(For additional information see “Acarbose: Patient drug information” and see “Acarbose: Pediatric drug information”)
- Antidiabetic Agent, Alpha-Glucosidase Inhibitor
Initial: 25 mg 3 times/day with the first bite of each main meal; to reduce GI effects, some patients may benefit from initiating at 25 mg once daily with gradual titration to 25 mg 3 times/day as tolerated
Maintenance dose: Should be adjusted at 4- to 8-week intervals based on 1-hour postprandial glucose levels and tolerance until maintenance dose is reached; maintenance dose: 50-100 mg 3 times/day. Dosage must be individualized on the basis of effectiveness and tolerance while not exceeding the maximum recommended dose.
≤60 kg: 50 mg 3 times/day
>60 kg: 100 mg 3 times/day
Patients receiving sulfonylureas or insulin: Acarbose given in combination with a sulfonylurea or insulin will cause a further lowering of blood glucose and may increase the hypoglycemic potential of the sulfonylurea or insulin. If hypoglycemia occurs, appropriate adjustments in the dosage of these agents should be made.
Significant renal dysfunction (Scr >2 mg/dL): Use is not recommended.
Tablet, oral: 25 mg, 50 mg, 100 mg
Precose®: 25 mg, 50 mg, 100 mg
Precose® may be confused with PreCare®
Precose® [U.S., Malaysia] may be confused with Precosa brand name for Saccharomyces boulardii [Finland, Sweden]
Gastrointestinal: Diarrhea (31%) and abdominal pain (19%) tend to return to pretreatment levels over time; frequency and intensity of flatulence (74%) tend to abate with time
Hepatic: Transaminases increased (≤4%)
Postmarketing and/or case reports: Edema, erythema, exanthema, hepatitis, ileus/subileus, jaundice, liver damage, pneumatosis cystoides intestinalis, rash, thrombocytopenia, urticaria
• Elevated serum transaminases: Treatment-emergent elevations of serum transaminases (AST and/or ALT) occurred in up to 14% of acarbose-treated patients in long-term studies. These serum transaminase elevations appear to be dose related. At doses >100 mg 3 times/day, the incidence of serum transaminase elevations greater than 3 times the upper limit of normal was 2-3 times higher in the acarbose group than in the placebo group. These elevations were asymptomatic, reversible, more common in females, and, in general, were not associated with other evidence of liver dysfunction. Fulminant hepatitis has been reported rarely.
• Renal impairment: Use not recommended in patients with significant impairment (Scr >2 mg/dL); use with caution in other patients with renal impairment.
• 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).
Concurrent drug therapy issues:
• Sulfonylureas/insulin: In combination with a sulfonylurea or insulin will cause a further lowering of blood glucose and may increase the hypoglycemic potential of the sulfonylurea or insulin.
Corticosteroids (Orally Inhaled): May diminish the hypoglycemic effect of Antidiabetic Agents. In some instances, corticosteroid-mediated HPA axis suppression has led to episodes of acute adrenal crisis, which may manifest as enhanced hypoglycemia, particularly in the setting of insulin or other antidiabetic agent use. Risk C: Monitor therapy
Corticosteroids (Systemic): May diminish the hypoglycemic effect of Antidiabetic Agents. In some instances, corticosteroid-mediated HPA axis suppression has led to episodes of acute adrenal crisis, which may manifest as enhanced hypoglycemia, particularly in the setting of insulin or other antidiabetic agent use. Risk C: Monitor therapy
Digoxin: Acarbose may decrease the serum concentration of Digoxin. Risk C: Monitor therapy
Herbs (Hypoglycemic Properties): May enhance the hypoglycemic effect of Hypoglycemic Agents. Risk C: Monitor therapy
Hypoglycemic Agents: May enhance the adverse/toxic effect of other Hypoglycemic Agents. Risk C: Monitor therapy
Luteinizing Hormone-Releasing Hormone Analogs: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Neomycin: May enhance the adverse/toxic effect of Acarbose. Neomycin may enhance the therapeutic effect of Acarbose. Neomycin may decrease the metabolism of Acarbose. Risk C: Monitor therapy
Pegvisomant: May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Somatropin: May diminish the hypoglycemic effect of Antidiabetic Agents. Risk D: Consider therapy modification
Thiazide Diuretics: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
25 mg (100): $81.99
50 mg (100): $87.99
100 mg (100): $89.99
25 mg (90): $85.51
50 mg (90): $88.49
100 mg (90): $109.99
Hb A1c: <7%
Preprandial capillary plasma glucose: 70-130 mg/dL
Peak postprandial capillary blood glucose: <180 mg/dL
- Accarb (NZ);
- Acrose (IL);
- Decarbay (TW);
- Deglu (TW);
- Dibose (MY);
- Eclid (ID);
- Garbose (MY);
- Glibos (TW);
- Glicobase (IT);
- Glucobay (AE, AR, AT, AU, BB, BD, BE, BF, BG, BH, BJ, BM, BR, BS, BZ, CH, CI, CL, CN, CO, CR, CY, CZ, DE, DK, DO, EC, EG, ES, ET, FI, GB, GH, GM, GN, GT, GY, HK, HN, HR, HU, IE, IN, IQ, IR, IT, JM, JO, JP, KE, KP, KW, LB, LR, LU, LY, MA, ML, MR, MU, MW, MX, MY, NE, NG, NI, NL, NO, OM, PA, PE, PK, PL, PT, PY, QA, RU, SA, SC, SD, SE, SG, SL, SN, SR, SV, SY, TH, TN, TR, TT, TZ, UG, UY, VE, YE, ZA, ZM, ZW);
- Gluconase (PH);
- Glucor (FR);
- Glucorid (MY);
- Glumida (ES);
- Incardel (MX);
- Kertonbose (TW);
- Prandase (IL);
- Precose (MY);
- Rebose (IN);
- Sincrosa (MX);
- Tardensone (TW)
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)
American Diabetes Association, “Standards of Medical Care in Diabetes Mellitus — 2011,” Diabetes Care, 2011, 34(Suppl 1):11-61. [PubMed 21193625]
Balfour JA and McTavish D, “Acarbose: A Reappraisal,” Drugs, 1993, 46(6):1025-54. [PubMed 7510610]
Bischoff H, “Pharmacology of α-Glucosidase Inhibition,” Eur J Clin Invest, 1994, 24(Suppl 3):3-10.
Handelsman Y, Mechanick JI, Blonde L, et al, “American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for Developing a Diabetes Mellitus Comprehensive Care Plan,” Endocr Pract, 2011, 17(Suppl 2):1-53. [PubMed 21474420]
Rodbard HW, Jellinger PS, Davidson JA, et al, “Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology Consensus Panel on Type 2 Diabetes Mellitus: An Algorithm for Glycemic Control,” Endocr Pract, 2009, 15(6):540-59. [PubMed 19858063]
Scheen AJ, de Magalhaes AC, Salvatore T, et al, “Reduction of the Acute Bioavailability of Metformin by the α-Glucosidase Inhibitor Acarbose in Normal Man,” Eur J Clin Invest, 1994, 24(Suppl 3):50-4.