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Miglitol

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Chemistry

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Also known as: 72432-03-2, Glyset, (2r,3r,4r,5s)-1-(2-hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol, Bay-m-1099, Bay m 1099, Miglitol (glyset)

Molecular Formula

C₈H₁₇NO₅

Molecular Weight

207.22 g/mol

InChI Key

IBAQFPQHRJAVAV-ULAWRXDQSA-N

FDA UNII

0V5436JAQW

Miglitol is a desoxynojirimycin derivative and inhibitor of alpha-glucosidase with antihyperglycemic activity. Miglitol binds to and inhibits alpha-glucosidase, an enteric enzyme found in the brush border of the small intestines that hydrolyzes oligosaccharides and disaccharides into glucose and other monosaccharides. This prevents the breakdown of larger carbohydrates into glucose and decreases the rise in postprandial blood glucose levels. Compared to acarbose, miglitol is systemically absorbed.

Miglitol is an alpha-Glucosidase Inhibitor. The mechanism of action of miglitol is as an alpha Glucosidase Inhibitor.

1 2D Structure

Miglitol

2 Identification

2.1 Computed Descriptors

2.1.1 IUPAC Name

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

2.1.2 InChI

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

2.1.3 InChI Key

IBAQFPQHRJAVAV-ULAWRXDQSA-N

2.1.4 Canonical SMILES

C1C(C(C(C(N1CCO)CO)O)O)O

2.1.5 Isomeric SMILES

C1[C@@H]([C@H]([C@@H]([C@H](N1CCO)CO)O)O)O

2.2 Other Identifiers

2.2.1 UNII

0V5436JAQW

2.3 Synonyms

2.3.1 MeSH Synonyms

1. Bay M 1099

2. Bay-m 1099

3. Bay-m-1099

4. Diastabol

5. Glyset

6. Miglitol, 4-methylbenzenesulfonate Salt, ((d)-isomer)

7. N-hydroxyethyl-1-desoxy-nojirimycin

8. N-hydroxyethyl-1-desoxynojirimycin

9. Plumarol

2.3.2 Depositor-Supplied Synonyms

1. 72432-03-2

2. Glyset

3. (2r,3r,4r,5s)-1-(2-hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol

4. Bay-m-1099

5. Bay M 1099

6. Miglitol (glyset)

7. Seibule

8. Chembl1561

9. (2r,3r,4r,5s)-1-(2-hydroxyethyl)-2-(hydroxymethyl)-3,4,5-piperidinetriol

10. 0v5436jaqw

11. Chebi:6935

12. Diastabol

13. Plumarol

14. Nsc-758702

15. Dsstox_cid_3323

16. Dsstox_rid_76977

17. Dsstox_gsid_23323

18. Miglitolum

19. N-(2-hydroxyethyl)-1-deoxynojirimycin

20. Smr000466381

21. Miglitolum [latin]

22. Cas-72432-03-2

23. Glyset (tn)

24. Unii-0v5436jaqw

25. Miglitol [usan:inn:ban]

26. Bay 1099

27. Hsdb 8022

28. Ncgc00095127-01

29. Einecs 276-661-6

30. Mfcd00867240

31. Sk-983

32. Baym1099

33. Miglitol [usan]

34. Miglitol [inn]

35. Miglitol [jan]

36. Miglitol [mi]

37. Miglitol [vandf]

38. Miglitol [mart.]

39. Bay M1009

40. Miglitol [who-dd]

41. Schembl22593

42. Mls000759514

43. Mls001424128

44. Mls006011963

45. Bidd:gt0732

46. Bay-m1099

47. Miglitol [orange Book]

48. Cid_441314

49. Gtpl4842

50. Miglitol (jp17/usan/inn)

51. Dtxsid0023323

52. Bay1099

53. Hms2051d05

54. Hms3713j07

55. N-hydroxylethyl-1-deoxynojirimycin

56. Hy-b0481

57. Zinc4097426

58. Tox21_111436

59. Bdbm50242271

60. Akos015969689

61. Tox21_111436_1

62. Ccg-100920

63. Db00491

64. Ks-1242

65. Nc00170

66. Nsc 758702

67. Ncgc00270540-02

68. M2302

69. S2589

70. C07708

71. C76308

72. D00625

73. Ab00639982-06

74. Ab00639982_08

75. 432m032

76. A837526

77. Q772735

78. Sr-01000759413

79. Sr-01000759413-4

80. W-104490

81. 1,5-dideoxy-1,5-((2-hydroxyethyl)imino)-d-glucitol

82. Brd-k44779798-001-06-5

83. Z1541638520

84. (2r,3r,4r,5s)-1-ethoxy-2-(hydroxymethyl)piperidine-3,4,5-triol

85. (4r,5r)-1-(2-hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol

86. (2r,3r,4r,5s)-1-(2-hydroxyethyl)-2-(2-hydroxymethyl)-3,4,5-piperidinetriol

87. 1204250-58-7

88. 3,4,5-piperidinetriol, 1-(2-hydroxyethyl)-2-(hydroxymethyl)-, (2r-(2.alpha.,3.beta.,4.alpha.,5.beta.))-

89. 3,4,5-piperidinetriol, 1-(2-hydroxyethyl)-2-(hydroxymethyl)-, (2r-(2alpha,3beta,4alpha,5beta))-

2.4 Create Date

2005-06-24

3 Chemical and Physical Properties

Molecular Formula	C₈H₁₇NO₅
Molecular Weight	207.22 g/mol
XLogP3	-2.6
Hydrogen Bond Donor Count	5
Hydrogen Bond Acceptor Count	6
Rotatable Bond Count	3
Exact Mass	207.11067264 g/mol
Monoisotopic Mass	207.11067264 g/mol
Topological Polar Surface Area	104 Å²
Heavy Atom Count	14
Formal Charge	0
Complexity	179
Isotope Atom Count	0
Defined Atom Stereocenter Count	4
Undefined Atom Stereocenter Count	0
Defined Bond Stereocenter Count	0
Undefined Bond Stereocenter Count	0
Covalently Bonded Unit Count	1

4 Drug and Medication Information

4.1 Drug Information

1 of 2
Drug Name	Glyset
PubMed Health	Miglitol (By mouth)
Drug Classes	Antidiabetic
Drug Label	GLYSET Tablets contain miglitol, an oral alpha-glucosidase inhibitor for use in the management of non-insulin-dependent diabetes mellitus (NIDDM). Miglitol is a desoxynojirimycin derivative, and is chemically known as 3,4,5-piperidinetriol, 1-(2-hydr...
Active Ingredient	Miglitol
Dosage Form	Tablet
Route	Oral
Strength	25mg; 100mg; 50mg
Market Status	Prescription
Company	Pharmacia And Upjohn

2 of 2
Drug Name	Glyset
PubMed Health	Miglitol (By mouth)
Drug Classes	Antidiabetic
Drug Label	GLYSET Tablets contain miglitol, an oral alpha-glucosidase inhibitor for use in the management of non-insulin-dependent diabetes mellitus (NIDDM). Miglitol is a desoxynojirimycin derivative, and is chemically known as 3,4,5-piperidinetriol, 1-(2-hydr...
Active Ingredient	Miglitol
Dosage Form	Tablet
Route	Oral
Strength	25mg; 100mg; 50mg
Market Status	Prescription
Company	Pharmacia And Upjohn

4.2 Therapeutic Uses

1-Deoxynojirimycin/*analogs & derivatives; alpha-Glucosidases/antagonists & inhibitors; Enzyme Inhibitors

National Library of Medicine's Medical Subject Headings online file (MeSH, 2009)

Reduction in postprandial blood glucose concentrations persists for 3-4 hours following a single dose in healthy individuals.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

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/

US Natl Inst Health; DailyMed. Current Medication Information for GLYSET (miglitol) tablet, film coated (October 2010). Available from, as of February 21, 2012: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=75711d16-2d27-476e-a312-d5af448a0e25

4.3 Drug Warning

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.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

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.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

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.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

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.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

For more Drug Warnings (Complete) data for Miglitol (11 total), please visit the HSDB record page.

4.4 Drug Indication

For use as an adjunct to diet to improve glycemic control in patients with non-insulin-dependent diabetes mellitus (NIDDM) whose hyperglycemia cannot be managed with diet alone.

5 Pharmacology and Biochemistry

5.1 Pharmacology

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.

5.2 MeSH Pharmacological Classification

Enzyme Inhibitors

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)

Glycoside Hydrolase Inhibitors

Compounds that inhibit or block the activity of GLYCOSIDE HYDROLASES such as ALPHA-AMYLASES and ALPHA-GLUCOSIDASES. (See all compounds classified as Glycoside Hydrolase Inhibitors.)

Hypoglycemic Agents

Substances which lower blood glucose levels. (See all compounds classified as Hypoglycemic Agents.)

5.3 FDA Pharmacological Classification

5.3.1 Active Moiety

MIGLITOL

5.3.2 FDA UNII

0V5436JAQW

5.3.3 Pharmacological Classes

alpha-Glucosidase Inhibitor [EPC]; alpha Glucosidase Inhibitors [MoA]

5.4 ATC Code

A - Alimentary tract and metabolism

A10 - Drugs used in diabetes

A10B - Blood glucose lowering drugs, excl. insulins

A10BF - Alpha glucosidase inhibitors

A10BF02 - Miglitol

5.5 Absorption, Distribution and Excretion

Absorption

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.

Route of Elimination

Miglitol is not metabolized in man or in any animal species studied. It is eliminated by renal excretion as an unchanged drug.

Volume of Distribution

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.

US Natl Inst Health; DailyMed. Current Medication Information for GLYSET (miglitol) tablet, film coated (October 2010). Available from, as of February 21, 2011: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=75711d16-2d27-476e-a312-d5af448a0e25

Therapeutic effects principally result from local actions on the small intestine; there is no evidence that systemic absorption contributes to therapeutic response.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

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.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

For more Absorption, Distribution and Excretion (Complete) data for Miglitol (9 total), please visit the HSDB record page.

5.6 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.

5.7 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...

PMID:9239452 Ahr HJ et al; Arzneimittelforschung 47 (6): 734-45 (1997)

The elimination half-life of miglitol from plasma is approximately 2 hours.

5.8 Mechanism of Action

In contrast to sulfonylureas, miglitol does not enhance insulin secretion. The antihyperglycemic action of miglitol results from a reversible inhibition of membrane-bound intestinal a-glucoside hydrolase enzymes. Membrane-bound intestinal a-glucosidases hydrolyze oligosaccharides and disaccharides to glucose and other monosaccharides in the brush border of the small intestine. In diabetic patients, this enzyme inhibition results in delayed glucose absorption and lowering of postprandial hyperglycemia.

Miglitol 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 tablets 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.

Miglitol inhibits alpha-glucosidase enzymes (e.g., sucrase, glucoamylase, maltase, isomaltase) that hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestinal brush border. The drug has little or no inhibitory effect on trehalase, lactase, or pancreatic alpha-amylase; it is not expected to produce lactose intolerance. Miglitol delays carbohydrate breakdown and glucose absorption and reduces postprandial hyperglycemia in diabetic patients; fasting blood glucose concentrations are mildly decreased.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

In contrast to sulfonylurea antidiabetic agents, miglitol does not enhance insulin secretion. The drug does not produce hypoglycemia when given as monotherapy in the fasted or postprandial state. When used in combination with sulfonylurea antidiabetic agents, miglitol reduces the insulinotropic and weight-increasing effects of sulfonylureas. Miglitol does not produce clinically important weight loss.

American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

Oral administration of miglitol has been reported to produce glucagon-like peptide 1 (GLP-1). /The authors/ hypothesized that p.o. administration of miglitol, an absorbable antidiabetic drug, reduces myocardial infarct size by stimulating GLP-1 receptors and inhibiting glycogenolysis in the myocardium. The effects of p.o. and i.v. administration of miglitol on myocardial infarct size were compared in a rabbit model of ischemia induced by 30 min of coronary occlusion and 48 hr of reperfusion. The levels of phospho(p)-PI3kinase and p-Akt were measured in cardiac tissue by use of Western blot analysis. Both p.o. and i.v. administration of miglitol reduced the infarct size, and this effect was greater after p.o. than after i.v. administration under similar plasma miglitol concentrations. The reduction in infarct size induced by p.o. miglitol but not that induced by i.v. miglitol was partially inhibited by treatment with exendin(9-39), a GLP-1 receptor blocker. Both p.o. and i.v. miglitol improved ejection fraction and +/-dP/dt after myocardial infarction. Miglitol administered p.o. but not i.v. up-regulated the myocardial expression of phospho(p)-PI3kinase and p-Akt following myocardial infarction; an effect that was inhibited by exendin(9-39). Administration of miglitol p.o. reduces myocardial infarct size through stimulation of GLP-1 receptors and activation of PI3kinase-Akt pathway in addition to the inhibition of glycogenolysis. These findings may have clinical implications for the p.o. administration of miglitol for the treatment of patients with diabetes mellitus combined with coronary artery disease.

PMID:21426318 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171865 Iwasa M et al; Br J Pharmacol 164 (1): 119-31 (2011)

Imino sugars are used to treat type 2 diabetes mellitus (miglitol (Glyset)) and lysosomal storage disorders (miglustat (Zavesca)) based on the inhibition of alpha-glucosidases and glucosyltransferases. In this substrate specificity study, /investigators/ examined the interactions of imino sugars with a novel human glucose sensor, sodium/glucose cotransporter type 3 (hSGLT3), using expression in Xenopus laevis oocytes and electrophysiology. The results for hSGLT3 are compared with those for alpha-glucosidases and human SGLT type 1 (hSGLT1), a well characterized sodium/glucose cotransporter of the SGLT family. In general, substrates have lower apparent affinities (K0.5) for hSGLT3 than hSGLT1 (D-glucose, alpha-methyl-D-glucose, 1-deoxy-D-glucose, and 4-deoxy-4-fluoro-D-glucose exhibit K0.5 values of 19, 21, 43, and 17 mM, respectively, for hSGLT3, and 0.5, 0.7, 10, and 0.07 mM, respectively, for hSGLT1). However, specificity of hSGLT3 binding is greater (D-galactose and 4-deoxy-4-fluoro-D-galactose are not hSGLT3 substrates, but have hSGLT1 K0.5 values of 0.6 and 1.3 mM). An important deviation from this trend is potent hSGLT3 activation by the imino sugars 1-deoxynojirimycin (DNJ), N-hydroxylethyl-1-deoxynojirimycin (miglitol), N-butyl-1-deoxynojirimycin (miglustat), N-ethyl-1-deoxynojirimycin, and 1-deoxynojirimycin-1-sulfonic acid, with K0.5 values of 0.5 to 9 microM. The diastereomer 1-deoxygalactonojirimycin activates hSGT3 with a K0.5 value of 11 mM, a 3000-fold less potent interaction than is observed for DNJ (4 microM). These imino sugar binding characteristics are similar to those for alpha-glucosidases, but there are no interactions with hSGLT1. This work provides insights into hSGLT3 and -1 substrate binding interactions, establishes a pharmacological profile to study endogenous hSGLT3, and may have important ramifications for the clinical application of imino sugars.

PMID:17110502 Voss AA et al; Mol Pharmacol 71 (2): 628-34 (2007)

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