AdipoGen Life Sciences


CHF 75.00
In stock
AG-CR1-3635-M01010 mgCHF 75.00
AG-CR1-3635-M05050 mgCHF 180.00
More Information
Product Details
Synonyms (2R,3R,4R,5S)-1-(2-Hydroxyethyl)-2-(2-hydroxymethyl)-3,4,5-piperidinetriol; BAY-1099; Diastabol; Glyset; Seibule
Product Type Chemical


MW 207.2
CAS 72432-03-2
RTECS TN4350170
Purity Chemicals ≥98% (NMR)
Appearance White solid.
Solubility Soluble in water or DMSO.
Identity Identity determined by 1H-NMR.
Smiles O[C@@H]1[C@@H](O)CN(CCO)[C@H](CO)[C@H]1O
Shipping and Handling
Shipping AMBIENT
Short Term Storage +20°C
Long Term Storage +4°C
Handling Advice Keep cool and dry.
Protect from moisture.
Use/Stability Stable for at least 2 years after receipt when stored at +4°C.
MSDS Download PDF
Product Specification Sheet
Datasheet Download PDF
  • Anti-diabetic agent with antihyperglycemic activity. α-Glucosidase inhibitor. Inhibits lysosomal α-glucosidase, sucrase, maltase and isomaltase (IC50= 0.35, 0.11, 1.3, and 1.2μM, respectively) as well as maltase-glucoamylase (IC50 = 1.0μM).
  • α-Glucosidase enzymes hydrolyze oligosaccharides and disaccharides into glucose and other monosaccharides. Inhibition by miglitol prevents the breakdown of larger carbohydrates into glucose. This suppresses postprandial hyperglycemia and reduces plasma glucose concentration in normal rats and in several animal models of diabetes without cardiovascular complications.
  • Anti-obesity drug. Shown to inhibit adipogenesis of white adipocytes in vitro and to activate brown adipose tissue (BAT) in mice.
  • Induces an enhanced and prolonged release of glucagon-like peptide-1, regulating appetite and stabilizing body weight in humans.
  • Influenced bile acid metabolism in mice and regulated the secretion of incretin hormones in humans.
  • Reduces plasma lipids and inhibits free radical generation. Inhibits oxidative stress-induced apoptosis and mitochondrial ROS overproduction in endothelial cells.
Product References
  1. Miglitol, a new α-glucosidase inhibitor:  J.P. Sels, et al.; Expert. Opin. Pharmacother. 1, 149 (1999) (Review)
  2. The effects of miglitol on glucagon-like peptide-1 secretion and appetite sensations in obese type 2 diabetics: A. Lee, et al.; Diabetes Obes. Metab. 4, 329 (2002)
  3. In vitro inhibition of glycogen-degrading enzymes and glycosidases by six-membered sugar mimics and their evaluation in cell cultures: C. Kuriyama, et al.; Biorg. Med. Chem. 16, 7330 (2008)
  4. Probing the active-site requirements of human intestinal N-terminal maltase-glucoamylase: Synthesis and enzyme inhibitory activities of a six-membered ring nitrogen analogue of kotalanol and its de-O-sulfonated derivative: S. Mohan, et al.;  Biorg. Med. Chem. 18, 7794 (2010)
  5. The synthesis and biological evaluation of 1-C-alkyl-L-arabinoiminofuranoses, a novel class of α-glucosidase inhibitors: Y. Natori, et al.; Bioorg. Med. Chem. Lett. 21, 738 (2011)
  6. Alpha-glucosidase inhibitors 2012 - cardiovascular considerations and trial evaluation: E. Standl & O. Schnell; Diab. Vasc. Dis. Res.  9, 163 (2012)
  7. Miglitol, an anti-diabetic drug, inhibits oxdiative stress-induced apoptosis and mitochondrial ROS over-production in endothelial cells by enhancement of AMP-activated protein kinase: C. Aoki, et al.; J. Pharmacol. Sci. 120, 121 (2012)
  8. Miglitol prevents diet-induced obesity by stimulating brown adipose tissue and energy expenditure independent of preventing the digestion of carbohydrates: T. Sasaki, et al.; Endocr. J. 60, 1117 (2013)
  9. Lipid lowering and antioxidant effect of miglitol in triton treated hyperlipidemic and high fat diet induced obese rats: A. Shrivastava, et al.; Lipids 48, 597 (2013)
  10. Miglitol increases energy expenditure by upregulating uncoupling protein 1 of brown adipose tissue and reduces obesity in dietary-induced obese mice: S. Sugimoto, et al.; Nutr. Metab. (Lond) 11, 14 (2014)
  11. Review: Miglitol has potential as a therapeutic drug against obesity: S. Sugimoto, et al.; Nutr. Metab. (Lond) 12, 51 (2015)
© 2017 Adipogen Life Sciences. Pictures: © 2012 Martin Oeggerli. All Rights Reserved.