VA Class:HS502
ATC Class:A10BF01
Acarbose is an α-glucosidase inhibitor antidiabetic agent.1, 6, 30
Acarbose is used as monotherapy as an adjunct to diet and exercise for the management of type 2 (noninsulin-dependent) diabetes mellitus (NIDDM) in patients whose hyperglycemia cannot be controlled by diet and exercise alone.1, 6, 14, 17, 47 Acarbose also may be used in combination with a sulfonylurea, metformin, or insulin as an adjunct to diet and exercise for the management of type 2 diabetes mellitus in patients whose hyperglycemia cannot be controlled with acarbose, metformin, insulin, or sulfonylurea monotherapy, diet, and exercise.1, 6, 23
Current guidelines for the treatment of type 2 diabetes mellitus generally recommend metformin as first-line therapy in addition to lifestyle modifications in patients with recent-onset type 2 diabetes mellitus or mild hyperglycemia because of its well-established safety and efficacy (i.e., beneficial effects on glycosylated hemoglobin [hemoglobin A1c; HbA1c], weight, and cardiovascular mortality).698, 704, 705 (See Uses: Type 2 Diabetes Mellitus, in Metformin 68:20.04.) In patients with contraindications or intolerance to metformin (e.g., risk of lactic acidosis, GI intolerance) or in selected other patients, some experts suggest that initial therapy with a drug from another class of antidiabetic agents (e.g., a glucagon-like peptide-1 [GLP-1] receptor agonist, sodium-glucose cotransporter 2 [SGLT2] inhibitor, dipeptidyl peptidase-4 [DPP-4] inhibitor, sulfonylurea, thiazolidinedione, basal insulin) may be acceptable based on patient factors.698, 704 Initiating antidiabetic therapy with 2 agents (e.g., metformin plus another drug) may be appropriate in patients with an initial HbA1c exceeding 7.5% or at least 1.5% above the target level.698, 704 In metformin-intolerant patients with high initial HbA1c levels, some experts suggest initiation of therapy with 2 agents from other antidiabetic drug classes with complementary mechanisms of action.698, 704
While α-glucosidase inhibitors (acarbose, miglitol) generally are not recommended as second-line therapy after failure of metformin monotherapy because of lesser efficacy, frequent adverse GI effects, and greater cost compared with other antidiabetic agents, some experts state that an α-glucosidase inhibitor may be appropriate for treatment of type 2 diabetes mellitus in selected patients.110, 698
Because of the progressive nature of type 2 diabetes mellitus, patients initially receiving an oral antidiabetic agent will eventually require multiple oral and/or injectable noninsulin antidiabetic agents of different therapeutic classes and/or insulin for adequate glycemic control.698, 704 Patients who have inadequate glycemic control with initial (e.g., metformin) monotherapy should receive treatment with additional antidiabetic agents; data suggest that the addition of each noninsulin agent to initial therapy lowers HbA1c by approximately 0.7-1%.704 In addition, early initiation of combination therapy may help to more rapidly attain glycemic goals and extend the time to treatment failure.704
Factors to consider when selecting additional antidiabetic agents for combination therapy in patients with inadequate glycemic control on metformin monotherapy include patient comorbidities (e.g., atherosclerotic cardiovascular disease [ASCVD], established kidney disease, heart failure), hypoglycemia risk, impact on weight, cost, risk of adverse effects, and patient preference.698, 699, 704, 705, 706 When the greater glucose-lowering effect of an injectable drug is needed in patients with type 2 diabetes mellitus, some experts currently state that an injectable GLP-1 receptor agonist is preferred over insulin in most patients because of beneficial effects on body weight and a lower risk of hypoglycemia, although adverse GI effects may diminish tolerability.698, 704 While addition of a GLP-1 receptor agonist may successfully control hyperglycemia, many patients will eventually require insulin therapy.698 Early introduction of insulin therapy should be considered when hyperglycemia is severe (e.g., blood glucose of at least 300 mg/dL or HbA1c exceeding 9-10%), especially in the presence of catabolic manifestations (e.g., weight loss, hypertriglyceridemia, ketosis) or symptoms of hyperglycemia.698, 704 For additional information regarding the initiation of insulin therapy in patients with diabetes mellitus, see Uses: Diabetes Mellitus, in the Insulins General Statement 68:20.08.
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, 23, 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 of about 0.4-1%.1, 17, 18, 20, 24, 27 In placebo-controlled trials in type 2 diabetic patients, monotherapy with acarbose (25-300 mg 3 times daily) produced greater lowering of postprandial plasma glucose and glycosylated hemoglobin concentrations 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., tolbutamide, 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
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, 23, 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, 23, 37, 44 Adequate glycemic control has been maintained for at least 1 year in compliant patients receiving the drug.6, 22, 23
Acarbose also may be useful as an adjunct to other antidiabetic drug therapy (e.g., sulfonylureas, metformin) in patients with type 2 diabetes mellitus, possibly because these drugs have different mechanisms of antihyperglycemic effect.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 glycosylated hemoglobin concentration 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 type 2 diabetic patients 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 glycosylated hemoglobin concentrations) 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 maximum dosage of a sulfonylurea, addition of acarbose (50-300 mg 3 times daily) to such therapy reduced glycosylated hemoglobin concentrations and allowed a reduction in sulfonylurea dosage compared with that in patients receiving sulfonylurea monotherapy.1, 3, 23 Addition of acarbose (50-100 mg 3 times daily for 6 months) to patients with type 2 diabetes mellitus receiving insulin (mean daily dosage of 61 units) has reduced glycosylated hemoglobin concentrations by a mean of 0.69% and has decreased 1-hour postprandial glucose concentrations by 36 mg/dL.1 In a long-term study in patients receiving acarbose alone or combined with a sulfonylurea, metformin, or insulin, the reduction in glycosylated hemoglobin concentration was sustained throughout the year-long study in those receiving acarbose alone or in combination with sulfonylureas or metformin; however, the statistically significant effect on glycosylated hemoglobin noted at 6 months in those receiving insulin and acarbose was no longer evident at 1 year.1
Precautions and Other Considerations
Patients should be advised fully and completely about the nature of diabetes mellitus, what they must do to prevent and detect complications, and how to control their condition.23, 62, 67 Patients should be instructed that dietary regulation is the principal consideration in the management of diabetes1, 54, 56 and that acarbose therapy is used only as an adjunct to,1 and not a substitute for, proper dietary regulation.1, 23, 65 Patients also should be advised that they should not neglect dietary restrictions, develop a careless attitude about their condition, or disregard instructions about body-weight control, exercise, hygiene, and avoidance of infection.23
Because of its mechanism of action, acarbose should not cause hypoglycemia when administered alone in the fasted or postprandial state.1 However, hypoglycemia, including hypoglycemic shock, may occur when the drug is used concomitantly with a sulfonylurea antidiabetic agent and/or insulin.1 If hypoglycemia occurs, appropriate adjustments in the dosage of these agents should be made.1 Oral glucose (dextrose), the absorption of which is not inhibited by acarbose, should be used instead of sucrose (table sugar) for the treatment of mild to moderate hypoglycemia in patients receiving acarbose.1 Severe hypoglycemia may require the use of either IV glucose or parenteral glucagon.1
Therapy with acarbose, particularly in dosages exceeding 150 mg daily (50 mg 3 times daily), may be associated with elevations in serum aminotransferase (i.e., ALT [SGPT], AST [SGOT]) concentrations and, in rare instances, hyperbilirubinemia.1, 23 The manufacturer recommends that serum aminotransferase determinations be performed every 3 months during the first year of acarbose therapy and periodically thereafter.1 If elevations in serum aminotransferase concentrations occur, the dosage of acarbose should be reduced; withdrawal of the drug may be necessary, particularly if the elevated serum aminotransferase concentrations persist.1
For additional information on this drug until a more detailed monograph is developed and published, the manufacturer's labeling should be consulted. It is essential that the labeling be consulted for information on the usual cautions, precautions, and contraindications concerning potential drug interactions and/or laboratory test interferences and for information on acute toxicity.
Acarbose is administered orally.1 The drug should be administered at the beginning (with the first bite) of each main meal.1, 23 If the prescribed diet designed to minimize adverse GI effects is not observed, adverse GI effects may be intensified.1 If symptoms 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
Safety and efficacy of acarbose in children younger than 18 years of age have not been established.1, 23
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 glycosylated hemoglobin (hemoglobin A1c [HbA1c]) values to normal or near normal using the lowest effective dosage of acarbose, either when used as monotherapy or in combination with a sulfonylurea antidiabetic agent, metformin, or insulin.1 (Glucose concentrations in plasma generally are 10-15% higher than those in whole blood; glucose concentrations also may vary according to the method and laboratory used for these determinations.) 62, 107 During initiation of therapy and titration of dosage, 1-hour postprandial glucose determinations should be performed to determine therapeutic response and the minimum effective dosage of acarbose; thereafter, glycosylated hemoglobin values should be monitored at intervals of approximately 3 months (the life-span of erythrocytes) to evaluate long-term glycemic control.1, 14, 17, 23 The manufacturer states that monitoring blood glucose concentrations with the 1,5-anhydroglucitol (1,5-AG) assay is not recommended because measurements of 1,5-anhydroglucitol are unreliable in assessing glycemic control in patients taking acarbose; alternative methods of monitoring glycemic control should be used.1
For the management of type 2 diabetes mellitus, the usual initial adult dosage of acarbose is 25 mg given at the beginning (with the first bite) of each main meal.1, 23 However, some patients may benefit from a more gradual dosage titration to reduce adverse GI effects.1, 2, 12, 23, 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 3 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 3 times daily has been reached, the dosage of acarbose may be increased at intervals of 4-8 weeks until the desired 1-hour postprandial glucose concentration (e.g., less than 180 mg/dL) is achieved or a maximum dosage of 50 mg 3 times daily (for patients weighing 60 kg or less) or 100 mg 3 times daily (for patients weighing more than 60 kg) is reached.1, 23, 34, 41 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 (4-8 weeks), although flatulence usually is only abated rather than returned to pretreatment levels.1 If adverse GI effects occur despite adherence to the prescribed diet, a clinician should be consulted, and the dosage of acarbose temporarily or permanently reduced.1 (See Dosage and Administration: Administration.) The usual maintenance dosage of acarbose ranges from 50-100 mg 3 times daily; use of the 50-mg dosage 3 times daily may be associated with fewer adverse effects and has efficacy similar to the 100-mg dosage 3 times daily.1, 6, 47 Since patients with low body weight may be at increased risk for elevated serum aminotransferase concentrations, only patients with body weight exceeding 60 kg should be considered for dosages exceeding 50 mg 3 times daily.1, 23 If no further reduction in postprandial glucose or glycosylated hemoglobin concentrations occurs at the maximum recommended dosage of acarbose (100 mg 3 times daily), consideration should be given to lowering the dosage.1 Dosages of acarbose higher than those recommended by the manufacturer (e.g., 200-300 mg 3 times daily) have been evaluated, but clinically important differences in postprandial plasma glucose and glycosylated hemoglobin concentrations have not been shown consistently; the manufacturer states that acarbose dosages exceeding 100 mg 3 times daily are not recommended since such dosages have been associated with an increased risk of elevated serum aminotransferase concentrations.1, 10, 18, 19, 20, 22, 23, 25, 27, 30, 37, 43 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, 23
Dosage in Renal and Hepatic Impairment
Acarbose is not recommended for use in diabetic patients with 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, 23 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, 23
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 diabetic patients, 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, 23, 24, 30 Acarbose has no inhibitory effect on lactase and would not be expected to produce lactose intolerance.1
In contrast to sulfonylurea antidiabetic agents, acarbose does not enhance insulin secretion.1 Acarbose also does not produce hypoglycemia when given as monotherapy in fasting individuals.1 Therefore, the drug is appropriately referred to as an antihyperglycemic agent rather than a hypoglycemic agent.19, 23, 46 Because the mechanisms of action of acarbose and sulfonylurea antidiabetic agents differ, the effects of these drugs on glycemic control are additive when used in combination; acarbose also reduces the insulinotropic and weight-increasing effects of sulfonylureas.1 However, since acarbose principally delays rather than prevents glucose absorption, the drug produces no clinically important loss of calories and generally does not cause weight loss in either diabetic or nondiabetic individuals.2, 6, 13, 14, 18, 21, 23, 28, 35, 37, 39
Additional Information
SumMon®(see Users Guide). For additional information on this drug until a more detailed monograph is developed and published, the manufacturer's labeling should be consulted. It is essential that the labeling be consulted for detailed information on the usual cautions, precautions, and contraindications.
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 June 21, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
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