Miglitol

Products

We are here to help in anything you need. Please use our online system or send an email to .

Miglitol

Inquiry

Catalog Number	PR72432032
CAS	72432-03-2
Structure
Description	Miglitol inhibits the breakdown complex carbohydrates into glucose. It is primarily used in diabetes mellitus type 2 for establishing greater glycemic control by preventing the digestion of carbohydrates (such as disaccharides, oligosaccharides, and polysaccharides) into monosaccharides which can be absorbed by the body.
Synonyms	Glyset; (2R,3R,4R,5S)-1-(2-hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol
IUPAC Name	(2R,3R,4R,5S)-1-(2-hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol
Molecular Weight	207.22
Molecular Formula	C8H17NO5
InChI	IBAQFPQHRJAVAV-ULAWRXDQSA-N
InChI Key	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
Drug Categories	Alimentary Tract and Metabolism; Alkaloids; Blood Glucose Lowering Agents; Carbohydrates; Drugs Used in Diabetes; Enzyme Inhibitors; Glycoside Hydrolase Inhibitors; Hypoglycemia-Associated Agents; Imines; Imino Pyranoses; Imino Sugars; Oral Hypoglycemics; Piperidines
Drug Interactions	Acarbose-The risk or severity of hypoglycemia can be increased when Acarbose is combined with Miglitol. Acebutolol-The therapeutic efficacy of Miglitol can be increased when used in combination with Acebutolol. Acetazolamide-The therapeutic efficacy of Miglitol can be increased when used in combination with Acetazolamide. Acetohexamide-The risk or severity of hypoglycemia can be increased when Miglitol is combined with Acetohexamide. Acetyl sulfisoxazole-The therapeutic efficacy of Miglitol can be increased when used in combination with Acetyl sulfisoxazole.
Half-Life	The elimination half-life of miglitol from plasma is approximately 2 hours.
Isomeric SMILES	C1[C@@H]([C@H]([C@@H]([C@H](N1CCO)CO)O)O)O
Standard	JP
Type	Small Molecule
Therapeutic Category	Antidiabetics

Pharmacology

Indications

Miglitol is indicated for use as an adjunct to diet in order to improve glycemic control in patients diagnosed with non-insulin-dependent diabetes mellitus (NIDDM). It is specifically prescribed for individuals whose hyperglycemia cannot be adequately managed through dietary modifications alone.

Pharmacodynamics

Miglitol functions as an oral alpha-glucosidase inhibitor and is derived from desoxynojirimycin. Its primary mechanism involves delaying the digestion of carbohydrates consumed, which leads to a reduced rise in blood glucose levels post-meal. This reduction in plasma glucose consequently decreases the levels of glycosylated hemoglobin in patients with Type II diabetes mellitus. Glycosylated hemoglobin levels serve as an indicator of average blood glucose concentration over time. When combined with sulfonylureas, miglitol offers an additive effect on glycemic control due to its distinct mechanism of action. Additionally, it mitigates the insulinotropic and weight-gaining effects associated with sulfonylureas. At recommended dosages, miglitol exhibits minimal inhibitory activity against lactase, and therefore, it is not expected to cause lactose intolerance.

Absorption

Miglitol exhibits saturable absorption at elevated doses. A 25 mg dose of miglitol is completely absorbed, whereas when the dose is increased to 100 mg, absorption efficiency ranges from 50% to 70%. Importantly, there is no evidence to suggest that systemic absorption of the drug contributes to its therapeutic efficacy.

Metabolism

Miglitol is not metabolized in humans or any animal species that have been studied. Its pharmacological activity is independent of metabolic conversion.

Mechanism of Action

Miglitol operates through a distinct mechanism that sets it apart from sulfonylureas, as it does not stimulate insulin secretion. Instead, miglitol exerts its antihyperglycemic effects by reversibly inhibiting the membrane-bound intestinal alpha-glucoside hydrolase enzymes. These enzymes are responsible for breaking down oligosaccharides and disaccharides into glucose and other monosaccharides within the brush border of the small intestine. In individuals with diabetes, this enzyme inhibition leads to a delay in glucose absorption, effectively reducing postprandial hyperglycemia.

It should be noted that our service is only used for research, not for clinical use.