Acarbose is an α-glucosidase inhibitor antidiabetic agent.1, 6, 30
Acarbose is used as an adjunct to diet and exercise to improve glycemic control in adult patients with type 2 diabetes mellitus.1, 6, 14, 17, 47 In clinical studies in adults, acarbose was evaluated as monotherapy and in combination with other antidiabetic agents (e.g., sulfonylurea, metformin, insulin).1, 6, 18, 19, 20, 21, 26, 44, 47
Acarbose lowers postprandial blood glucose concentrations and thereby reduces fluctuations in the daily blood glucose concentration-time profile in patients with type 2 diabetes mellitus and in lean or obese nondiabetic individuals; fasting blood glucose concentrations either are not affected or are mildly decreased.1, 2, 3, 5, 6, 7, 17, 19, 20, 21, 24, 35, 37, 39, 47 Reductions in blood glucose produced by acarbose as monotherapy in patients with type 2 diabetes mellitus generally have been associated with reductions in glycosylated hemoglobin concentration (hemoglobin A1c; HbA1c) of about 0.4-1%.1, 17, 18, 20, 24, 27 In placebo-controlled trials in patients with type 2 diabetes mellitus, monotherapy with acarbose (25-300 mg 3 times daily) produced greater lowering of postprandial plasma glucose and HbA1c than dietary therapy alone.1, 2, 3, 6, 19, 20 A limited number of comparative clinical studies indicate that acarbose monotherapy is as effective as monotherapy with a sulfonylurea (e.g., glyburide) or a biguanide (e.g., metformin) for the management of mild to moderate postprandial hyperglycemia in patients with type 2 diabetes mellitus.1, 2, 3, 6, 19, 21
Adequate glycemic control has been maintained for at least 1 year in patients receiving the drug.6, 22 Primary failure with acarbose may be the result of individual variations in the sensitivity of intestinal α-glucosidases to the drug, impaired insulin secretion, severe insulin resistance, or poor compliance with a diet low in simple sugars.6, 18, 20, 22, 27, 48 Data on the incidence of primary failures in patients receiving initial monotherapy with acarbose are limited, and data comparing the probabilities of primary failure with acarbose and other oral antidiabetic agents are lacking.18, 19, 20, 22, 37, 44
Acarbose also may be useful as an adjunct to other antidiabetic drug therapy (e.g., sulfonylureas, metformin, insulin) in patients with type 2 diabetes mellitus.1, 6, 18, 19, 22, 34, 40, 44, 49, 51 Reductions in blood glucose produced by acarbose combined with other oral antidiabetic agents (e.g., sulfonylurea given at maximum dose, metformin given at 2-5.5 g daily) in patients with type 2 diabetes mellitus generally have resulted in reductions in HbA1c of about 0.5-0.65% and decreases in 1-hour postprandial glucose concentrations of about 34 mg/dL.1, 27
In a comparative clinical trial in patients with type 2 diabetes receiving acarbose or tolbutamide alone or in combination as an adjunct to dietary therapy, combined therapy with acarbose (200 mg 3 times daily) and tolbutamide (250-1000 mg 3 times daily) resulted in better glycemic control (as determined by postprandial plasma glucose and HbA1c) and less weight gain than therapy with diet alone, acarbose alone, or tolbutamide alone; in addition, the mean daily dosage of tolbutamide when used as adjunctive therapy (1.9 g) was less than that when the drug was given as monotherapy (2.4 g).1, 19 In patients receiving a maximum dosage of a sulfonylurea, addition of acarbose (50-300 mg 3 times daily) to such therapy reduced HbA1c and allowed a reduction in sulfonylurea dosage compared with that in patients receiving sulfonylurea monotherapy.1, 3 The addition of acarbose (50-100 mg 3 times daily for 6 months) to insulin therapy (mean daily dosage of 61 units) in patients with type 2 diabetes mellitus reduced HbA1c by a mean of 0.69% and decreased 1-hour postprandial glucose concentrations by 36 mg/dL.1 In a long-term study in patients receiving acarbose alone or in combination with a sulfonylurea, metformin, or insulin, the reduction in HbA1c was sustained throughout the year-long study in those receiving acarbose alone or in combination with a sulfonylurea or metformin; however, the statistically significant effect on HbA1c noted at 6 months in those receiving insulin and acarbose was no longer evident at 1 year.1
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, hypoglycemia risk, presence of overweight or obesity, cost, access, and patient preferences.707 The α-glucosidase inhibitors do not have additional beneficial effects on cardiovascular or renal outcomes.707 Therefore, their use should be considered only as add-on therapy in patients who require additional glycemic control or when more effective medications are not tolerated, are contraindicated, or are unavailable.707
The American Association of Clinical Endocrinology (AACE) also publishes guidelines for the management of type 2 diabetes.708, 709 The principles of diabetes management outlined in the guidelines are similar to those recommended by the ADA.708, 709 The α-glucosidase inhibitors can be considered as an alternative for add-on therapy when other preferred alternatives are either contraindicated or not tolerated.708, 709
Acarbose is administered orally 3 times daily.1 The drug should be administered at the beginning (with the first bite) of each main meal.1 If the prescribed diet designed to minimize adverse GI effects is not observed, adverse GI effects may be intensified.1 Common adverse GI effects (e.g., flatulence, diarrhea, abdominal discomfort) usually develop during the first few weeks of therapy and generally diminish in frequency and intensity with time, although flatulence usually is only abated rather than returned to pretreatment levels.1 If adverse GI effects are strongly distressing despite adherence to the prescribed diabetic diet, a clinician should be consulted and the dosage of acarbose temporarily or permanently reduced.1
Store acarbose tablets at 20—25°C in a tightly closed container protected from moisture.1
Dosage of acarbose must be individualized carefully based on patient response and tolerance.1 The goal of therapy should be to reduce both postprandial blood (or plasma) glucose and HbA1c values to normal or near normal using the lowest effective dosage.1
For the management of type 2 diabetes mellitus, the usual initial adult dosage of acarbose is 25 mg orally three times daily given at the beginning (with the first bite) of each main meal.1 However, some patients may benefit from a more gradual dosage titration to reduce adverse GI effects.1, 2, 12, 34 Therapy with the drug in these patients should be initiated at a low dosage (25 mg once daily) and increased gradually as necessary to the usual initial dosage of 25 mg three times daily.1 Subsequent dosage should be adjusted according to the patient's therapeutic response and tolerance, using the lowest possible effective dosage.1, 34, 43, 45
Once an acarbose dosage of 25 mg three times daily has been reached, the dosage of acarbose may be increased at intervals of 4-8 weeks based on 1-hour postprandial glucose or HbA1c levels, and on tolerance.1, 34, 41 The dosage can increased from 25 mg three times daily to 50 mg three times daily, with some patients benefiting from a further increase to 100 mg three times daily.1 The usual maintenance dosage of acarbose ranges from 50-100 mg three times daily; use of the 50-mg dosage three times daily may be associated with fewer adverse effects and has efficacy similar to the 100-mg dosage three times daily.1, 6, 47 Since patients with low body weight may be at increased risk for elevated serum transaminases, only patients with body weight exceeding 60 kg should be considered for dosages exceeding 50 mg three times daily.1 If no further reduction in postprandial glucose or HbA1c occurs at the maximum recommended dosage of acarbose (100 mg three times daily), consideration should be given to lowering the dosage.1 Once an effective and tolerated dosage of acarbose is established, that dosage should be maintained.1 Although satisfactory control of blood glucose concentrations may be achieved within a few days after dosage adjustment, the full effect of the drug may be delayed for up to 2 weeks.18
Dosages of acarbose higher than those recommended by the manufacturer (e.g., 200-300 mg three times daily) have been evaluated, but clinically important differences in postprandial plasma glucose and HbA1c have not been shown consistently.1, 10, 18, 19, 20, 22, 25, 27, 30, 37, 43
Acarbose is contraindicated in patients with cirrhosis; however, data are lacking and the manufacturer makes no specific recommendations regarding use of the drug in other conditions associated with hepatic impairment.1
Acarbose is not recommended for use in patients with significant renal impairment (i.e., serum creatinine exceeding 2 mg/dL) since no information is available concerning the use of the drug in such patients; however, in a study in nondiabetic individuals with renal impairment, plasma concentrations of acarbose increased in proportion to the degree of renal dysfunction.1
The manufacturer makes no specific dosage recommendations for geriatric patients.1
There are no clinical studies establishing conclusive evidence of macrovascular risk reduction with acarbose.1
Based on its mechanism of action, acarbose should not cause hypoglycemia in the fasted or postprandial state when used as monotherapy or when used concomitantly with metformin.1
The potential for hypoglycemia may be increased when acarbose is used concomitantly with insulin or an insulin secretagogue (e.g., sulfonylurea).1
Oral glucose (i.e., dextrose) absorption is not inhibited by acarbose and should be used instead of sucrose (e.g., cane sugar) for the treatment of mild to moderate hypoglycemia.1 The hydrolysis of sucrose to glucose and fructose is inhibited by acarbose and is therefore unsuitable for rapid correction of hypoglycemia.1 Severe hypoglycemia may require the use of either an IV glucose infusion or glucagon injection.1
Elevations in serum transaminase (i.e., ALT, AST) concentrations and, in rare instances, hyperbilirubinemia may occur, particularly with acarbose dosages exceeding 150 mg daily (50 mg 3 times daily).1 Jaundice and fatal hepatitis have been reported during postmarketing experience; the relationship to acarbose is unclear.1
In long-term studies (up to a duration of 12 months and including dosages up to 300 mg three times daily), treatment-emergent elevations of serum transaminases (AST and/or ALT) above the upper limit of normal (ULN), greater than 1.8 times the ULN, and greater than 3 times the ULN occurred in 14%, 6%, and 3%, respectively, of acarbose-treated patients compared to 7%, 2%, and 1%, respectively, of placebo-treated patients.1 These elevations appeared to be dose-related, asymptomatic, reversible, more common in females, and, in general, were not associated with other evidence of liver dysfunction.1 In clinical studies including those using acarbose doses up to the maximum approved dosage of 100 mg three times daily, treatment-emergent elevations of AST and/or ALT at any level of severity were similar between patients who received acarbose and those who received placebo.1 In postmarking experience with acarbose, 62 cases of serum transaminase elevations greater than 500 IU/L (29 of which were associated with jaundice) were reported.1 Of these 62 patients, 41 patients received a dosage of ≥100 mg three times daily and 33 patients had a reported weight <60 kg.1 In the 59 cases in which follow-up information was available, hepatic abnormalities improved or resolved upon discontinuation of acarbose in 55 patients and were unchanged in 2 patients.1
Monitor serum transaminase concentrations every 3 months during the first year of acarbose therapy and periodically thereafter.1 If elevations occur, reduce dosage.1 It may be necessary to discontinue the drug, particularly if elevated serum transaminase concentrations persist.1
Temporary loss of glycemic control may occur during periods of stress, such as fever, infection, or surgery.1 At such times, alternate therapy (including temporary insulin therapy) may be necessary.1
The manufacturer states that monitoring blood glucose concentrations with the 1,5-anhydroglucitol assay is not recommended because measurements are unreliable in assessing glycemic control in patients taking acarbose; alternative methods of monitoring glycemic control should be used.1
There are no adequate and well-controlled studies of acarbose in pregnancy.1 In animal reproduction studies conducted in rats, acarbose doses up to 480 mg/kg (corresponding to 9 times the exposure in humans based on plasma levels) revealed no evidence of impaired fertility or harm to the fetus.1 In rabbits, acarbose doses up to 160 mg/kg (corresponding to 10 times the human dose based on body surface area) showed no evidence of embryotoxicity and there was no evidence of teratogenicity at a dose 32 times the human dose (based on body surface area).1 However, in rabbits, reduced maternal body weight gain, likely the result of the pharmacodynamic activity of high doses of acarbose in the intestines, may have been responsible for a slight increase in embryonic losses.1
Abnormal glucose levels during pregnancy are associated with a higher incidence of congenital anomalies as well as increased neonatal morbidity and mortality; acarbose should be used during pregnancy only if clearly needed as safety in pregnant women has not been established.1
There is no information regarding the presence of acarbose in human milk.1 Acarbose is distributed into milk in rats.1 Acarbose is not recommended for use while breast-feeding.1
Safety and efficacy of acarbose have not been established in pediatric patients younger than 18 years of age.1
No overall differences in safety or efficacy of acarbose have been observed between patients ≥65 years of age and younger patients.1 In clinical studies of acarbose, 27% of patients were ≥65 years of age and 4% of patients were ≥75 years of age.1 The mean steady-state AUC and maximum concentration of acarbose are approximately 1.5-times higher in geriatric patients compared to younger patients; these differences are not considered significant.1
Acarbose is contraindicated in patients with cirrhosis.1
The plasma concentration of acarbose increases proportionally relative to the degree of renal dysfunction.1 In patients with severe renal impairment (creatinine clearance <25 mL/minute per 1.73 m2), peak plasma concentrations and AUCs were 5- and 6-times higher, respectively, than those with normal renal function.1 Long-term studies in patients with significant renal dysfunction (serum creatinine >2 mg/dL) have not been conducted; use of acarbose in these patients is not recommended.1
The most common adverse effects of acarbose are GI symptoms, including flatulence, diarrhea, and abdominal pain.1
Drugs That May Antagonize Hypoglycemic Effects
Drugs that cause hyperglycemia and may lead to loss of glycemic control in patients with diabetes mellitus include calcium-channel blocking agents, corticosteroids, estrogens, isoniazid, nicotinic acid (niacin), oral contraceptives, phenothiazines, phenytoin, sympathomimetics, thiazide and other diuretics, and thyroid preparations.1 When such drugs are added to or withdrawn from therapy in patients receiving acarbose, patients should be closely observed for evidence of altered glycemic control.1
Concomitant use of digestive enzyme supplements containing carbohydrate-splitting enzymes (e.g., amylase, pancreatin) and acarbose may reduce the efficacy of acarbose; avoid concomitant use.1
Concomitant use of acarbose and digoxin may affect bioavailability, maximum plasma concentration (decreased 26%), and mean trough concentration (decreased 9%) of digoxin.1 Dosage adjustment of digoxin may be required if used concomitantly with acarbose.1
Insulin and Insulin Secretagogues
Concomitant use of acarbose with insulin or insulin secretagogues (e.g., sulfonylureas) may increase the risk of hypoglycemia.1 If hypoglycemia occurs, dosage adjustment of insulin or the insulin secretagogue may be required.1
Acarbose does not affect the absorption or distribution of glyburide.1
Concomitant use of intestinal adsorbents (e.g., charcoal) and acarbose may reduce the efficacy of acarbose; avoid concomitant use.1
The peak plasma concentration of metformin is reduced by approximately 20% when administered concomitantly with acarbose due to a delay in the absorption of metformin; metformin absorption, as indicated by plasma AUC levels, is not affected.1 This interaction is not considered to be clinically meaningful.1
Acarbose has no effect on the pharmacokinetics or pharmacodynamics of nifedipine.1
Due to the effects on gastric emptying, pramlintide should not be used concomitantly with medications that cause delayed gastric emptying, including α-glucosidase inhibitors.112
Acarbose has no effect on the pharmacokinetics or pharmacodynamics of propranolol.1
Acarbose is an α-glucosidase inhibitor antidiabetic agent.1, 6, 30 The drug is a complex oligosaccharide produced by fermentation of Actinoplanes utahensis .1, 6, 30 Acarbose is a reversible, competitive inhibitor of α-glucosidase enzymes (e.g., glucoamylase, sucrase, maltase, isomaltase) that hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the intestinal brush-border.2, 6, 14, 24, 29, 30 Acarbose also has a small inhibitory effect on pancreatic α-amylase, which hydrolyzes starch into maltose, maltotriose, and dextrins in the lumen of the small intestine.2, 14, 17, 30, 33 In patients with diabetes, inhibition of these enzymes results in delayed carbohydrate breakdown and glucose absorption and in a resultant reduction in postprandial hyperglycemia.1, 2, 5, 6, 7, 10, 14, 24, 30 Acarbose has no inhibitory effect on lactase and would not be expected to produce lactose intolerance.1
The systemic bioavailability of acarbose is low, with less than 2% absorbed as the active parent drug.1 Peak plasma concentrations of the active drug are attained at approximately 1 hour.1 Acarbose is metabolized in the GI tract, principally by intestinal bacteria but also by digestive enzymes to multiple metabolites, one of which is active.1 Acarbose is excreted principally in the feces (51%) as unabsorbed drug and in the urine as metabolites (34% of the dose).1 The plasma half-life of acarbose is approximately 2 hours; accumulation does not occur with the recommended multiple daily dosing frequency (i.e., three times daily).1 Mean steady-state AUC and peak plasma concentrations of acarbose were approximately 1.5-times higher in geriatric patients compared to younger adults; however, these differences were not statistically significant.1 The plasma concentration of acarbose increases proportionally relative to the degree of renal dysfunction.1 In patients with severe renal impairment (creatinine clearance <25 mL/minute per 1.73 m2), peak plasma concentrations and AUC of acarbose were 5- and 6-times higher, respectively, than those with normal renal function.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 | 25 mg* | Acarbose Tablets | |
50 mg* | Acarbose Tablets | |||
100 mg* | Acarbose Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
AHFS® Drug Information. © Copyright, 1959-2025, Selected Revisions December 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.
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