Miglitol was orally administered at 40 mg/100 g of high-fat diet containing 45% kcal as fat to 12-week-old rats for 29 days, and age-matched rats without the agent were used as the respective controls

Absorption, Distribution and Excretion
Absorption of miglitol is saturable at high doses with 25 mg being completely absorbed while a 100-mg dose is only 50-70% absorbed. No evidence exists to show that systemic absorption of miglitol adds to its therapeutic effect.
Miglitol is not metabolized in man or in any animal species studied. It is eliminated by renal excretion as an unchanged drug.
0.18 L/kg
Absorption of miglitol is saturable at high doses: a dose of 25 mg is completely absorbed, whereas a dose of 100 mg is only 50% - 70% absorbed. For all doses, peak concentrations are reached in 2-3 hours.
Therapeutic effects principally result from local actions on the small intestine; there is no evidence that systemic absorption contributes to therapeutic response.
The protein binding of miglitol is negligible (<4.0%). Miglitol has a volume of distribution of 0.18 L/kg, consistent with distribution primarily into the extracellular fluid.
Miglitol is distributed principally into extracellular fluid and concentrated in enterocytes of the small intestine.
For more Absorption, Distribution and Excretion (Complete) data for Miglitol (9 total), please visit the HSDB record page.

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Metabolism / Metabolites
Miglitol is not metabolized in man or in any animal species studied.
Miglitol is not metabolized in man or in any animal species studied. No metabolites have been detected in plasma, urine, or feces, indicating a lack of either systemic or pre-systemic metabolism.

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Biological Half-Life
The elimination half-life of miglitol from plasma is approximately 2 hours.
... Miglitol is rapidly eliminated from plasma with apparent elimination half-lives of 0.4-1.8 hr. ... At very low concentration levels a terminal elimination phase of radioactivity characterized by half-lives of 50-110 hr...
The elimination half-life of miglitol from plasma is approximately 2 hours.

Hepatotoxicity
In several large clinical trials, serum aminotransferase elevations were no more common with miglitol than with placebo, and all elevations that occurred were asymptomatic and resolved rapidly with stopping therapy. Neither during these studies nor since approval and wide clinical use have reports of clinically apparent liver injury due to miglitol been published. Thus, liver injury from miglitol must be very rare if it occurs at all. There also have been no reports of patients who developed liver injury while on acarbose being switched to miglitol.
Likelihood score: E (unlikely cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Limited data indicate that miglitol is poorly excreted into breastmilk. Because miglitol is also poorly absorbed orally, it is unlikely to adversely affect the breastfed infant.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
The protein binding of miglitol is negligible (<4.0%).

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Interactions
Several studies investigated the possible interaction between miglitol and glyburide. In six healthy volunteers given a single dose of 5-mg glyburide on a background of 6 days treatment with miglitol (50 mg 3 times daily for 4 days followed by 100 mg 3 times daily for 2 days) or placebo, the mean Cmax and AUC values for glyburide were 17% and 25% lower, respectively, when glyburide was given with miglitol. In a study in diabetic patients in which the effects of adding miglitol 100 mg 3 times daily x 7 days or placebo to a background regimen of 3.5 mg glyburide daily were investigated, the mean AUC value for glyburide was 18% lower in the group treated with miglitol, although this difference was not statistically significant. Further information on a potential interaction with glyburide was obtained from one of the large U.S. clinical trials (Study 7) in which patients were dosed with either miglitol or placebo on a background of glyburide 10 mg twice daily. At the 6-month and 1-year clinic visits, patients taking concomitant miglitol 100 mg 3 times daily exhibited mean Cmax values for glyburide that were 16% and 8% lower, respectively, compared to patients taking glyburide alone. However, these differences were not statistically significant. Thus, although there was a trend toward lower AUC and Cmax values for glyburide when co-administered with miglitol, no definitive statement regarding a potential interaction can be made based on the foregoing three studies.
The effect of miglitol on the pharmacokinetics of a single 1000-mg dose of metformin was investigated in healthy volunteers. Mean AUC and Cmax values for metformin were 12% to 13% lower when the volunteers were given miglitol as compared with placebo, but this difference was not statistically significant.
In a healthy volunteer study, co-administration of miglitol 3 times daily together with digoxin reduced the average plasma concentrations of digoxin by 19% and 28%, respectively. However, in diabetic patients under treatment with digoxin, plasma digoxin concentrations were not altered by co-administration of miglitol ...
Other healthy volunteer studies have demonstrated that miglitol may significantly reduce the bioavailability of ranitidine and propranolol by 60% and 40%, respectively. No effect of miglitol was observed on the pharmacokinetics or pharmacodynamics of nifedipine.
For more Interactions (Complete) data for Miglitol (9 total), please visit the HSDB record page.

Eur J Pharmacol.2009 Dec 10;624(1-3):51-7;Horm Metab Res.2009 Mar;41(3):213-20.

Therapeutic Uses
1-Deoxynojirimycin/*analogs & derivatives; alpha-Glucosidases/antagonists & inhibitors; Enzyme Inhibitors
Reduction in postprandial blood glucose concentrations persists for 3-4 hours following a single dose in healthy individuals.
Miglitol is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus./Included in US product label/

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Drug Warnings
Miglitol is contraindicated in patients with known hypersensitivity to the drug or diabetic ketoacidosis. The drug is also contraindicated in patients with inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or predisposition to this condition, chronic intestinal diseases associated with marked disorders of digestion or absorption, and coexisting conditions that may deteriorate as a result of increased intestinal gas formation.
Miglitol should not cause hypoglycemia when administered alone in the fasting or postprandial state. There is an increased risk of hypoglycemia when miglitol is used concomitantly with insulinor a sulfonylurea antidiabetic agent. If hypoglycemia occurs, dosage of these agents should be adjusted appropriately.
Oral glucose (dextrose) should be used for the treatment of mild to moderate hypoglycemia instead of sucrose (table sugar, a disaccharide); absorption of oral glucose (a monosaccharide) is not delayed by miglitol. Severe hypoglycemia may require the use of either iv glucose infusion or parenteral glucagon.
There is a risk of possible loss of glycemic control in patients receiving miglitol during periods of stress (e.g., fever, trauma, infection, surgery); temporary administration of insulin may be required.
For more Drug Warnings (Complete) data for Miglitol (11 total), please visit the HSDB record page.

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Pharmacodynamics
Miglitol, an oral alpha-glucosidase inhibitor, is a desoxynojirimycin derivative that delays the digestion of ingested carbohydrates, thereby resulting in a smaller rise in blood glucose concentration following meals. As a consequence of plasma glucose reduction, miglitol reduce levels of glycosylated hemoglobin in patients with Type II (non-insulin-dependent) diabetes mellitus. Systemic nonenzymatic protein glycosylation, as reflected by levels of glycosylated hemoglobin, is a function of average blood glucose concentration over time. Because its mechanism of action is different, the effect of miglitol to enhance glycemic control is additive to that of sulfonylureas when used in combination. In addition, miglitol diminishes the insulinotropic and weight-increasing effects of sulfonylureas. Miglitol has minor inhibitory activity against lactase and consequently, at the recommended doses, would not be expected to induce lactose intolerance.

C8H17NO5

207.22

207.11

72432-03-2

Miglitol-d4;2714473-10-4

441314

White to pale-yellow powder
Crystals from ethanol

1.5±0.1 g/cm3

453.7±45.0 °C at 760 mmHg

114ºC

284.3±27.4 °C

0.0±2.5 mmHg at 25°C

1.598

-1.4

5

6

3

14

179

4

O([H])[C@@]1([H])[C@@]([H])([C@]([H])(C([H])([H])N(C([H])([H])C([H])([H])O[H])[C@]1([H])C([H])([H])O[H])O[H])O[H]

IBAQFPQHRJAVAV-ULAWRXDQSA-N

InChI=1S/C8H17NO5/c10-2-1-9-3-6(12)8(14)7(13)5(9)4-11/h5-8,10-14H,1-4H2/t5-,6+,7-,8-/m1/s1

(2R,3R,4R,5S)-1-(2-hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: 100 mg/mL (482.58 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)