Mitiglinide CalciumCAS# 145525-41-3 |
- Guanfacine hydrochloride
Catalog No.:BCC1609
CAS No.:29110-48-3
- (R,R)-Formoterol
Catalog No.:BCC1293
CAS No.:67346-49-0
- Doxazosin Mesylate
Catalog No.:BCC1257
CAS No.:77883-43-3
- Medetomidine
Catalog No.:BCC1736
CAS No.:86347-14-0
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 145525-41-3 | SDF | Download SDF |
| PubChem ID | 5478927 | Appearance | Powder |
| Formula | C38H48CaN2O6 | M.Wt | 668.88 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : 5 mg/mL (14.95 mM; Need ultrasonic) | ||
| Chemical Name | calcium;(2S)-4-[(3aS,7aR)-1,3,3a,4,5,6,7,7a-octahydroisoindol-2-yl]-2-benzyl-4-oxobutanoate | ||
| SMILES | C1CCC2CN(CC2C1)C(=O)CC(CC3=CC=CC=C3)C(=O)[O-].C1CCC2CN(CC2C1)C(=O)CC(CC3=CC=CC=C3)C(=O)[O-].[Ca+2] | ||
| Standard InChIKey | PMRVFZXOCRHXFE-FMEJWYFOSA-L | ||
| Standard InChI | InChI=1S/2C19H25NO3.Ca/c2*21-18(20-12-15-8-4-5-9-16(15)13-20)11-17(19(22)23)10-14-6-2-1-3-7-14;/h2*1-3,6-7,15-17H,4-5,8-13H2,(H,22,23);/q;;+2/p-2/t2*15-,16+,17-;/m00./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. |
||
| 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. |
||
| 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. | ||
Mitiglinide Calcium Dilution Calculator
Mitiglinide Calcium Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.495 mL | 7.4752 mL | 14.9504 mL | 29.9007 mL | 37.3759 mL |
| 5 mM | 0.299 mL | 1.495 mL | 2.9901 mL | 5.9801 mL | 7.4752 mL |
| 10 mM | 0.1495 mL | 0.7475 mL | 1.495 mL | 2.9901 mL | 3.7376 mL |
| 50 mM | 0.0299 mL | 0.1495 mL | 0.299 mL | 0.598 mL | 0.7475 mL |
| 100 mM | 0.015 mL | 0.0748 mL | 0.1495 mL | 0.299 mL | 0.3738 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. | |||||
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
Mitiglinide is a drug for the treatment of type 2 diabetes. It is a highly selective KATP channel antagonist.
- 1,7-Dimethoxy-2,3-methylenedioxyxanthone
Catalog No.:BCN7539
CAS No.:145523-71-3
- (2R,3S)-Boc-3-Phenylisoserine
Catalog No.:BCN8362
CAS No.:145514-62-1
- MRS 2179 tetrasodium salt
Catalog No.:BCC5685
CAS No.:1454889-37-2
- PF-06463922
Catalog No.:BCC5568
CAS No.:1454846-35-5
- 4-Benzoylpyridine
Catalog No.:BCC8697
CAS No.:14548-46-0
- LY3009120
Catalog No.:BCC3985
CAS No.:1454682-72-4
- Furano(2'',3'',7,6)-4'-hydroxyflavanone
Catalog No.:BCN6405
CAS No.:1454619-70-5
- PU-WS13
Catalog No.:BCC6425
CAS No.:1454619-14-7
- Isolintetralin
Catalog No.:BCN3052
CAS No.:145459-30-9
- Heterophyllin B
Catalog No.:BCN2768
CAS No.:145459-19-4
- L-692,585
Catalog No.:BCC7305
CAS No.:145455-35-2
- Homalomenol A
Catalog No.:BCN1647
CAS No.:145400-03-9
- Eucamalol
Catalog No.:BCN1648
CAS No.:145544-91-8
- Sophocarpine
Catalog No.:BCN5971
CAS No.:145572-44-7
- Cyclocommunol
Catalog No.:BCN3375
CAS No.:145643-96-5
- NNC 711
Catalog No.:BCC7176
CAS No.:145645-62-1
- 2'-O-Benzoylpaeoniflorin
Catalog No.:BCN7803
CAS No.:1456598-64-3
- SH-4-54
Catalog No.:BCC5483
CAS No.:1456632-40-8
- HG-9-91-01
Catalog No.:BCC4071
CAS No.:1456858-58-4
- 3-Allylrhodanine
Catalog No.:BCC8604
CAS No.:1457-47-2
- AR-C 66096 tetrasodium salt
Catalog No.:BCC6004
CAS No.:145782-74-7
- 4,6-Dichloro-5-nitro-2-propylthiopyrimidine
Catalog No.:BCC8667
CAS No.:145783-14-8
- 4,6-Dichloro-2-(propylthio)pyrimidin-5-amine
Catalog No.:BCC8666
CAS No.:145783-15-9
- G-749
Catalog No.:BCC4009
CAS No.:1457983-28-6
Nateglinide and mitiglinide, but not sulfonylureas, induce insulin secretion through a mechanism mediated by calcium release from endoplasmic reticulum.[Pubmed:17409272]
J Pharmacol Exp Ther. 2007 Jul;322(1):1-7.
Nateglinide and mitiglinide (glinides) are characterized as rapid-onset and short-acting insulinotropic agents. Although both compounds do not have a sulfonylurea structure, it has been postulated that insulin secretion is preceded by their binding to Kir6.2/SUR1 complex, and a mechanism of insulin secretion of glinides has been accounted for by this pathway. However, we hypothesized the involvement of additional mechanisms of insulin secretion enhanced by glinides, and we analyzed the pattern of time course of insulin secretion from MIN6 cells with the existence of agents that have specific pharmacologic actions. Dose-dependent effects of tolbutamide, glibenclamide, nateglinide, and mitiglinide were observed. Insulin secretion induced by 3 microM tolbutamide and 1 nM glibenclamide was completely inhibited by 10 microM diazoxide and 3 microM verapamil, although the latter half-component of insulin secretion profile induced by 3 microM nateglinide or 30 nM mitiglinide remained with the existence of those agents. Glinides enhanced insulin secretion even in Ca2+-depleted medium, and its pattern of secretion was same as the pattern with existence of verapamil. The latter half was suppressed by 1 microM dantrolene, and concomitant addition of verapamil and dantrolene completely suppressed the entire pattern of insulin secretion enhanced by nateglinide. Thus, we conclude that glinide action is demonstrated through two pathways, dependently and independently, from the pathway through K(ATP) channels. We also demonstrated that the latter pathway involves the intracellular calcium release from endoplasmic reticulum via ryanodine receptor activation.
[Pharmacological and clinical profile of mitiglinide calcium hydrate (Glufast), a new insulinotropic agent with rapid onset].[Pubmed:15467258]
Nihon Yakurigaku Zasshi. 2004 Oct;124(4):245-55.
Mitiglinide Calcium hydrate (mitiglinide, Glufast) is a new insulinotropic agent of the glinide class with rapid onset. Mitiglinide is thought to stimulate insulin secretion by closing the ATP-sensitive K(+) (K(ATP)) channels in pancreatic beta-cells, and its early insulin release and short duration of action would be effective in improving postprandial hyperglycemia. In studies of various cloned K(ATP) channels, mitiglinide shows a higher selectivity for the beta-cell type of SUR1/Kir6.2 than the cardiac and smooth muscle types of K(ATP) channels in comparison with glibenclamide and glimepiride. In vitro and in vivo studies demonstrated the insulinotropic effect of mitiglinide is more potent than that of nateglinide, and mitiglinide surpassed in controlling postprandial hyperglycemia in normal and diabetic animals. In clinical trials, treatment with mitiglinide provided lasting improvement of postprandial hyperglycemia in Type 2 diabetic patients and decreased the fasting plasma glucose levels and HbA(1C) values. The incidence of adverse events related to mitiglinide were nearly equivalent to placebo; in particular there was no difference with the frequency of hypoglycemia. The results from these studies indicated that mitiglinide could be expected to possess good therapeutic features of being effective in reducing postprandial glucose excursions in the early stage of Type 2 diabetes and less incidence of events suggestive of hypoglycemia.
Comparison Between Effectiveness of 100 mg/day Sitagliptin and a Switch to Mitiglinide Calcium Hydrate/Voglibose from 50 mg/day Sitagliptin in Patients with Type 2 Diabetes.[Pubmed:28331117]
J UOEH. 2017;39(1):1-9.
We analyzed the effects of 100 mg/day sitagliptin and a switch to Mitiglinide Calcium hydrate/voglibose compound tablets (MIT/VOG) in patients with type 2 diabetes mellitus (T2DM) treated with 50 mg/day sitagliptin. Five patients with T2DM treated with 50 mg/day sitagliptin and hemoglobin A1c (HbA1c) of >/=6.5% were switched to MIT/VOG, or the dose of sitagliptin was increased to 100 mg/day. The effects of the changes in therapy were compared in a crossover fashion by continuous glucose monitoring. The primary endpoint was mean amplitude of glycemic excursions (MAGE), and the secondary end points were 24-hour mean blood glucose level and mean blood glucose level from 0:00 a.m. to 7:00 a.m. and from 7:00 a.m. to 0:00 a.m., percentage of time with blood glucose level of >/=200 mg/dl and <70 mg/dl, maximum and minimum blood glucose levels, and increases in postprandial blood glucose levels. MAGE was significantly lower with MIT/VOG (P = 0.016), whereas mean blood glucose levels were lower between 0:00 a.m. and 7:00 a.m. with 100 mg/day sitagliptin. The percentage of time with blood glucose level >/=200 mg/dl was significantly shorter with MIT/VOG (P = 0.041). The maximum blood glucose level was significantly lower with MIT/VOG (P = 0.043), and the minimum was significantly lower with 100 mg/day sitagliptin (P = 0.043). Blood glucose levels after dinner and mean increases in postprandial blood glucose levels were significantly lower with MIT/VOG (P = 0.090 and P = 0.045 respectively). In patients with T2DM, treatment with MIT/VOG improves MAGE and postprandial hyperglycemia and 100 mg/day sitagliptin lowers early morning glucose levels. This trial was registered with the University Hospital Medical Information Network (UMIN) (No. UMIN R000008274).
