Acarbose: The Starch-Blocking Diabetes Drug and Its Trials

Table of Contents

1. A Drug Made by Soil Bacteria That Stays in the Gut
2. How Blocking Two Enzymes Slows Starch and Sugar Digestion
3. What the US Label Covers: Use, Dosing and Blood Sugar Effect
4. Gas, Diarrhea and Abdominal Pain in the Label Trials
5. The Liver-Enzyme Warning on the Label
6. Low Blood Sugar, Table Sugar and Other Medicines
7. STOP-NIDDM: Fewer New Cases of Diabetes
8. The STOP-NIDDM Heart Findings and the Dispute Over Them
9. The ACE Trial: No Heart Benefit, Fewer New Diabetes Cases
10. The Mouse Lifespan Results From the Interventions Testing Program
11. What Is Not Known
12. Key Research Papers
13. Connections
14. Featured Videos

A Drug Made by Soil Bacteria That Stays in the Gut

Acarbose is not built in a chemistry lab from scratch. The US prescribing information describes it as an oligosaccharide — a short chain of sugar-like units — obtained by fermentation of a microorganism, Actinoplanes utahensis. Its shape resembles a small piece of starch closely enough that the body's starch-digesting enzymes grab onto it, but it cannot be cut apart the way real starch can. That is the whole trick: the enzymes get stuck on acarbose instead of working on food.

Because acarbose acts where food is digested, it does not need to reach the blood. The label reports that in a study of six healthy men, less than 2% of an oral dose was absorbed as active drug. The rest stays in the intestine, where it is broken down mainly by gut bacteria and partly by digestive enzymes. The small fraction that does get absorbed is cleared by the kidneys, and the label gives a plasma half-life of acarbose activity of about 2 hours, so the drug does not build up when taken three times a day.

The same enzyme target is shared by two other prescription drugs in this family, miglitol and voglibose, and by a natural compound: 1-deoxynojirimycin from white mulberry leaf. The White Mulberry Leaf page describes that plant compound and the small trials of the leaf with carbohydrate meals.

How Blocking Two Enzymes Slows Starch and Sugar Digestion

Starch from bread, rice, potatoes and grains is a long chain of glucose units. The body cannot absorb a chain; it can only absorb single sugars. Breaking the chain down happens in two steps, and acarbose slows both of them. According to the label's description of the mechanism:

• Step one — pancreatic alpha-amylase. This enzyme, released by the pancreas into the small intestine, cuts long starch chains into shorter pieces called oligosaccharides.
• Step two — the alpha-glucosidases. These enzymes sit on the surface of the cells lining the small intestine (the brush border). They cut the short pieces, and sugars such as sucrose (table sugar), into single sugars like glucose that can be absorbed.

Acarbose blocks both enzymes in a competitive and reversible way: it competes with food for the same spot on the enzyme, and the block wears off as the drug leaves the gut. The label states that in people with diabetes this delays glucose absorption and lowers the blood sugar peak after meals. Because the effect is tied to food in the gut, the label directs that the tablet be taken with the first bite of each main meal.

Three details from the label explain much of how acarbose behaves in practice:

• It does not raise insulin. Unlike the sulfonylurea drugs, acarbose does not increase insulin release. Its effect adds to that of sulfonylureas, insulin or metformin when they are combined, because each works in a different way.
• It leaves milk sugar alone. The label states acarbose has no inhibitory activity against lactase, the enzyme that digests lactose, so it would not be expected to cause lactose intolerance.
• Undigested carbohydrate travels further down. Starch and sugar that are not broken down in the small intestine move on to the large intestine, where gut bacteria ferment them. The label links the drug's common gas and bowel symptoms directly to this undigested carbohydrate. In mice, the same flow of starch to the large intestine changes the gut bacteria and the fatty acids they make (see the mouse section below).

What the US Label Covers: Use, Dosing and Blood Sugar Effect

The current US prescribing information for generic acarbose tablets (revised August 2025, on DailyMed) gives one indication: acarbose is indicated as an add-on to diet and exercise to improve blood sugar control in adults with type 2 diabetes. It is not approved in the United States for preventing diabetes or for any other use. Tablets come in 25 mg, 50 mg and 100 mg strengths.

Dosing as the label describes it

• The label's starting dose is 25 mg three times a day with the first bite of each main meal; it also describes starting at 25 mg once a day and building up, to lessen stomach and bowel side effects.
• The dose is adjusted at 4–8 week intervals according to the one-hour after-meal glucose or glycated hemoglobin (HbA1c) and to tolerance. The usual maintenance range is 50 mg to 100 mg three times a day.
• The maximum is 50 mg three times a day for people weighing 60 kg or less, and 100 mg three times a day above 60 kg. The label ties the lower ceiling to the higher risk of raised liver enzymes in people with low body weight.

How much it lowers blood sugar

The label pools six fixed-dose studies of acarbose alone in people with type 2 diabetes on diet treatment. Compared with placebo, glycated hemoglobin fell by 0.44 percentage points at 25 mg three times a day, 0.77 at 50 mg, 0.74 at 100 mg, 0.86 at 200 mg and 1.00 at 300 mg. The label notes there were no statistically significant differences among doses from 50 to 300 mg three times a day, and the two highest doses are above today's maximum. In four US add-on studies, the placebo-subtracted change in glycated hemoglobin was −0.78 with diet alone, −0.54 on top of maximum sulfonylurea therapy, −0.65 on top of maximum metformin therapy and −0.69 on top of insulin.

An independent Cochrane review of 41 trials with 8,130 participants (30 of the trials tested acarbose) came to a similar picture: compared with placebo, acarbose lowered glycated hemoglobin by 0.8 percentage points, fasting blood glucose by 1.1 mmol/L and post-load blood glucose by 2.3 mmol/L, with no clinically relevant effect on blood fats or body weight. The reviewers found that doses above 50 mg three times a day gave no extra effect on glycated hemoglobin but more side effects, and that it remained unclear whether the drug changes death rates or diabetes complications. For what glycated hemoglobin measures, see the Hemoglobin A1C page.

Who the label excludes

The label lists acarbose as contraindicated in diabetic ketoacidosis, cirrhosis, inflammatory bowel disease, colonic ulceration, partial bowel obstruction or a tendency to bowel obstruction, chronic intestinal diseases with marked problems of digestion or absorption, conditions that could worsen from more gas in the intestine, and known allergy to the drug. Long-term trials were not run in people with a serum creatinine above 2.0 mg/dL, and the label states that treatment of these patients is not recommended. Safety in pregnancy and in children has not been established.

Gas, Diarrhea and Abdominal Pain in the Label Trials

The side effects of acarbose follow directly from how it works. Carbohydrate that is not digested in the small intestine is fermented by bacteria in the large intestine, and fermentation makes gas. The label calls the bowel symptoms “a manifestation of the mechanism of action.”

In US placebo-controlled trials, among 1,255 people taking acarbose at 50–300 mg three times a day and 999 taking placebo, the label reports:

• Flatulence: 74% on acarbose versus 29% on placebo.
• Diarrhea: 31% versus 12%.
• Abdominal pain: 19% versus 9%.

The label states that these effects usually develop during the first few weeks, are mostly mild to moderate, and generally lessen with time. In a one-year study where patients kept symptom diaries, abdominal pain and diarrhea tended to return to pre-treatment levels and flatulence tended to ease. The label also states the symptoms can be stronger when the prescribed diet is not followed — a meal heavy in sugar and starch sends more undigested carbohydrate to the colon.

The trials show the same pattern. In STOP-NIDDM, flatulence and diarrhea were the most frequent side effects, and 31% of people on acarbose stopped treatment early compared with 19% on placebo. In the ACE trial, stomach and bowel disorders were the most common adverse event leading to stopping the drug or changing the dose (7% on acarbose versus 5% on placebo).

Rare bowel reports

From worldwide use after approval, the label lists ileus and subileus (a stalled bowel), and rare reports of pneumatosis cystoides intestinalis — gas-filled cysts in the bowel wall — linked to alpha-glucosidase inhibitors including acarbose. The label describes its symptoms as diarrhea, mucus discharge, rectal bleeding and constipation, and its possible complications as free air in the abdomen, a twisted or blocked bowel, intussusception, bleeding and perforation; it directs that acarbose be stopped and imaging done if this condition is suspected. Other postmarketing reports on the label include skin rashes and hives, swelling (edema) and a low platelet count.

The Liver-Enzyme Warning on the Label

Although very little acarbose enters the blood, the label carries a specific warning about the liver. It is based on two kinds of evidence.

In the US trials

In US studies lasting up to 12 months, including doses up to 300 mg three times a day, rises in the liver enzymes aspartate aminotransferase and alanine aminotransferase were more common on acarbose:

• above the upper limit of normal: 14% on acarbose versus 7% on placebo;
• more than 1.8 times the upper limit: 6% versus 2%;
• more than 3 times the upper limit: 3% versus 1%.

The label describes these rises as without symptoms, reversible, more common in women, dose-related and generally not accompanied by other signs of liver damage. In US studies limited to the current maximum of 100 mg three times a day, liver-enzyme rises at any level were similar on acarbose and placebo.

After approval

In about 3 million patient-years of use worldwide, the label reports 62 cases of liver enzymes above 500 IU/L, 29 of them with jaundice. Forty-one of the 62 people took 100 mg three times a day or more, and 33 of the 45 whose weight was recorded weighed under 60 kg. In 55 of the 59 cases with follow-up, the liver results improved or returned to normal after acarbose was stopped, and in two they were unchanged. The label also reports cases of fulminant hepatitis with a fatal outcome, and states that the relationship to acarbose is unclear.

The label's monitoring schedule is a check of liver enzymes every 3 months during the first year and periodically after that, with a lower dose or stopping the drug as possible responses when enzymes stay raised. This is why the 50 mg ceiling for people of 60 kg or less appears in the dosing section. Background on these blood tests is on the liver function test pages of the Lab Tests section.

Low Blood Sugar, Table Sugar and Other Medicines

Taken alone, acarbose does not cause low blood sugar (hypoglycemia), the label states, either when fasting or after meals; an overdose produces more gas, diarrhea and abdominal discomfort rather than low blood sugar. The picture changes when it is combined with a sulfonylurea or insulin. Those drugs can lower blood sugar on their own, and adding acarbose lowers it further, so the label states it may increase the potential for hypoglycemia. The label notes no increase in hypoglycemia when acarbose was added to metformin.

This creates an unusual practical point. Table sugar (sucrose) has to be split into glucose and fructose before it can be absorbed — and that split is exactly what acarbose slows. The label therefore names oral glucose (dextrose), whose absorption acarbose does not block, rather than sucrose for treating mild to moderate low blood sugar, and states that sucrose is unsuitable for rapid correction. It adds that people taking acarbose together with a sulfonylurea or insulin are to have a source of glucose readily available, and that severe hypoglycemia may need intravenous glucose or a glucagon injection.

Interactions named on the label

• Intestinal adsorbents and digestive enzymes. Charcoal, and enzyme preparations that split carbohydrate (amylase, pancreatin), may reduce the effect of acarbose; the label states they are not to be taken at the same time.
• Digoxin. Acarbose may change how much digoxin is absorbed; the label reports a 26% lower average peak level of digoxin and states that a digoxin dose adjustment may be needed.
• Metformin. Total metformin absorption was unchanged, but its peak level was about 20% lower because absorption was slightly delayed; the label calls this of little if any clinical significance.
• Drugs that raise blood sugar. Thiazide and other diuretics, corticosteroids, thyroid products, estrogens and oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazid can loosen blood sugar control.
• A blood test that stops working. The label states the 1,5-anhydroglucitol test is unreliable for judging blood sugar control in people taking acarbose.

STOP-NIDDM: Fewer New Cases of Diabetes

Impaired glucose tolerance is a stage before type 2 diabetes in which blood sugar climbs too high after a sugar drink but not high enough to count as diabetes (see Prediabetes). Because acarbose targets the after-meal rise, researchers asked whether it could slow the move from impaired glucose tolerance to diabetes. The Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) tested this in hospitals in Canada, Germany, Austria, Norway, Denmark, Sweden, Finland, Israel and Spain.

The trial gave 100 mg of acarbose or placebo three times a day to 1,429 people with impaired glucose tolerance (714 acarbose, 715 placebo), with a yearly glucose tolerance test to detect diabetes. Their average age was 54.5 years and average body mass index 30.9, and they were followed for a mean of 3.3 years. The 2002 report in The Lancet found:

• Diabetes developed in 221 people (32%) on acarbose and 285 (42%) on placebo, a relative hazard of 0.75 — about a quarter lower.
• Acarbose increased the number of people whose glucose tolerance went back to normal.
• At the end of the study, three months on placebo was followed by a rise in the number of people turning diabetic — a sign that the effect depended on continuing the drug.
• Dropping out was common: 211 of 682 people (31%) on acarbose stopped early, compared with 130 of 686 (19%) on placebo.

Sixty-one people (4%) were left out of the analysis because they did not have impaired glucose tolerance or had no data after randomisation. That exclusion later became one of the points of dispute described in the next section.

The STOP-NIDDM Heart Findings and the Dispute Over Them

In 2003 the STOP-NIDDM investigators published a second report in JAMA on heart disease and high blood pressure. They found that people on acarbose had:

• a 49% lower relative risk of cardiovascular events (hazard ratio 0.51, 95% confidence interval 0.28–0.95), which was a 2.5% absolute risk reduction;
• a lower risk of heart attack (hazard ratio 0.09, 95% confidence interval 0.01–0.72);
• a 34% lower relative risk of new high blood pressure (hazard ratio 0.66), a 5.3% absolute risk reduction;
• results that stayed statistically significant after adjusting for major risk factors (hazard ratio 0.47 for cardiovascular events).

A hazard ratio of 0.51 means about half the rate of events. The confidence intervals show how uncertain those numbers are: for heart attack the interval stretches from 0.01 to 0.72, a very wide range. The investigators themselves concluded that the study “suggests” a reduction in risk.

A separate 2004 meta-analysis pooled seven placebo-controlled acarbose trials of at least 52 weeks in people who already had type 2 diabetes (1,248 on acarbose, 932 on placebo). It reported a lower risk of heart attack (hazard ratio 0.36) and of any cardiovascular event (hazard ratio 0.65) on acarbose.

The critique

In 2004 two researchers from Cologne, Thomas Kaiser and Peter Sawicki, published a critical analysis of everything published about STOP-NIDDM. They reported “several serious flaws” — selection bias, inadequate blinding, bias in data analysis and reporting, and potential sponsoring bias — and concluded that the validity of the results was seriously flawed and that the clinical benefit of acarbose and of lowering after-meal blood sugar was unproven.

The investigators' reply

The STOP-NIDDM investigators answered in the same journal. They stated that the 61 people left out were excluded before unblinding for two reasons — 17 did not meet major entry criteria and 44 had no data after randomisation — and that blinding and randomisation were handled by an independent biostatistician. They reported that 9.3% of participants had a fasting glucose of 7.0 mmol/L or more at screening and might have counted as diabetic under newer criteria, but that removing them still left a significant reduction in diabetes (p=0.0027), and that the effect also held after adjusting for weight change. They stated that the cardiovascular endpoints were set in the original protocol and judged by an independent adjudication committee, and that they stood behind the results. Sawicki and Kaiser published a further response in the same issue.

The disagreement was not settled by argument. It was put to a direct test a decade later in a much larger trial built to measure heart outcomes as its main question: the ACE trial.

The ACE Trial: No Heart Benefit, Fewer New Diabetes Cases

The Acarbose Cardiovascular Evaluation (ACE) trial was a randomised, double-blind, placebo-controlled trial run in 176 hospital outpatient clinics in China and funded by the drug's original manufacturer. Between 2009 and 2015 it enrolled 6,522 Chinese patients who had both established coronary heart disease and impaired glucose tolerance — more than four times the size of STOP-NIDDM. The trial gave acarbose 50 mg three times a day or placebo, on top of standard heart-disease treatment, and followed people for a median of 5.0 years.

The main question was a five-part combined outcome: death from cardiovascular causes, non-fatal heart attack, non-fatal stroke, hospital admission for unstable angina and hospital admission for heart failure. The 2017 report in The Lancet Diabetes & Endocrinology found:

• No difference in heart outcomes. The combined outcome occurred in 470 people (14%) on acarbose and 479 (15%) on placebo, a hazard ratio of 0.98 (95% confidence interval 0.86–1.11).
• No difference in any of the secondary heart or death outcomes — including the three-part outcome of cardiovascular death, heart attack and stroke, death from any cause, cardiovascular death, heart attack, stroke, unstable angina, heart failure admissions and impaired kidney function.
• Fewer new cases of diabetes. Diabetes developed in 436 people (13%) on acarbose and 513 (16%) on placebo, a rate ratio of 0.82.
• Bowel side effects led to more changes. Stomach and bowel disorders were the most common adverse event behind stopping or changing the dose: 215 (7%) on acarbose versus 150 (5%) on placebo.
• Deaths from non-cardiovascular causes and from cancer did not differ between the groups.

The authors' conclusion was that in Chinese patients with coronary heart disease and impaired glucose tolerance, acarbose did not reduce the risk of major cardiovascular events but did reduce the incidence of diabetes. The diabetes result matched the direction of STOP-NIDDM; the heart result did not. The current US label states that there have been no clinical studies establishing conclusive evidence of large-blood-vessel (macrovascular) risk reduction with acarbose or any other diabetes drug. For a broader view of the condition, see Type 2 Diabetes.

The Mouse Lifespan Results From the Interventions Testing Program

Everything in this section was found in mice, not people.

The National Institute on Aging (NIA) Interventions Testing Program tests compounds for lifespan effects in genetically mixed mice. Each compound is tested in parallel at three sites, and all results are published, including the failures. Acarbose has now been tested there several times.

Harrison 2014: the first result

In the 2014 report in Aging Cell, acarbose increased median lifespan by 22% in male mice but by only 5% in female mice. Maximum lifespan (measured as the age at the 90th percentile) rose 11% in males and 9% in females. The difference between the sexes could not be explained by differences in effects on weight. In the same report, 17-alpha-estradiol and nordihydroguaiaretic acid extended male median lifespan, and methylene blue did not change median lifespan.

Strong 2016: a repeat, and a late start

The program's 2016 report tested acarbose again at the original concentration of 1,000 parts per million in the diet. In mice, it again significantly increased median lifespan in males and 90th-percentile lifespan in both sexes, even when treatment was started at 16 months of age — middle age for a mouse. The same report found that metformin alone, at 0.1% of the diet, did not significantly extend mouse lifespan.

Harrison 2019: three doses and health measures

A 2019 study compared 400, 1,000 and 2,500 parts per million in mice. Each dose changed survival significantly in both sexes, with larger effects in males, and the three doses did not differ from each other. The two higher doses raised male median lifespan by 16% and 17%, but female median lifespan by only 4% and 5%. Age at the 90th percentile rose 8–11% in males at each dose, and 3% in females only at 1,000 ppm. Acarbose cut weight and fat more in female mice than in males, so weight loss did not explain the sex difference. At 1,000 ppm, the treated mice had fewer lung tumors (males), less liver degeneration (both sexes), less kidney scarring called glomerulosclerosis (females), smaller blood sugar responses to refeeding (males) and better balance on a rotating rod (older females).

Smith 2019: the gut bacteria

Because acarbose sends more starch to the lower gut, researchers compared the droppings of treated and untreated mice from all three sites. In mice on acarbose, one group of bacteria (the family Muribaculaceae) bloomed at every site, and the short-chain fatty acid propionate was consistently higher. Levels of acetate, butyrate and propionate together predicted how long the mice lived. The authors described this as a correlation that suggests a role for the gut bacteria and called for studies testing whether the fatty acids actually cause the longer life.

No trial has tested whether acarbose lengthens human life. In these studies the drug was mixed into the mouse diet at fixed concentrations, which is not how the tablet is taken by people.

What Is Not Known

• Whether acarbose prevents heart attacks or strokes. STOP-NIDDM and a pooled analysis reported fewer cardiovascular events; the larger ACE trial, designed with heart outcomes as its main question, found none. Whether the difference reflects the people studied (ACE enrolled only Chinese patients who already had coronary heart disease), the dose (ACE gave 50 mg three times a day, STOP-NIDDM 100 mg) or chance in a small number of events is not settled by either trial.
• Whether delaying diabetes changes long-term health. Both trials found fewer new diabetes diagnoses, but STOP-NIDDM saw new cases rise again within three months of stopping the drug. Neither trial showed fewer deaths.
• Whether the mouse lifespan effect applies to people. There are no human lifespan data. Why the effect is so much larger in male mice is also unexplained.
• How much of the mouse effect comes from gut bacteria. The link between short-chain fatty acids and lifespan in mice is a correlation, not a tested cause.
• Long-term effects on diabetes complications and death. The Cochrane review found too few data on mortality, complications and quality of life to say whether alpha-glucosidase inhibitors change them, and most trials lasted about 24 weeks.
• Who is most at risk of the liver reaction. The label links serious liver-enzyme rises to higher doses and low body weight, but most mild rises cause no symptoms, and the cause of the rare fatal hepatitis cases is unclear.

Decisions about diabetes medicines belong with a clinician who knows the person's full medical history and other drugs.

Key Research Papers

1. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M; STOP-NIDDM Trail Research Group. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. Lancet. 2002;359(9323):2072-7. PubMed PMID: 12086760
2. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M; STOP-NIDDM Trial Research Group. Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM trial. JAMA. 2003;290(4):486-94. PubMed PMID: 12876091
3. Kaiser T, Sawicki PT. Acarbose for prevention of diabetes, hypertension and cardiovascular events? A critical analysis of the STOP-NIDDM data. Diabetologia. 2004;47(3):575-580. PubMed PMID: 14727025
4. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M; STOP-NIDDM Trial Research Group. Acarbose for the prevention of Type 2 diabetes, hypertension and cardiovascular disease in subjects with impaired glucose tolerance: facts and interpretations concerning the critical analysis of the STOP-NIDDM Trial data. Diabetologia. 2004;47(6):969-75; discussion 976-7. PubMed PMID: 15164169
5. Sawicki PT, Kaiser T. Response to Chiasson et al.: Acarbose for the prevention of Type 2 diabetes, hypertension and cardiovascular disease in subjects with impaired glucose tolerance: facts and interpretations concerning the critical analysis of the STOP-NIDDM Trial data. Diabetologia. 2004;47(6):976-7. PubMed PMID: 15150689
6. Hanefeld M, Cagatay M, Petrowitsch T, Neuser D, Petzinna D, Rupp M. Acarbose reduces the risk for myocardial infarction in type 2 diabetic patients: meta-analysis of seven long-term studies. Eur Heart J. 2004;25(1):10-6. PubMed PMID: 14683737
7. Holman RR, Coleman RL, Chan JCN, Chiasson JL, Feng H, Ge J, Gerstein HC, Gray R, Huo Y, Lang Z, McMurray JJ, Rydén L, Schröder S, Sun Y, Theodorakis MJ, Tendera M, Tucker L, Tuomilehto J, Wei Y, Yang W, Wang D, Hu D, Pan C; ACE Study Group. Effects of acarbose on cardiovascular and diabetes outcomes in patients with coronary heart disease and impaired glucose tolerance (ACE): a randomised, double-blind, placebo-controlled trial. Lancet Diabetes Endocrinol. 2017;5(11):877-886. PubMed PMID: 28917545
8. Van de Laar FA, Lucassen PL, Akkermans RP, Van de Lisdonk EH, Rutten GE, Van Weel C. Alpha-glucosidase inhibitors for type 2 diabetes mellitus. Cochrane Database Syst Rev. 2005;2005(2):CD003639. PubMed PMID: 15846673
9. Harrison DE, Strong R, Allison DB, Ames BN, Astle CM, Atamna H, Fernandez E, Flurkey K, Javors MA, Nadon NL, Nelson JF, Pletcher S, Simpkins JW, Smith D, Wilkinson JE, Miller RA. Acarbose, 17-α-estradiol, and nordihydroguaiaretic acid extend mouse lifespan preferentially in males. Aging Cell. 2014;13(2):273-82. PubMed PMID: 24245565
10. Strong R, Miller RA, Antebi A, Astle CM, Bogue M, Denzel MS, Fernandez E, Flurkey K, Hamilton KL, Lamming DW, Javors MA, de Magalhães JP, Martinez PA, McCord JM, Miller BF, Müller M, Nelson JF, Ndukum J, Rainger GE, Richardson A, Sabatini DM, Salmon AB, Simpkins JW, Steegenga WT, Nadon NL, Harrison DE. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an α-glucosidase inhibitor or a Nrf2-inducer. Aging Cell. 2016;15(5):872-84. PubMed PMID: 27312235
11. Harrison DE, Strong R, Alavez S, Astle CM, DiGiovanni J, Fernandez E, Flurkey K, Garratt M, Gelfond JAL, Javors MA, Levi M, Lithgow GJ, Macchiarini F, Nelson JF, Sukoff Rizzo SJ, Slaga TJ, Stearns T, Wilkinson JE, Miller RA. Acarbose improves health and lifespan in aging HET3 mice. Aging Cell. 2019;18(2):e12898. PubMed PMID: 30688027
12. Smith BJ, Miller RA, Ericsson AC, Harrison DC, Strong R, Schmidt TM. Changes in the gut microbiome and fermentation products concurrent with enhanced longevity in acarbose-treated mice. BMC Microbiol. 2019;19(1):130. PubMed PMID: 31195972

Label figures on this page come from the current US prescribing information for generic acarbose tablets (revised August 2025), available on DailyMed.

PubMed Topic Searches

1. PubMed: acarbose and impaired glucose tolerance trials
2. PubMed: acarbose and cardiovascular outcomes
3. PubMed: acarbose and lifespan in mice
4. PubMed: acarbose and the gut microbiome
5. PubMed: acarbose and liver injury

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Connections

• Drugs — every drug page on the site
• Caloric Restriction and Mimetics — acarbose beside rapamycin, metformin and SGLT2 inhibitors
• White Mulberry Leaf — a plant compound that blocks the same enzyme
• Metformin — the first-line diabetes drug acarbose is often combined with
• Rapamycin — another drug tested by the Interventions Testing Program
• Type 2 Diabetes — the condition on the label
• Prediabetes — the stage studied in STOP-NIDDM and ACE
• Hemoglobin A1C — the blood test used to measure its effect

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