MiglitolCAS# 72432-03-2 |
2D Structure
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Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
Cas No. | 72432-03-2 | SDF | Download SDF |
PubChem ID | 441314 | Appearance | Powder |
Formula | C8H17NO5 | M.Wt | 207.22 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | Bay m1009 | ||
Solubility | H2O : ≥ 200 mg/mL (965.16 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | (2R,3R,4R,5S)-1-(2-hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol | ||
SMILES | C1C(C(C(C(N1CCO)CO)O)O)O | ||
Standard InChIKey | IBAQFPQHRJAVAV-ULAWRXDQSA-N | ||
Standard 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 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Inhibitor of α-glucosidase; antihyperglycemic. Suppresses postprandial hyperglycemia in vivo and reduces plasma glucose concentration in normal rats and in several animal models of diabetes. Shown to inhibit the loss of pancreatic β cells in type 2 diabetic rats. Also inhibits apoptosis and mitochondrial overproduction of reactive oxygen species in endothelial cells in vitro. |
Miglitol Dilution Calculator
Miglitol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.8258 mL | 24.1289 mL | 48.2579 mL | 96.5158 mL | 120.6447 mL |
5 mM | 0.9652 mL | 4.8258 mL | 9.6516 mL | 19.3032 mL | 24.1289 mL |
10 mM | 0.4826 mL | 2.4129 mL | 4.8258 mL | 9.6516 mL | 12.0645 mL |
50 mM | 0.0965 mL | 0.4826 mL | 0.9652 mL | 1.9303 mL | 2.4129 mL |
100 mM | 0.0483 mL | 0.2413 mL | 0.4826 mL | 0.9652 mL | 1.2064 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Development and Validation of Miglitol and Its Impurities by RP-HPLC and Characterization Using Mass Spectrometry Techniques.[Pubmed:27754407]
Sci Pharm. 2016 Oct 14;84(4):654-670.
Alpha glucoside inhibitors used to treat type-2 diabetes mellitus (DM) are likely to be safe and effective. These agents are most effective for postprandial hyperglycemia. Miglitol is a type of drug used to treat type-2 DM. A simple, selective, linear, precise and accurate reversed-phase high-performance liquid chromatography (RP-HPLC) method was developed and validated for a related substance of Miglitol and its identification, and characterization was done by different mass spectrometry techniques. The gradient method at a flow rate of 1.0 mL/min was employed on a prevail carbohydrate ES column (250 x 4.6 mm, 5 mum particle size) at a temperature of 35 degrees C. Mobile phase A consisted of 10 mM dipotassium hydrogen orthophosphate adjusted to pH 8.0 using concentrated phosphoric acid and mobile phase B consisted of acetonitrile. The ultraviolet detection wavelength was 210 nm and 20 muL of the sample were injected. The retention time for Miglitol was about 24.0 min. Forced degradation of the Miglitol sample was conducted in accordance with the International Conference on Harmonisation (ICH) guidelines. Acidic, basic, neutral, and oxidative hydrolysis, thermal stress, and photolytic degradation were used to assess the stability-indicating the power of the method. Substantial degradation was observed during oxidative hydrolysis. No degradation was observed under the other stress conditions. The method was optimized using samples generated by forced degradation and sample solutions spiked with impurities and epimers. Good resolution of the analyte peak from peaks, corresponding to process-related impurities, epimers and degradation products, was achieved and the method was validated as per the ICH guidelines. The method can successfully be applied for routine analysis of Miglitol.
Add-on therapy with anagliptin in Japanese patients with type-2 diabetes mellitus treated with metformin and miglitol can maintain higher concentrations of biologically active GLP-1/total GIP and a lower concentration of leptin.[Pubmed:27780736]
Peptides. 2016 Dec;86:118-125.
Metformin, alpha-glucosidase inhibitors (alpha-GIs), and dipeptidyl peptidase 4 inhibitors (DPP-4Is) reduce hyperglycemia without excessive insulin secretion, and enhance postprandial plasma concentration of glucagon-like peptide-1 (GLP-1) in type-2 diabetes mellitus (T2DM) patients. We assessed add-on therapeutic effects of DPP-4I anagliptin in Japanese T2DM patients treated with metformin, an alpha-GI Miglitol, or both drugs on postprandial responses of GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), and on plasma concentration of the appetite-suppressing hormone leptin. Forty-two Japanese T2DM patients with inadequately controlled disease (HbA1c: 6.5%-8.0%) treated with metformin (n=14), Miglitol (n=14) or a combination of the two drugs (n=14) received additional treatment with anagliptin (100mg, p.o., b.i.d.) for 52 weeks. We assessed glycemic control, postprandial responses of GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), and on plasma concentration of leptin in those patients. Add-on therapy with anagliptin for 52 weeks improved glycemic control and increased the area under the curve of biologically active GLP-1 concentration without altering obesity indicators. Total GIP concentration at 52 weeks was reduced by add-on therapy in groups treated with Miglitol compared with those treated with metformin. Add-on therapy reduced leptin concentrations. Add-on therapy with anagliptin in Japanese T2DM patients treated with metformin and Miglitol for 52 weeks improved glycemic control and enhanced postprandial concentrations of active GLP-1/total GIP, and reduce the leptin concentration.
Effect of miglitol on the suppression of nonalcoholic steatohepatitis development and improvement of the gut environment in a rodent model.[Pubmed:28349245]
J Gastroenterol. 2017 Nov;52(11):1180-1191.
BACKGROUND: The gut environment has been considered to play a role in the development of nonalcoholic steatohepatitis (NASH). alpha-glucosidase inhibitors (alpha-GIs) delay carbohydrate absorption and may change the gut environment. We considered that the protective effect of alpha-GIs against NASH development is related to changes in the gut environment and thus investigated the effects of Miglitol, an alpha-GI, on NASH development and the gut environment. METHODS: Mice were divided into three groups and fed a normal chow diet (NCD), a high-fat high-sucrose diet (HFHSD), or HFHSD plus 0.04% Miglitol (HFHSD plus M) for 12 weeks. RESULTS: Insulin resistance developed more in the HFHSD group than in the NCD group, whereas it was suppressed in the HFHSD plus M group. NASH was evaluated histologically, biochemically, and on the basis of messenger RNA expression levels. Miglitol treatment suppressed HFHSD-induced NASH development with the suppression of hepatic Toll-like receptor 4 expression, increased glucagon-like peptide 1 (GLP-1) concentration, and reduced lipopolysaccharide concentration in portal plasma. Regarding the gut environment, the intestinal transit time was shortened and colon inflammation was suppressed in the HFHSD plus M group compared with the HFHSD group. Regarding the gut microbiota, the abundances of Erysipelotrichaceae and Coriobacteriaceae were increased in the HFHSD group compared with the NCD group, whereas the increase was suppressed in the HFHSD plus M group. CONCLUSIONS: We demonstrated that Miglitol has a protective effect against HFHSD-induced NASH development. The increased GLP-1 secretion and the suppression of endotoxemia, associated with the changes in the gut environment, including the gut microbiota, could contribute to the underlying mechanisms.
Reappraisal and perspectives of clinical drug-drug interaction potential of alpha-glucosidase inhibitors such as acarbose, voglibose and miglitol in the treatment of type 2 diabetes mellitus.[Pubmed:28010166]
Xenobiotica. 2018 Jan;48(1):89-108.
1. Amidst the new strategies being developed for the management of type 2 diabetes mellitus (T2DM) with both established and newer therapies, alpha glucosidase inhibitors (AGIs) have found a place in several treatment protocols. 2. The objectives of the review were: (a) to compile and evaluate the various clinical pharmacokinetic drug interaction data for AGIs such as acarbose, Miglitol and voglibose; (b) provide perspectives on the drug interaction data since it encompasses coadministered drugs in several key areas of comorbidity with T2DM. 3. Critical evaluation of the interaction data suggested that the absorption and bioavailability of many coadministered drugs were not meaningfully affected from a clinical perspective. Therefore, on the basis of the current appraisal, none of the AGIs showed an alarming and/or overwhelming trend of interaction potential with several coadministered drugs. Hence, dosage adjustment is not warranted in the use of AGIs in T2DM patients in situations of comorbidity. 4. The newly evolving fixed dose combination strategies with AGIs need to be carefully evaluated to ensure that the absorption and bioavailability of the added drug are not impaired due to concomitant food ingestion.
Miglitol, an anti-diabetic drug, inhibits oxidative stress-induced apoptosis and mitochondrial ROS over-production in endothelial cells by enhancement of AMP-activated protein kinase.[Pubmed:23018899]
J Pharmacol Sci. 2012;120(2):121-8. Epub 2012 Sep 26.
Endothelial dysfunction caused by oxidative stress plays a key role in atherogenesis. This study investigated whether the anti-diabetic drug Miglitol, an alpha-glucosidase inhibitor, which is currently available in clinical practice, can prevent endothelial cell apoptosis and whether it might restore impaired vascular relaxation under oxidative stress. The bEnd.3 cells, a microvascular endothelial cell line, were pre-treated with various concentrations of Miglitol and then were incubated with H(2)O(2) for 1 - 2 h. Treatment of bEnd.3 cells with Miglitol resulted in the protection of cell viability, suppression of mitochondrial superoxide production, and DNA strand breakage under the oxidative stress. These effects of Miglitol were associated with the activation of AMP-activated protein kinase (AMPK) and the phosphorylation of endothelial nitric oxide synthase (eNOS). In aortic rings with endothelium, acetylcholine (Ach)-induced relaxation was attenuated by H(2)O(2). We found that this impaired relaxation was restored by acute treatment with Miglitol. Compound C, an AMPK inhibitor, inhibited the amelioration of vascular relaxations treated with Miglitol. These results suggest that Miglitol might protect against endothelial cells damage under oxidative stress via inhibition of endothelial cell apoptosis and mitochondrial superoxide production, which are mediated by the activation of AMPK and the phosphorylation of eNOS.
Effects of miglitol, an alpha-glucosidase inhibitor, on glycaemic status and histopathological changes in islets in non-obese, non-insulin-dependent diabetic Goto-Kakizaki rats.[Pubmed:17537288]
Br J Nutr. 2007 Oct;98(4):702-10.
Miglitol, a 1-deoxynojirimycin derivative, is an alpha-glucosidase inhibitor. In the present study, the effects of acute (single-dose) and chronic (8-week) oral administration of Miglitol in Goto-Kakizaki (GK) rats, an animal model of type 2 diabetes, were investigated. Dose-dependent decreases in incremental blood glucose concentrations integrated over a period of 2 h (deltaAUC0-2 h) for values of blood glucose after sucrose-loading in Miglitol-treated GK rats were observed following an acute oral administration of Miglitol (1, 3 or 10 mg/kg body weight). At 10 mg/kg, the deltaAUC0-2 h of blood glucose was decreased by 45 % compared with the control group. Following the oral administration of Miglitol in a dietary mixture (10 mg, 20 mg or 40 mg Miglitol/100 g control diet) for 8 weeks, the ratio of HbA1c at 8 weeks compared with 0 weeks in GK rats treated with 40 mg Miglitol/100 g control diet Miglitol was significantly decreased compared with control GK rats without changes in body weight. In oral glucose tolerance testing, Miglitol caused a slight decrease in the deltaAUC0-2 h of plasma glucose concentration. In addition, Miglitol treatment slightly inhibited the reduction in beta-cell mass, and lessened the irregular contours and fibrosis of the islets in GK rats. These results indicate that Miglitol ameliorates the hyperglycaemic state of GK rats and the impaired function of the pancreatic islets, as well as preventing the degeneration of islets in GK rats.
Miglitol, a new alpha-glucosidase inhibitor.[Pubmed:11249557]
Expert Opin Pharmacother. 1999 Nov;1(1):149-56.
Miglitol (Bay m 1099, Bayer) is a second generation alpha-glucosidase inhibitor. It is a derivative of 1-desoxynojirimycin, and binds reversibly to the brushborder alpha-glucosidase enzymes. In contrast to its parent drug (acarbose, Bay g 5421, Bayer), Miglitol is almost completely absorbed in the small intestine. It has to be taken with each main meal, and through its effect on carbohydrate digestion it blunts the postprandial blood glucose increase. Miglitol has no or a very small effect on fasting blood glucose levels. The blood-glucose lowering effects of Miglitol in patients with Type 2 diabetes are lower than those of the frequently-used sulphonylurea compounds. Long-term studies show that a moderate average reduction of HbA1c of 0.3-0.7% point from baseline can be achieved. An advantage over sulphonylurea is the effect on serum insulin levels: Miglitol therapy leads to slightly lower postprandial levels of serum insulin, whereas chronic sulphonylurea treatment usually increases serum insulin levels. This insulin-sparing effect may, in theory, lead to a lesser weight gain or even no weight gain and reduced risk of hypoglycaemia during chronic treatment. Long-term experience in Type 1 diabetic patients is limited. Similarly, Miglitol may lead to reduced postprandial glucose excursions, slightly reduced insulin requirements and perhaps, as a consequence, a lower risk of hypoglycaemia. More long-term data are needed to fully assess to the clinical use of Miglitol in these patients.