Version May 2024
Note: Dosage must be individualized on the basis of effectiveness and tolerance.
Diabetes mellitus, type 2: Limited data available: Note: Alpha glucosidase inhibitors could be considered an additional therapeutic option in pediatric patients with type 2 diabetes mellitus who are ≥3 months post diagnosis and if target HbA1c <7% not attained while on metformin therapy (maximized) in addition to a healthy lifestyle (eg, diet and exercise) with or without insulin. However, due to limited data and adverse effects, use of acarbose is limited to those who cannot tolerate other therapies; based on mechanism of action, acarbose will be more effective in those in whom carbohydrates make up a large part of the diet (Ref).
Children ≥10 years and Adolescents: Oral: Initial dose: 25 mg 3 times daily with the first bite of each main meal; may also initiate at 25 mg once daily with gradual titration to 25 mg 3 times daily as tolerated; then increase in 25 mg/dose increments in 2- to 4-week intervals as tolerated (Ref). Weight-based maximum dose: ≤60 kg: 50 mg/dose, >60 kg: 100 mg/dose. Clinical trials in pediatric patients are lacking; dosing based on expert-reported clinical experience; overall dosing is similar to that used in adult patients (Ref).
Dumping syndrome (reactive hypoglycemia) after Nissen fundoplication: Limited data available:
Infants ≥4 months and young children who have failed nutritional manipulations: Oral: Initial dose: 12.5 to 25 mg before each bolus feeding of formula containing complex carbohydrates. Increase in 12.5 to 25 mg/dose increments until postprandial serum glucose stable (>60 mg/dL was used in clinical reports). Reported dose range: 12.5 to 100 mg/dose. Dosing based on a few small studies (total n=11). Acarbose was well tolerated in most patients, except for a few patients who experienced flatulence (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
(For additional information see "Acarbose: Drug information")
Diabetes mellitus, type 2, treatment: Note: Dosage must be individualized on the basis of effectiveness and tolerance.
Oral: Initial: 25 mg 3 times daily with the first bite of each main meal (may also initiate at 25 mg once daily with gradual titration to 25 mg 3 times daily as tolerated); increase dose at 4- to 8-week intervals based on 1-hour postprandial glucose or HbA1c levels and tolerance until maintenance dose of 50 to 100 mg 3 times daily is reached (maximum dose: ≤60 kg: 50 mg 3 times daily; >60 kg: 100 mg 3 times daily).
Postprandial hyperinsulinemic hypoglycemia after gastric bypass surgery (off label): Oral: 25 to 100 mg 3 times daily just prior to the start of each meal, or if more frequent meals may consider 25 to 50 mg up to 6 times daily. Administer in conjunction with dietary modifications aimed at reducing the glycemic index of each meal (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Serum creatinine ≤2 mg/dL or CrCl ≥25 mL/ minute/1.73 m2: There are no dosage adjustments provided in the manufacturer’s labeling.
Serum creatinine >2 mg/dL or CrCl <25 ml/minute/1.73 m2: Use is not recommended; systemic AUC increased 6-fold in patients with CrCl <25 mL/ minute/1.73 m2.
There are no dosage adjustments provided in the manufacturer's labeling; contraindicated in patients with cirrhosis.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
>10%: Gastrointestinal: Frequency and intensity of flatulence (74%) tend to abate with time; diarrhea (31%) and abdominal pain (19%) tend to return to pretreatment levels over time
1% to 10%: Hepatic: Increased serum transaminases (≤4%)
<1%, postmarketing, and/or case reports: Edema, erythema, hepatic injury, hepatitis, intestinal obstruction, jaundice, pneumatosis cystoides intestinalis, skin rash, thrombocytopenia, urticaria
Hypersensitivity to acarbose or any component of the formulation; diabetic ketoacidosis; cirrhosis; inflammatory bowel disease, colonic ulceration, partial intestinal obstruction, patients predisposed to intestinal obstruction; chronic intestinal diseases associated with marked disorders of digestion or absorption; conditions that may deteriorate as a result of increased gas formation in the intestine
Concerns related to adverse effects:
• Elevated serum transaminases: Treatment-emergent elevations of serum transaminases (AST and/or ALT) and hyperbilirubinemia may occur (dose-related). These elevations were asymptomatic, reversible, more common in females, and, in general, were not associated with other evidence of liver dysfunction. Fulminant hepatitis (may be fatal) has been reported. If elevations are observed, a reduction in dosage or withdrawal of therapy may be indicated, particularly if the elevations persist.
• Hypoglycemia: Hypoglycemia is unlikely to occur with acarbose monotherapy but may occur with combination therapy (eg, sulfonylureas, insulin, metformin). In patients taking acarbose, oral glucose (dextrose) should be used instead of sucrose (cane sugar) in the treatment of mild-to-moderate hypoglycemia since the hydrolysis of sucrose to glucose and fructose is inhibited by acarbose.
Disease-related concerns:
• Hepatic impairment: Use with caution in patients with hepatic impairment.
• Renal impairment: Not recommended in patients with significant impairment (serum creatinine >2 mg/dL or CrCl <25 mL/minute/1.73 m2).
• Stress-related states: It may be necessary to discontinue acarbose and administer insulin if the patient is exposed to stress (ie, fever, trauma, infection, surgery).
Other warnings/precautions:
• Appropriate use: Diet: Increased intake of sucrose (cane sugar) and food that contains sucrose during treatment can lead to GI symptoms (eg, flatulence and bloating), loose stools, and occasionally diarrhea. If a diabetic diet is not followed, the GI side effects may be intensified. If severe symptoms develop in spite of adherence to a diabetic diet, temporarily or permanently reduce dose.
• Patient education: Diabetes self-management education (DSME) is essential to maximize the effectiveness of therapy.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
Precose: 25 mg [DSC], 50 mg [DSC], 100 mg [DSC]
Generic: 25 mg, 50 mg, 100 mg
Yes
Tablets (Acarbose Oral)
25 mg (per each): $0.90 - $0.91
50 mg (per each): $0.97 - $0.98
100 mg (per each): $1.16 - $1.17
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
Glucobay: 50 mg [DSC], 100 mg [DSC] [contains corn starch]
Generic: 50 mg, 100 mg
Oral: Administer with first bite of each main meal.
Oral: Administer with the first bite of each main meal.
Store at <25°C (77°F). Protect from moisture.
Management of type 2 diabetes mellitus (noninsulin-dependent) when hyperglycemia cannot be managed by diet and exercise alone (FDA approved in adults); has also been used for prevention of reactive hypoglycemia caused by dumping syndrome after Nissen fundoplication.
Precose may be confused with PreCare
Precose [US, Malaysia] may be confused with Precosa brand name for Saccharomyces boulardii [Finland, Sweden]
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Alpha-Lipoic Acid: May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Androgens: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Beta-Blockers (Beta1 Selective): May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Beta-Blockers (Nonselective): May enhance the hypoglycemic effect of Antidiabetic Agents. Beta-Blockers (Nonselective) may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Bortezomib: May enhance the therapeutic effect of Antidiabetic Agents. Bortezomib may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Digoxin: Acarbose may decrease the serum concentration of Digoxin. Risk C: Monitor therapy
Direct Acting Antiviral Agents (HCV): May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Etilefrine: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Guanethidine: May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Hyperglycemia-Associated Agents: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Hypoglycemia-Associated Agents: Antidiabetic Agents may enhance the hypoglycemic effect of Hypoglycemia-Associated Agents. Risk C: Monitor therapy
Insulins: Alpha-Glucosidase Inhibitors may enhance the hypoglycemic effect of Insulins. Management: Consider a decrease in insulin dose when initiating therapy with an alpha-glucosidase inhibitor and monitor patients for hypoglycemia. Risk D: Consider therapy modification
Maitake: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Monoamine Oxidase Inhibitors: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Neomycin (Systemic): May enhance the adverse/toxic effect of Acarbose. Neomycin (Systemic) may decrease the metabolism of Acarbose. Risk C: Monitor therapy
Pegvisomant: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Prothionamide: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Quinolones: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Quinolones may diminish the therapeutic effect of Agents with Blood Glucose Lowering Effects. Specifically, if an agent is being used to treat diabetes, loss of blood sugar control may occur with quinolone use. Risk C: Monitor therapy
Ritodrine: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Salicylates: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Selective Serotonin Reuptake Inhibitors: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Sulfonylureas: Alpha-Glucosidase Inhibitors may enhance the hypoglycemic effect of Sulfonylureas. Management: Consider a decrease in sulfonylurea dose when initiating therapy with an alpha-glucosidase inhibitor and monitor patients for hypoglycemia. Risk D: Consider therapy modification
Thiazide and Thiazide-Like Diuretics: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Information related to the use of acarbose in pregnancy is limited (Bertini 2005; Narayanan 2016). Less than 2% of an oral dose of acarbose is absorbed systemically, which should limit fetal exposure.
Poorly controlled diabetes during pregnancy can be associated with an increased risk of adverse maternal and fetal outcomes, including diabetic ketoacidosis, preeclampsia, spontaneous abortion, preterm delivery, delivery complications, major malformations, stillbirth, and macrosomia (ACOG 201 2018). To prevent adverse outcomes, prior to conception and throughout pregnancy, maternal blood glucose and HbA1c should be kept as close to target goals as possible but without causing significant hypoglycemia (ADA 2023; Blumer 2013).
Agents other than acarbose are currently recommended to treat diabetes mellitus in pregnancy (ADA 2023).
Fasting blood glucose; postprandial glucose, serum creatinine, HbA1c (at least twice yearly in patients who have stable glycemic control and are meeting treatment goals; quarterly in patients not meeting treatment goals or with therapy change [ADA 2022]); liver enzymes every 3 months for the first year of therapy and periodically thereafter.
Plasma blood glucose and HbA1c goals for patients with diabetes: Note: Postprandial blood glucose should be measured when there is a discrepancy between preprandial blood glucose concentrations and HbA1c values and to help assess glycemia for patients who receive basal/bolus or pump regimens. It is usually drawn 1 to 2 hours after starting a meal and is considered to be the "peak."
Children and Adolescents:
Blood glucose:
Type 2 diabetes:
Fasting plasma glucose: 70 to 110 mg/dL (SI: 3.9 to 6.1 mmol/L) (ISPAD [Shah 2022]).
Postprandial glucose: 70 to 140 mg/dL (SI: 3.9 to 7.8 mmol/L) (ISPAD [Shah 2022]).
HbA1c: <7%; target should be individualized; a more stringent goal (<6.5%) may be reasonable if it can be achieved without significant hypoglycemia; lower targets may also be recommended when using insulin pumps and/or continuous glucose monitoring and during the "honeymoon" phase; less aggressive goals (<7.5% or <8%) may be appropriate in patients who cannot articulate symptoms of hypoglycemia, cannot check glucose frequently, have a history of severe hypoglycemia, have extensive comorbid conditions, or lack access to analog insulins, advanced insulin delivery technology, or continuous glucose monitoring (ADA 2023; ISPAD [de Bock 2022]).
Competitive inhibitor of pancreatic α-amylase and intestinal brush border α-glucosidases, resulting in delayed hydrolysis of ingested complex carbohydrates and disaccharides and absorption of glucose; dose-dependent reduction in postprandial serum insulin and glucose peaks; inhibits the metabolism of sucrose to glucose and fructose
Absorption: <2% as active drug; ~35% as metabolites
Metabolism: Exclusively via GI tract, principally by intestinal bacteria and digestive enzymes; 13 metabolites identified (major metabolites are sulfate, methyl, and glucuronide conjugates)
Bioavailability: Low systemic bioavailability of parent compound; acts locally in GI tract
Half-life elimination: ~2 hours
Time to peak: Active drug: ~1 hour
Excretion: Urine (~34% as inactive metabolites, <2% parent drug and active metabolite); feces (~51% as unabsorbed drug)
Altered kidney function: In patients with CrCl <25 mL/minute/1.73 m2, the Cmax was ~5 times higher, and the AUC was 6 times larger.
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