1,5-dideoxy-1,5-((2-hydroxyethyl)imino)-D-glucitol

DescriptionMiglitol was introduced in Germany as an auxiliary treatment for non-insulin dependent diabetes (NIDDM). A simple two-step synthesis of Miglitol consists of converting 6-desoxy-6-aminosorbose into desoxynojirimycin by reductive cyclization, then selectively hydroxyethylating the cyclic nitrogen. Miglitol is a short-acting intestinal alpha-D-glucosidase inhibitor, reducing postprandial glucose excursions by helping to delay absorption of complex carbohydrates. Acarbose and voglibose are the previous compounds marketed in this class. At low doses, orally administered miglitol was shown to be rapidly and completely absorbed then removed by renal excretion.

UsesAn inhibitor of alpha-glucosidases.

Usesantibacterial

UsesA potent α-glucosidase inhibitor. A new antidiabetic drug.

General DescriptionMiglitol is (2R,3R,4R,5S)-1-(2-hydroxyethyl)-2-(hydroxymethyl)-3,4,5-piperidinetriol, or N-hydroxyethyl-1-deoxynorjirimycin. The drug is available as 25-, 50-, and100-mg tablets (Glyset), for administration 25 to 100 mgt.i.d. with meals. In contrast to acarbose, miglitol is highlyabsorbed from a 25-mg oral dose, although absorption is reportedto be saturable, and accordingly less complete athigher doses. Binding to plasma proteins is minimal, andthe volume of distribution (0.18 L/kg, corresponding to12–13 L in a 70-kg adult) is characteristic of compoundsdistributed only to blood and extracellular fluids. Practicallyno systemic biotransformation of miglitol occurs in humans;essentially 100% of an orally administered dose is excretedintact in urine.

General DescriptionMiglitol, 1-(2-hydroxyethyl)-2-(hydroxymethyl)-[2R-(2α,3β ,4α,5β)]-piperidine (Glyset), a desoxynojirimycinderivative, is chemically known as 3,4,5-piperidinetriol. It is a white to pale yellow powder that issoluble in water, with a pKa of 5.9. In chemical structure,this agent is very similar to a sugar, with the heterocyclic nitrogenserving as an isosteric replacement of the sugar oxygen.This feature allows recognition by the -glucosidase asa substrate. This results in competitive inhibition of the enzymeand delays complex carbohydrate absorption from thegastrointestinal tract.