Glimepiride is a sulfonylurea antidiabetic agent.1
Glimepiride is used as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.1, 54 Sulfonylureas, including glimepiride, also may be used in combination with one or more other oral antidiabetic agents or insulin as an adjunct to diet and exercise in patients with type 2 diabetes mellitus who are unable to achieve adequate glycemic control with oral antidiabetic agent monotherapy.1, 5, 54, 102, 103, 104, 105, 106, 117, 707, 708
Glimepiride is commercially available as a single-entity preparation and also in fixed combination with pioglitazone for this use.1, 117 The fixed combination of glimepiride and pioglitazone is used as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus who are already receiving a thiazolidinedione and a sulfonylurea separately or who do not achieve adequate glycemic control with thiazolidinedione or sulfonylurea monotherapy.117
Glimepiride is not indicated for the treatment of type 1 diabetes mellitus or for patients with diabetic ketoacidosis.1
When given as monotherapy for the treatment of type 2 diabetes mellitus, glimepiride improves glycemic control compared with placebo as evidenced by reductions in fasting and postprandial blood glucose concentrations and glycosylated hemoglobin (hemoglobin A1c; HbA1c); these reductions are dose dependent over a range of 1-4 mg daily.1, 5, 6, 20 Some patients, particularly those with high fasting plasma glucose concentrations, may benefit from the maximum dosage of glimepiride (8 mg daily).5 For patients receiving the maximum dosage, the average reduction in HbA1c is 2% in absolute units.1, 5 Clinical studies suggest that glimepiride is as effective as glyburide for the management of hyperglycemia in patients with type 2 diabetes mellitus.5, 7, 20, 54 The efficacy of glimepiride is not affected by age, sex, weight, or race.1
Efficacy of glimepiride for the management of type 2 diabetes mellitus in adult patients was established in a 14-week, multicenter, randomized, double-blind, placebo-controlled trial in 304 patients with a mean baseline HbA1c of 7.9—8%.1 Patients discontinued their baseline sulfonylurea therapy and then entered a 3-week washout period followed by randomization to either placebo or glimepiride (1 mg, 4 mg, or 8 mg daily).1 All patients were initiated on glimepiride 1 mg daily.1 Patients randomized to the glimepiride 4 or 8 mg groups where then titrated at weekly intervals, first to 4 mg and then to 8 mg, as long as the dose was tolerated, until the assigned dose was reached.1 Once the randomized target dosage of glimepiride was reached, patients were maintained at that dosage until week 14.1 Glimepiride showed significant improvements in HbA1c of -1.2% (1 mg group), -1.8% (4 mg group), and -1.8% (8 mg group) compared to placebo.1
In a multicenter, randomized, double-blind, placebo-controlled, dose-titration trial, 249 adult patients who were either treatment-naïve or had received limited treatment with antidiabetic therapy were randomized to receive glimepiride or placebo for 22 weeks.1 The mean baseline HbA1cwas 9.1% (placebo group) or 9.3% (glimepiride group).1 All patients assigned to glimepiride were initiated on a dosage of 1 mg daily; dosage was subsequently titrated (upward or downward) at 2-week intervals to a goal fasting plasma glucose of 90—150 mg/dL.1 Following 10 weeks of dosage adjustment, patients were maintained at their optimal dosage (1, 2, 3, 4, 6, or 8 mg daily) for the remaining 12 weeks of the trial.1 In this study, glimepiride was associated with significant improvements in fasting plasma glucose and HbA1c.1 The improvement observed in HbA1c in the glimepiride group was -1.1% compared to placebo.1
In a comparative, single-blind (patients only), dose titration trial in children and adolescents 8-17 years of age with type 2 diabetes mellitus, glimepiride (titrated to a mean last daily dosage of 4 mg) was as effective as metformin (titrated to a mean last dosage of 1.4 g daily) in reducing HbA1c values from baseline.1 Patients received glimepiride at an initial dosage of 1 mg daily or metformin hydrochloride at an initial dosage of 500 mg twice daily; dosage was titrated until a fasting blood glucose concentration of less than 126 mg/dL was achieved or a maximum dosage of 8 mg daily of glimepiride or 1 g twice daily of metformin hydrochloride was reached.1 The adverse effect profile in pediatric patients receiving glimepiride was similar to that observed in adults.1 However, the manufacturer states that data are insufficient to recommend the use of glimepiride in pediatric patients.1
Primary or secondary failure to sulfonylureas has been attributed to a progressive decline in pancreatic beta-cell function, but data are limited concerning the incidence of failure with glimepiride.17, 19, 26, 28, 54 Secondary failure to sulfonylurea drugs is characterized by progressively decreasing diabetic control following 1 month to several years of good control.44 Interim data from a substudy (UKPD 26) of the UKPD study in patients with newly diagnosed type 2 diabetes mellitus who were receiving intensive antidiabetic therapy (maintenance of fasting plasma glucose in a range from 108 mg/dL to less than 270 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.62, 67 The failure rate at 6 years was 48% among patients receiving glyburide and about 40% among patients receiving chlorpropamide.67 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.59, 60, 61, 63, 65, 67, 68 In another substudy (UKPD 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.59 At diagnosis, risk factors predisposing toward sulfonylurea failure included higher fasting plasma glucose concentrations, younger age, and lower pancreatic β-cell reserve.59, 67
Sulfonylureas also 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.103, 104, 105, 106, 117, 707, 708
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.22, 46, 48, 97 In general, combined sulfonylurea and insulin therapy for type 2 diabetes mellitus results in glycemic control comparable to that achieved with insulin alone but at a substantially reduced (e.g., by 40-50%) insulin dosage.22, 46, 47, 48 However, such combined therapy may increase the risk of hypoglycemic reactions.11, 19, 707, 708
When glimepiride is used in fixed combination with other antidiabetic agents, the cautions, precautions, and contraindications associated with other concomitant drug(s) must be considered in addition to those associated with glimepiride.117
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 other 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 kidney 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 the guidelines are similar to those recommended by the ADA.708 The AACE 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
Glimepiride is administered orally once daily.1, 5, 6 Glimepiride should be administered with breakfast or with the first main meal of the day.1 The fixed combination of glimepiride and pioglitazone is administered orally once daily with the first main meal of the day.117 See the full prescribing information for additional administration instructions for the combination product.117 Although food slightly decreases the extent and slightly delays absorption of glimepiride, the manufacturer recommends that the drug be taken with the first meal of the day.1 Once-daily dosing of glimepiride provides adequate control of blood glucose concentration throughout the day.1
Dosage of glimepiride must be individualized carefully based on patient response and tolerance.1 The goal of therapy should be to reduce both fasting glucose and glycosylated hemoglobin (hemoglobin A1c [HbA1c]) values to normal or near normal using the lowest effective dosage of glimepiride, when used either as monotherapy or in combination with other antidiabetic agents.1, 707, 708
Store glimepiride tablets at 20-25°C in well-closed containers with safety closures.1
For the management of type 2 diabetes mellitus, the usual initial adult dosage of glimepiride is 1 or 2 mg orally once daily administered with breakfast or the first main meal.1 In debilitated, malnourished, or geriatric patients and in other patients at increased risk of hypoglycemia, the initial dosage of glimepiride should be 1 mg orally once daily.1
In patients receiving 1 mg of glimepiride daily, the dosage may be increased to 2 mg daily if adequate glycemic control has not been achieved after 1-2 weeks.1 After reaching the 2-mg dosage, subsequent dosage should be adjusted according to the patient's tolerance and therapeutic response, increasing the dosage in increments of no more than 1 or 2 mg daily at 1- to 2-week intervals.1 A conservative titration scheme is recommended for patients at increased risk for hypoglycemia.1 The maximum recommended dosage of glimepiride is 8 mg once daily.1
When transferring from most sulfonylurea antidiabetic agents to glimepiride, a transition period generally is not required, and administration of the sulfonylurea antidiabetic agent may be discontinued abruptly.1 Because an exaggerated hypoglycemic response may occur in some patients during the transition from a sulfonylurea antidiabetic agent with a prolonged half-life (e.g., chlorpropamide [no longer commercially available in the US]) to glimepiride, patients being transferred from such agents should be monitored closely for the occurrence of hypoglycemia during the initial 1-2 weeks of the transition period.1
Glimepiride/Pioglitazone Fixed-combination Therapy
The initial dosage of glimepiride in fixed combination with pioglitazone should be based on the patient's current regimen with glimepiride (or another sulfonylurea agent) and/or pioglitazone.117 Bioequivalence has been demonstrated between the fixed combination of glimepiride and pioglitazone and each drug given concurrently at the currently approved dosage strengths.117
Patients currently receiving glimepiride: When the commercially available preparation containing glimepiride in fixed combination with pioglitazone is used in patients inadequately controlled on glimepiride monotherapy, the usual initial dosage of the glimepiride component is 2 or 4 mg with 30 mg of pioglitazone orally once daily with the first main meal.117
Patients currently receiving pioglitazone: In patients inadequately controlled on pioglitazone monotherapy, the usual initial dosage of the fixed-combination product is 2 mg of glimepiride and 30 mg of pioglitazone orally once daily.117 Subsequent dosage should be adjusted according to the patient's therapeutic response and tolerability.117
Patients currently receiving glimepiride and pioglitazone as separate tablets: When the fixed-combination preparation is used to replace concurrent therapy with separate tablets of glimepiride and pioglitazone, the initial dosage of the fixed combination should be as close as possible to the patient's existing dosage of glimepiride and pioglitazone; adjust subsequent dosage based on response.117, 117
Patients transferring from monotherapy with a sulfonylurea other than glimepiride or from combination therapy with pioglitazone and a sulfonylurea other than glimepiride: The usual initial dosage of the fixed combination is 2 mg of glimepiride and 30 mg of pioglitazone orally once daily; adjust based on response.117
The manufacturer makes no specific dosage recommendations for patients with hepatic impairment.1
Glimepiride/Pioglitazone Fixed-Combination Therapy
The manufacturer makes no specific dosage recommendations for patient with hepatic impairment; use with caution in patients with liver disease.1
The manufacturer states that an initial dosage of glimepiride 1 mg daily is recommended to reduce the risk of hypoglycemia in patients with type 2 diabetes and renal impairment.1 Further dosage increases can be made based upon the patient's glycemic response; a conservative titration scheme is recommended.1
The manufacturer makes no specific dosage recommendations for patients with renal impairment.1 To minimize the risk of hypoglycemia, the initial dosage, dosage increments, and maintenance dosage of the fixed combination of glimepiride and pioglitazone should be conservative.1 Patients with renal impairment should be closely monitored for hypoglycemia during initiation and subsequent dosage adjustment of combination therapy.1
Although no overall differences in safety or efficacy were observed between geriatric and younger adults in clinical studies, the possibility that some older patients may exhibit increased sensitivity to the drug cannot be ruled out.1 Because geriatric patients may have decreased renal function and hypoglycemia may be more difficult to recognize, the manufacturer states that caution should be used when initiating and increasing the dosage of glimepiride in geriatric patients.1 Geriatric patients initially are recommended to receive 1 mg of glimepiride once daily.1 Further dosage increases can be made based upon the patient's glycemic response; a conservative titration scheme is recommended.1
Glimepiride/Pioglitazone Fixed-combination Therapy
The manufacturer makes no specific dosage recommendations for geriatric patients.1 To minimize the risk of hypoglycemia, the initial dosage, dosage increments, and maintenance dosing of the fixed combination of glimepiride and pioglitazone should be conservative.1 During initiation and any subsequent dosage adjustments of the fixed combination of glimepiride and pioglitazone, geriatric patients should be observed carefully for hypoglycemia.1
Glimepiride/Pioglitazone Fixed-combination Therapy
As fluid retention and heart failure (HF) have been reported with pioglitazone, patients with systolic dysfunction should receive pioglitazone 15 mg once daily as monotherapy and safely tolerate dosage titration to 30 mg once daily as monotherapy before receiving the lowest approved dosage of the fixed-combination preparation (consisting of glimepiride 2 mg and pioglitazone 30 mg).117 If subsequent dosage adjustment is necessary with the fixed-combination preparation, patients should be closely monitored for weight gain, edema, or other manifestations of HF exacerbation.117
All sulfonylureas, including glimepiride, can cause severe hypoglycemia.1 The patient's ability to concentrate and react may be impaired as a result of hypoglycemia.1 These impairments may present a risk in situations where these abilities are important, such as driving or operating machinery.1 Severe hypoglycemia can lead to unconsciousness or convulsions and may result in temporary or permanent impairment of brain function or death.1
Hypoglycemia may occur in patients receiving glimepiride alone or in combination with other antidiabetic agents.1, 117 Appropriate patient selection and careful attention to dosage are important to avoid glimepiride-induced hypoglycemia.1 Hypoglycemia (i.e., blood glucose concentrations less than 60 mg/dL) occurred in 0.9-1.7% of patients receiving glimepiride in two long-term (1 year), controlled clinical trials.1, 5, 54
Geriatric patients, debilitated, or malnourished patients, or those with adrenal, pituitary, renal, or hepatic impairment may be particularly susceptible to hypoglycemia induced by sulfonylureas, including glimepiride.1, 57, 117 Use caution when initiating and increasing the dosage of glimepiride in patients who may be predisposed to hypoglycemia.1 Hypoglycemia is more likely to occur when caloric intake is deficient, after severe or prolonged exercise, and when alcohol is ingested.1 Hypoglycemia may be more difficult to recognize in geriatric patients, in patients with autonomic neuropathy, and in patients who also are receiving β-adrenergic blocking agents or other sympatholytic agents.1, 117 In these situations, severe hypoglycemia may occur before the patient is aware of the hypoglycemia.1
Management of glimepiride-induced hypoglycemia depends on the severity of the reaction; severe reactions (e.g., coma, seizures) occur infrequently but require immediate hospitalization and treatment and observation until complete recovery is ensured.1 Mild hypoglycemia without loss of consciousness or neurologic findings should be treated aggressively by administration of oral glucose and adjustments in glimepiride dosage and/or the patient's meal and exercise pattern.1
Patients receiving glimepiride and responsible family members should be informed of the risks of hypoglycemia, symptoms and treatment of hypoglycemic reactions, and conditions that predispose to the development of such reactions.1
There have been postmarketing reports of hypersensitivity reactions in patients treated with glimepiride, including serious reactions including anaphylaxis, angioedema, and Stevens-Johnson syndrome.1
If a hypersensitivity reaction is suspected, promptly discontinue glimepiride, assess for other potential causes for the reaction, and initiate alternate treatment for diabetes mellitus.1
Sulfonylureas, including glimepiride, can cause hemolytic anemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency.1 There have been reports of hemolytic anemia in patients receiving glimepiride who did not have a known history of G6PD deficiency.1
Use caution in patients with G6PD deficiency and consider the use of a non-sulfonylurea alternative.1
Increased Risk of Cardiovascular Mortality
Oral hypoglycemic drugs have been reported to be associated with increased cardiovascular mortality as compared to diet alone or diet plus insulin.1
This warning is based on the study conducted by the University Group Diabetes Program (UGDP), a long-term, prospective clinical trial designed to evaluate the effectiveness of glucose-lowering drugs in preventing or delaying vascular complications in patients with non-insulin-dependent diabetes.1 UGDP reported that patients treated for 5—8 years with diet plus a fixed dosage of tolbutamide had a rate of cardiovascular mortality approximately 2.5 times that of patients treated with diet alone.1 A significant increase in total mortality was not observed, but the use of tolbutamide was discontinued based on the increase in cardiovascular mortality, thus limiting the opportunity for the study to show an increase in overall mortality.1 Despite controversy regarding the interpretation of these results, the findings of the UGDP study provide an adequate basis for this warning.1 Although only one drug in the sulfonylurea class (tolbutamide) was included in this study, it is prudent to consider this warning may apply to other drugs in this class based on their similarities in mechanism of action and chemical structure.1
Inform patients of the potential risks and advantages of glimepiride and of alternative therapy.1
There have been no clinical studies establishing conclusive evidence of macrovascular risk reduction with glimepiride.1
When used in fixed combination with pioglitazone or other drugs, the cautions, precautions, contraindications, and drug interactions associated with both drugs must be considered.117
Available data from a small number of published studies and decades of postmarketing experience with glimepiride in pregnancy have not identified any drug associated risk for major birth defects, miscarriage, or adverse maternal outcomes.1 However, sulfonylureas (including glimepiride) cross the placenta and have been associated with neonatal adverse reactions such as hypoglycemia.1 Prolonged hypoglycemia, lasting 4—10 days, has been reported in neonates born to mothers receiving a sulfonylurea at the time of delivery and has been reported with the use of agents with a prolonged half-life.1
In animal studies, there was no increase in congenital anomalies, but an increase in fetal deaths occurred in rats and rabbits at glimepiride doses 50 times and 0.1 times the maximum recommended human dose (based on body surface area), respectively.1 This fetotoxicity was observed only at doses inducing maternal hypoglycemia and is believed to be directly related to the pharmacologic (hypoglycemic) action of glimepiride, as has been similarly noted with other sulfonylureas.1
Poorly controlled diabetes in pregnancy is associated with risks to both the mother and fetus.1 Poorly controlled diabetes in pregnancy is associated with increased maternal risk for diabetic ketoacidosis, preeclampsia, spontaneous abortions, preterm delivery, and delivery complications.1 Poorly controlled diabetes also increases the fetal risk for major birth defects, still birth, and macrosomia-related morbidity.1
Due to reports of prolonged hypoglycemia in neonates born to mothers receiving a sulfonylurea at the time of delivery, glimepiride should be discontinued at least 2 weeks before expected delivery.1 Observe newborns for symptoms of hypoglycemia and respiratory distress and manage accordingly.1
There is no information regarding the presence of glimepiride in human milk or the effects on milk production.1 Glimepiride is distributed into milk in rats.1 During prenatal and postnatal studies in rats, significant concentrations of glimepiride were present in breast milk and the serum of the pups.1 Offspring of rats exposed to high levels of glimepiride during pregnancy and lactation developed skeletal deformities consisting of shortening, thickening, and bending of the humerus during the postnatal period.1 These skeletal deformities were determined to be the result of nursing from mothers exposed to glimepiride.1
The developmental and health benefits of breastfeeding should be considered along with any potential adverse effects on the breast-fed child from glimepiride or from the underlying maternal condition.1 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).1
Glimepiride is not recommended in pediatric patients because of its adverse effects on body weight and hypoglycemia.1
The pharmacokinetics of a single dose of glimepiride were evaluated in 30 pediatric patients (aged 10—17 years) with type 2 diabetes mellitus.1 The results of this study found that the maximum plasma concentration, AUC, and half-life were comparable to historical data in adults.1 The safety and efficacy of glimepiride in pediatric patients were evaluated in a single-blind, 24-week trial that randomized 272 patients (aged 8—17 years) with type 2 diabetes to receive either glimepiride or metformin.1 Treatment naïve and previously treated patients were enrolled; previously treated patients were required to discontinue other oral antidiabetic agents at randomization.1 After 24 weeks, the overall mean treatment difference in glycosylated hemoglobin (hemoglobin A1c; HbA1c) was 0.2%, favoring metformin.1 Based on this result, the trial did not meet its primary objective of showing a similar reduction in HbA1c with glimepiride compared to metformin.1 Adverse effects reported in pediatric patients treated with glimepiride were similar to those reported in adult patients.1 Hypoglycemic events documented by a blood glucose <36 mg/dL were observed in 4% of patients treated with glimepiride compared to 1% treated with metformin.1 One patient in each treatment group experienced a severe hypoglycemic episode.1
In clinical trials of glimepiride, 1053 of 3491 patients (30%) were >65 years of age. No overall differences in safety or effectiveness were observed between these patients and younger patients, but greater sensitivity of some older individuals cannot be ruled out.1 There were no significant differences in the pharmacokinetics of glimepiride between patients with type 2 diabetes ≤65 years and those >65 years of age.1
Glimepiride is substantially excreted by the kidney.1 Geriatric patients are more likely to have renal impairment.1 Additionally, hypoglycemia may be difficult to recognize in geriatric patients.1 Use caution when initiating glimepiride and increasing the dosage of glimepiride in geriatric patients.1
The pharmacokinetics of glimepiride have not been adequately evaluated in patients with hepatic impairment.1
In a single-dose, open-label study, glimepiride 3 mg was administered to 15 patients with mild (creatinine clearance >50 mL/minute), moderate (creatinine clearance 20—50 mL/minute), and severe (creatinine clearance <20 mL/minute) renal impairment.1 Although serum glimepiride concentrations decreased with decreasing renal function, patients with severe renal impairment had a 2.3-fold higher mean AUC for the M1 metabolite and an 8.6-fold higher mean AUC for the M2 metabolite compared to those with mild renal impairment.1 The apparent terminal half-life for glimepiride did not change, while the half-lives for the M1 and M2 metabolites increased as renal function decreased.1 Mean urinary excretion of the M1 and M2 metabolites as a percentage of the dose decreased from 44% in patients with mild renal impairment to 21.9% in moderate renal impairment and 9.3% in severe renal impairment.1 A multiple-dose titration study was conducted in 16 patients with type 2 diabetes and renal impairment (baseline creatinine clearance 10—60 mL/minute) using dosages ranging from 1 to 8 mg daily for 3 months.1 The results were consistent with those observed in the single-dose study.1 In both studies, the relative total clearance of glimepiride increased when renal function was impaired and the elimination of the 2 major metabolites (M1 and M2) was reduced in renal impairment.1
To minimize the risk of hypoglycemia, the recommended starting dosage of glimepiride is 1 mg daily for all patients with type 2 diabetes and renal impairment.1
The pharmacokinetics of glimepiride and its metabolites were measured in a single-dose study involving 28 patients with type 2 diabetes who either had normal body weight or were morbidly obese.1 While the time to maximum plasma concentration (Tmax), clearance, and volume of distribution of glimepiride in the morbidly obese patients were similar to those in the normal weight group, the morbidly obese patients had a lower maximum plasma concentration (Cmax) and AUC than those of normal body weight.1
The most common adverse effects of glimepiride (≥5% of patients and more common than placebo) reported in clinical trials were hypoglycemia, headache, nausea, and dizziness.1
Glimepiride is metabolized by cytochrome P-450 (CYP) isoenzyme 2C9.1
Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes
There may be an interaction between glimepiride and inhibitors (e.g., fluconazole) and inducers (e.g., rifampin) of CYP2C9.1
Fluconazole may inhibit the metabolism of glimepiride, causing increased plasma concentrations of glimepiride, which may lead to hypoglycemia.1
Rifampin may induce the metabolism of glimepiride, causing decreased plasma concentrations of glimepiride, which may lead to worsening glycemic control.1
Medications that are highly protein bound, such as chloramphenicol, coumarins, fluoxetine, monoamine oxidase inhibitors, non-steroidal anti-inflammatory agents, probenecid, salicylates, and sulfonamides, may increase the glucose-lowering effect of sulfonylureas (including glimepiride), increasing the susceptibility to and/or intensity of hypoglycemia.1 When these medications are administered to a patient receiving glimepiride, monitor the patient closely for hypoglycemia.1 When these medications are withdrawn from a patient receiving glimepiride, monitor the patient closely for worsening glycemic control.1
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.1
The following medications may increase the glucose-lowering effect of sulfonylureas, including glimepiride, increasing the susceptibility to and/or intensity of hypoglycemia: anabolic steroids and androgens, angiotensin-converting enzyme inhibitors, oral antidiabetic agents, clarithromycin, cyclophosphamide, disopyramide, fibrates, fluconazole, histamine H2-receptor antagonists, insulin, pentoxifylline, pramlintide acetate, quinolones, somatostatin analogs, sulfinpyrazone, and tetracyclines.1 When these medications are administered to a patient receiving glimepiride, monitor the patient closely for hypoglycemia.1 When these medications are withdrawn from a patient receiving glimepiride, monitor the patient closely for worsening glycemic control.1
The following medications may reduce the glucose-lowering effect of sulfonylureas, including glimepiride, leading to worsening glycemic control: atypical antipsychotics (e.g., clozapine, olanzapine), barbiturates, oral contraceptives, corticosteroids, danazol, diazoxide, diuretics (thiazides and others), estrogens, glucagon, isoniazid, laxatives, nicotinic acid, phenothiazines, phenytoin, protease inhibitors, rifampin, somatropin, sympathomimetics (e.g., epinephrine, albuterol, terbutaline), and thyroid hormones.1 When these medications are administered to a patient receiving glimepiride, monitor the patient closely for worsening glycemic control.1 When these medications are withdrawn from a patient receiving glimepiride, monitor the patient closely for hypoglycemia.1
Additional agents, including both acute and chronic alcohol ingestion, β-adrenergic blocking agents, and clonidine may lead to either potentiation or weakening of glimepiride's glucose-lowering effect.1
The signs of hypoglycemia may be reduced or absent in patients taking sympatholytic drugs such as β-adrenergic blocking agents and clonidine.1
Administration of aspirin (1 g three times daily for 5 days) and glimepiride (single dose of 1 mg on day 4 of study period) resulted in a 34% decrease in mean glimepiride AUC and a 4% decrease in the mean glimepiride maximum plasma concentration.1
Colesevelam may reduce the maximum plasma concentration (by 8%) and total exposure of glimepiride (by 18%) when the two are administered concurrently.1 However, absorption is not reduced when glimepiride is administered 4 hours prior to colesevelam.1 Therefore, glimepiride should be administered at least 4 hours prior to colesevelam.1
Histamine H2-receptor Antagonists
Concomitant administration of a single 4-mg oral dose of glimepiride (on day 3 of the study period) with either cimetidine or ranitidine (given for a study period of 4 days) did not significantly alter the absorption and disposition of glimepiride.1
A potential interaction between oral miconazole and sulfonylureas leading to severe hypoglycemia has been reported.1 Whether this interaction occurs with other dosage forms of miconazole is not known.1
Concomitant administration of a single 2-mg dose of glimepiride (on day 4 of the study period) with propranolol (40 mg three times daily for 5 days) significantly increased glimepiride maximum plasma concentration, AUC, and half-life by 23%, 22%, and 15%, respectively.1
Concomitant administration of warfarin (single 25 mg dose administered 6 days before starting glimepiride and on day 4 of glimepiride administration) with glimepiride (4 mg daily for 10 days) did not alter the pharmacokinetics or plasma protein binding of warfarin.1 Glimepiride did decrease the pharmacodynamic response to warfarin, resulting in a reduction in the mean area under the prothrombin time curve and maximum prothrombin time by 3.3% and 9.9%, respectively; this is not considered clinically significant.1
Glimepiride is a sulfonylurea antidiabetic agent.1 The drug is structurally similar to glyburide and glipizide.3 Like other sulfonylurea antidiabetic agents, glimepiride lowers blood glucose concentration in diabetic patients and in healthy nondiabetic individuals.2, 20 Although the hypoglycemic action of the various sulfonylureas generally is similar, the drugs may differ quantitatively and/or possibly qualitatively in the extent to which they produce specific effects, and the effects may vary as a function of duration of treatment.9, 10 The precise mechanism(s) of hypoglycemic action of sulfonylurea antidiabetic agents has not been clearly established, but the drugs, including glimepiride, initially appear to lower blood glucose concentration principally by stimulating secretion of endogenous insulin from the beta cells of the pancreas.1, 9, 10, 11, 28, 54 During prolonged administration, sulfonylureas, including glimepiride, provide overall glycemic control without appreciable increases in fasting insulin secretion; therefore, extrapancreatic effects (e.g., enhanced peripheral sensitivity to insulin) appear to contribute substantially to the hypoglycemic action of the drugs.1, 2, 3, 5, 6, 50 Like other sulfonylureas, glimepiride alone is ineffective in the absence of functioning beta cells.1 Following single oral doses as low as 0.5-0.6 mg of the drug in healthy individuals, the hypoglycemic action generally is maximal within 2-3 hours.1 In patients with type 2 diabetes mellitus receiving 1-8 mg of glimepiride once daily, glycemic effects are maintained over 24 hours.1, 5
Following oral administration, peak drug concentration and maximal therapeutic effect is achieved in approximately 2—3 hours.1 Glimepiride demonstrates linear pharmacokinetics over the dosage range of 1—8 mg.1 Administration with food decreases the peak plasma concentration and AUC by 8 and 9%, respectively.1 Glimepiride is highly protein bound (>99.5%).1 Glimepiride is completely metabolized by oxidative biotransformation by cytochrome P-450 2C9 to the metabolite M1, which is further metabolized to M2 by cytosolic enzymes.1 M1 possess approximately one-third of the pharmacological activity in animal models, although it is unclear whether M1 results in clinical meaningful effects on blood glucose in humans; M2 is inactive.1 Glimepiride is excreted in the urine (60%) and the feces (40%) as metabolites.1 In geriatric patients, the mean AUC is reduced by 13% and weight-adjusted clearance is approximately 11% higher than that of younger patients.1 There is no difference in the pharmacokinetics of glimepiride based on sex (when adjusted for body weight) or race.1 The pharmacokinetics of glimepiride do not differ between healthy subjects and patients with diabetes mellitus.1 In patients with decreased renal function, glimepiride serum concentrations decrease while the AUC and half-lives of the metabolites (M1 and M2) increase.1 The effect of hepatic impairment on the pharmacokinetics of glimepiride is unknown.1 Morbid obesity is associated with a lower maximum plasma concentration and AUC compared to patients with normal body weight.1 There were no significant differences in the pharmacokinetics of glimepiride between patients with type 2 diabetes who were ≤65 years and those >65 years of age.1
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, 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)* | ||
Pioglitazone and Glimepiride Tablets | ||||
4 mg with Pioglitazone Hydrochloride 30 mg (of pioglitazone)* | Duetact® | Takeda | ||
Pioglitazone and Glimepiride 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. Florida Pharmaceutical Products, LLC. Glimepiride tablets prescribing information. Boca Raton, FL; 2024 Oct.
2. Anon. Glimepiride. Drug Future . 1992; 17:774-8.
3. Sato J, Ohsawa I, Oshida Y et al. Comparison between effects of glimepiride and glibenclamide on in vivo insulin action. Intl Congress Series . 1994; 1057:341-4.
5. Draeger E. Clinical profile of glimepiride. Diabetes Res Clin Pract . 1995; 28(Suppl):S139-46. [PubMed 8529506]
6. Hatziagelaki E, Diamantopoulos E, Halvatsiotis P et al. The effect of a new sulfonylurea glimepiride (HOE 490) on the blood glucose control of type II diabetics. Diabetes Res Clin Pract . 1988; 5(Suppl 1):S481. [PubMed 2901329]
7. Ladik T, Lotz N, Rupp P et al. Efficiency of the new sulfonylurea glimepiride in the treatment of type 2 diabetes. Diabetes Res Clin Pract . 1988; 5(Suppl 1):S487.
9. Jackson JE, Bressler R. Clinical pharmacology of sulphonylurea hypoglycaemic agents: part 1. Drugs . 1981; 22:211-45. [PubMed 7021124]
10. 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]
11. Krentz AJ, Ferner RE, Bailey CJ. Comparative tolerability profiles of oral antidiabetic agents. Drug Safety . 1994; 11:223-41. [PubMed 7848543]
13. Kerr CP. Improving outcomes in diabetes: a review of the outpatient care of NIDDM patients. J Fam Pract . 1995; 40:63-75. [PubMed 7807040]
15. Anon. Diabetes mellitus. NIH Cons Dev Conf Statement . 1986; 6:1-7.
16. Blake GH. Control of type II diabetes: reaping the rewards of exercise and weight loss. Postgrad Med . 1992; 92:129-32. [PubMed 1437899]
17. United Kingdom prospective diabetes study group. United Kingdom prospective diabetes study (UKPDS) 16: overview of 6 years' therapy of type II diabetes: a progressive disease. Diabetes . 1995; 44:1240-58.
18. Expert Committee of the Canadian Diabetes Advisory Board. Clinical practice guidelines for treatment of diabetes mellitus. CMAJ . 1992; 147:697-712. [PubMed 1521215]
19. Zimmerman B, Espenshade J, Fujimoto W et al. The pharmacological treatment of hyperglycemia in NIDDM. Diabetes Care . 1995; 18:1510-18. [PubMed 8722084]
20. Tsumura K. Clinical evaluation of glimepiride (HOE490) in NIDDM, including a double blind comparative study versus gliclazide. Diabetes Res Clin Pract . 1995; 28(Suppl):S147-9. [PubMed 8529507]
22. Williams G. Management of non-insulin-dependent diabetes mellitus. Lancet . 1994; 343:95-100. [PubMed 7903785]
24. Henry R R. Glucose control and insulin resistance in non-insulin-dependent diabetes mellitus. Ann Intern Med . 1996; 124:97-103. [PubMed 8554221]
26. Polonsky KS, Sturis J, Bell GI. Non-insulin-dependent diabetes mellitus—a genetically programmed failure of the beta cell to compensate for insulin resistance. N Engl J Med . 1996; 334:777-83. [PubMed 8592553]
28. Bailey C, Turner R. Metformin. N Engl J Med . 1996; 334:374-. [PubMed 8538710]
35. Clark CM Jr. Where do we go from here? Ann Intern Med . 1996; 124(1 Part 2):184-6. Editorial.
44. 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]
46. Raskin P. Combination therapy in NIDDM N Engl J Med . 1992; 327:1453-4. Editorial.
47. Yki-Järvinen H, Kauppila M, Kajanssu E et al. Comparison of insulin regimens in patients with non-insulin-dependent diabetes mellitus. N Engl J Med . 1992; 327:1426- 33. [PubMed 1406860]
48. 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]
49. Roerig. Glucotrol® prescribing information. In: Huff BB, ed. Physicians' desk reference. 43rd ed. Oradell, NJ: Medical Economics Company Inc; 1989:1782-3.
50. Fineberg SE, Schneider SH. Glipizide versus tolbutamide, an open trial: effects on insulin secretory patterns and glucose concentrations. Diabetologia . 1980; 18:49-54. [PubMed 6988265]
54. Bloomgarden ZT. New and traditional treatment of glycemia in NIDDM. Diabetes Care . 1996; 19:295-9. [PubMed 8742586]
57. Turner R, Cull C, Holman R et al. United Kingdom Prospective Diabetes Study 17: a 9-year update of a randomized, controlled trial on the effect of improved metabolic control on complications in non-insulin-dependent diabetes mellitus. Ann Intern Med . 1996; 124(1 Pt 2):136-45. [PubMed 8554206]
59. 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]
60. 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]
61. Nathan DM. Some answers, more controversy, from UKDS. Lancet . 1998; 352:832-3. [PubMed 9742972]
62. American Diabetes Association. Implications of the United Kingdom Prospective Diabetes Study. Diabetes Care . 1999; 22(Suppl. 1):S27-31.
63. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet . 1998; 352:854-65. [PubMed 9742977]
65. Genuth P. United Kingdom prospective diabetes study results are in. J Fam Pract . 1998; 47:(Suppl.
67. 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]
68. Watkins PJ. UKPDS: a message of hope and a need for change. Diabet Med . 1998; 15:895-6. [PubMed 9827842]
97. 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]
102. 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]
103. 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]
104. 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.
105. 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]
106. 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.
117. Takeda Pharmaceuticals, Inc. Duetact® (pioglitazone hydrochloride and glimepiride) prescribing information. Lexington, MA; 2020 Jun.
118. Nathan DM, Buse JB, Davidson MB et al. Management of hyperglycemia in type 2 diabetes: a consensus algorithm for initiation and adjustment of therapy. A consensus statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care . 2006; 29:1963-72. [PubMed 16873813]
119. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2003 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes . 2003; 27(Suppl 2):S1-152.
122. Klein S, Allison DB, Heymsfield SB et al. Waist circumference and cardiometabolic risk: a consensus statement from shaping America's health: Association for Weight Management and Obesity Prevention; NAASO, the Obesity Society; the American Society for Nutrition; and the American Diabetes Association. Diabetes Care . 2007; 30:1647-52. [PubMed 17360974]
123. American Diabetes Association. Summary of revisions for the 2009 clinical practice recommendations. Diabetes Care . 2009; 32:S3-S5. [PubMed 19118287]
124. DluhyRG, McMahon GT. Intensive glycemic control in the ACCORD and ADVANCE trials. N Engl J Med . 2008; 358:2630-33. Editorial.
125. Stratton IM, Adler AI, Neil HA et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ . 2000; 321:405-12. [PubMed 10938048]
126. 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]
127. Skyler JS, Bergenstal R, Bonow RO et al. Intensive glycemic control and the prevention of cardiovascular events: implications of the ACCORD, ADVANCE, and VA diabetes trials: a position statement of the American Diabetes Association and a scientific statement of the American College of Cardiology Foundation and the American Heart Association. Diabetes Care . 2009; 32:187-92. [PubMed 19092168]
128. , Patel A, MacMahon S et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med . 2008; 358:2560-72. [PubMed 18539916]
129. Action to Control Cardiovascular Risk in Diabetes Study Group, Gerstein HC, Miller ME et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med . 2008; 358:2545-59. [PubMed 18539917]
130. Duckworth W, Abraira C, Moritz T et al. Glucose control and vascular complications in veterans with type 2 diabetes. N Engl J Med . 2009; 360:129-39. [PubMed 19092145]
131. American Diabetes Association. Aspirin therapy in diabetes: position statement. Diabetes Care . 2001; 24(Suppl.1):S62-3.
132. Weiss IA, Valiquette G, Schwarcz MD. Impact of glycemic treatment choices on cardiovascular complications in type 2 diabetes. Cardiol Rev . 2009; 17(4):165-75. [PubMed 19525678]
133. Holman RR, Paul SK, Bethel MA et al. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med . 2008; 359:1577-89. [PubMed 18784090]
134. Nathan DM, Cleary PA, Backlund JY et al. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med . 2005; 353:2643-53. [PubMed 16371630]
135. Skyler JS. Non-insulin-dependent diabetes mellitus: a clinical strategy. Diabetes Care . 1984; 7(Suppl 1):118-29. [PubMed 6376024]
136. Ismail-Beigi F, Moghissi ES. Glycemia management and cardiovascular risk in type 2 diabetes: an evolving perspective. Endocr Pract . 2008 Jul-Aug; 14:639-43.
137. US Food and Drug Administration. FDA significantly restricts access to the diabetes drug Avandia. Rockville, MD; 2010 Sep 23. News release from FDA web site. Accessed 2010 Nov 15. [Web]
138. Woodcock J (US Food and Drug Administration). Decision on continued marketing of rosiglitazone (Avandia, Avandamet, Avandaryl). Rockville, MD; Available at FDA website. Accessed 2010 Nov 15. [Web]
139. Food and Drug Administration. FDA drug safety communication: Updated risk evaluation and mitigation strategy (REMS) to restrict access to rosiglitazone-containing medicines including Avandia, Avandamet, and Avandaryl. Rockville, MD; 2011 May 18. Available from FDA website. Accessed 2011 Jun 20. [Web]
140. Avandia® (rosiglitazone maleate), Avandamet (rosiglitazone maleate and metformin hydrochloride), and Avandaryl (rosiglitazone maleate and glimepiride) tablets risk evaluation and mitigation strategy (REMS). Available from FDA web site. Accessed 2011 Aug 25. [Web]
141. Food and Drug Administration. FDA advisory committee meeting briefing document for NDA 21071 Avandia (rosiglitazone maleate). Rockville, MD; July 13 and 14, 2010. From FDA website. [Web]
142. Lipska KJ, Ross JS. Switching from rosiglitazone: thinking outside the class. JAMA . 2011; 305:820-1. [PubMed 21304068]
143. Niemi M, Backman JT, Neuvonen M et al. Effects of fluconazole and fluvoxamine on the pharmacokinetics and pharmacodynamics of glimepiride. Clin Pharmacol Ther . 2001; 69:194-200. [PubMed 11309547]
144. Niemi M, Kivisto KT, Backman JT. Effect of rifampicin on the pharmacokinetics and pharmacodynamics of glimepiride. Br J Clin Pharmacol . 2000; 50:591-5. [PubMed 11136298]
698. Garber AJ, Handelsman Y, Grunberger G et al. Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm 2020 executive summary. Endocr Pract . 2020; 26:107-139. [PubMed 32022600]
699. Zelniker TA, Wiviott SD, Raz I et al. Comparison of the effects of glucagon-like peptide receptor agonists and sodium-glucose cotransporter 2 inhibitors for prevention of major adverse cardiovascular and renal outcomes in type 2 diabetes mellitus. Circulation . 2019; 139:2022-2031. [PubMed 30786725]
704. American Diabetes Association. 9. Pharmacologic approaches to glycemic treatment: Standards of Medical Care in Diabetes-2020 . Diabetes Care . 2020; 43:S98-S110. [PubMed 31862752]
705. American Diabetes Association. 10. Cardiovascular disease and risk management: Standards of Medical Care in Diabetes-2020 . Diabetes Care . 2020; 43:S111-S134. [PubMed 31862753]
706. American Diabetes Association. 11. Microvascular complications and foot care: Standards of Medical Care in Diabetes-2020 . Diabetes Care . 2020; 43:S135-S151. [PubMed 31862754]
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-S206.
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; 29:305-340.
709. Institute for Safe Medication Practices (ISMP). ISMP list of high-alert medications in acute care settings. ISMP; 2024.
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.