P, Huupponen R et al. Potential CYP2C9-mediated drug-drug interactions in hospitalized type 2 diabetes mellitus patients treated with the sulphonylureas glibenclamide, glimepiride or glipizide. J Intern Med . 2010; 268:359-66.
712. Niemi M, Backman JT, Neuvonen M et al. Effects of rifampin on the pharmacokinetics and pharmacodynamics of glyburide and glipizide. Clin Pharmacol Ther . 2011; 69:400-6.
999. By the 2023 American Geriatrics Society Beers Criteria® Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria® for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2023 Jul;71(7):2052-2081. doi: 10.1111/jgs.18372. Epub 2023 May 4. PMID: 37139824.