IpragliflozinSGLT2 inhibitor CAS# 761423-87-4 |
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Quality Control & MSDS
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| Cas No. | 761423-87-4 | SDF | Download SDF |
| PubChem ID | 10453870 | Appearance | Powder |
| Formula | C21H21FO5S | M.Wt | 404.45 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | ASP1941 | ||
| Solubility | DMSO : ≥ 100 mg/mL (247.25 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | (2S,3R,4R,5S,6R)-2-[3-(1-benzothiophen-2-ylmethyl)-4-fluorophenyl]-6-(hydroxymethyl)oxane-3,4,5-triol | ||
| SMILES | C1=CC=C2C(=C1)C=C(S2)CC3=C(C=CC(=C3)C4C(C(C(C(O4)CO)O)O)O)F | ||
| Standard InChIKey | AHFWIQIYAXSLBA-RQXATKFSSA-N | ||
| Standard InChI | InChI=1S/C21H21FO5S/c22-15-6-5-12(21-20(26)19(25)18(24)16(10-23)27-21)7-13(15)9-14-8-11-3-1-2-4-17(11)28-14/h1-8,16,18-21,23-26H,9-10H2/t16-,18-,19+,20-,21+/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 | Ipragliflozin (ASP1941) is a highly potent and selective SGLT2 inhibitor with IC50 of 2.8 nM; little and NO potency for SGLT1/3/4/5/6.
IC50 value: 2.8 nM [1][2]
Target: SGLT2
in vitro: Ipragliflozin potently and selectively inhibited human, rat, and mouse SGLT2 at nanomolar ranges and exhibited stability against intestinal glucosidases [3].
in vivo: Ipragliflozin showed good pharmacokinetic properties following oral dosing, and dose-dependently increased urinary glucose excretion, which lasted for over 12 h in normal mice [3]. Oral administration of ipragliflozin increased urinary glucose excretion in a dose-dependent manner, an effect which was significant at doses of 0.3 mg/kg or higher and lasted over 12 h [4]. Single administration of ipragliflozin dose-dependently increased urinary glucose excretion, reduced blood glucose and plasma insulin levels, and improved glucose intolerance [5]. References: | |||||
Ipragliflozin Dilution Calculator
Ipragliflozin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4725 mL | 12.3625 mL | 24.7249 mL | 49.4499 mL | 61.8123 mL |
| 5 mM | 0.4945 mL | 2.4725 mL | 4.945 mL | 9.89 mL | 12.3625 mL |
| 10 mM | 0.2472 mL | 1.2362 mL | 2.4725 mL | 4.945 mL | 6.1812 mL |
| 50 mM | 0.0494 mL | 0.2472 mL | 0.4945 mL | 0.989 mL | 1.2362 mL |
| 100 mM | 0.0247 mL | 0.1236 mL | 0.2472 mL | 0.4945 mL | 0.6181 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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Ipragliflozin is a selective inhibitor of sodium–glucose cotransporter 2 (SGLT2) with IC50 value of 7.38nM [1].
Ipragliflozin is a derivative of phlorizin. It shows inhibition activity for mouse, rat and human SGLT2 with IC50 values of 7.38nM, 6.73nM and 5.64nM, respectively. It is not effective for SGLT1 with IC50 value of 1876nM. In the radioligand binding and enzyme assays, lpragliflozin shows no interaction with other receptors, channels, and transporters like adrenergic, muscarinic and calcium channel, demonstrating a specific inhibition of SGLT2. As a glucitol compound, ipragliflozin is stable against glucosidases in mouse small intestine [1].
Since SGLT2 plays a critical role in renal glucose reabsorption, ipragliflozin is therapeutic potent to treat hyperglycemia in diabetes through increasing glucose excretion into urine. In STZ-induced type 1 diabetic rats and KK-Ay type 2 diabetic mice, the single administration of ipragliflozin significantly decreases the blood glucose levels [1].
References:
[1] Tahara A, Kurosaki E, Yokono M, Yamajuku D, Kihara R, Hayashizaki Y, Takasu T, Imamura M, Qun L, Tomiyama H, Kobayashi Y, Noda A, Sasamata M, Shibasaki M. Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo. Naunyn Schmiedebergs Arch Pharmacol. 2012 Apr;385(4):423-36.
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Drug-induced Liver injury Caused by Ipragliflozin Administration with Causality Established by a Positive Lymphocyte Transformation Test (LTT) and the Roussel Uclaf Causality Assessment Method (RUCAM): A Case Report.[Pubmed:28233736]
Ann Hepatol. 2017 March-April;16(2):308-311.
A 75-year old male patient had been regularly visiting our hospital for the management of his type 2 diabetes mellitus since he was diagnosed at age 64 years. When he developed hypoglycemic episodes with sulfonylurea, Ipragliflozin (50 mg/day) was started to replace the sulfonylurea therapy. However, 49 days after starting Ipragliflozin, his AST increased from 13 to 622 U/L, ALT increased from 9 to 266 U/L, ALP increased from 239 to 752 U/L, and (Upsilon-GTP) increased from 19 to 176 U/L. ZTT was 3.5 U, TTT was 0.4 U, and total bilirubin was 0.7 mg/dL. IgM hepatitis A antibody, hepatitis B antigen, hepatitis C virus antibody, IgM CMV antibody, and IgM EB VCA antibody were negative, whereas a lymphocyte transformation test for Ipragliflozin was positive. Abdominal CT scan showed mild fatty liver but no sign of nodular lesions. Following admission to our hospital, he received liver supportive therapy with the discontinuation of Ipragliflozin therapy. He was discharged from the hospital 18 days later with AST and ALT levels reduced to 20 U/L and 13 U/L, respectively. Based on the clinical presentation of this patient, it is highly important to monitor liver function along with other possible clinical complications (e.g., dehydration, ketosis, and urinary tract infection) associated with SGLT2 inhibitortherapy.
Effects of Ipragliflozin on Diabetic Nephropathy and Blood Pressure in Patients With Type 2 Diabetes: An Open-Label Study.[Pubmed:28090231]
J Clin Med Res. 2017 Feb;9(2):154-162.
BACKGROUND: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are novel agents used to treat type 2 diabetic patients. We investigated the efficacy of the SGLT2 inhibitor Ipragliflozin on diabetic nephropathy in Japanese patients with type 2 diabetes. METHODS: A 50 mg dose of Ipragliflozin was administered for 24 weeks to 50 patients with type 2 diabetes who were concomitantly managed with diet and exercise therapy alone or antidiabetic medications other than SGLT2 inhibitors. RESULTS: At the end of the 24-week Ipragliflozin treatment, significant decreases in mean glycated hemoglobin (HbA1c) (1.0+/-1.2%) and body weight (2.7 +/- 2.5 kg) were observed; in addition, median urinary albumin-to-creatinine ratio (UACR) significantly decreased from 15.5 (8.0 - 85.7) to 12.9 (7.4 - 36.3) mg/gCr. Sub-analysis by renal function at baseline revealed that median UACR in patients with estimated glomerular filtration rate (eGFR) >/= 90 mL/min/1.73 m(2) decreased significantly from 12.3 (7.5 - 89.6) to 10.6 (5.8 - 27.3) mg/gCr. Furthermore, mean eGFR decreased significantly from 102.4 +/- 8.6 to 93.6 +/- 10.5 mL/min/1.73 m(2) in these patients. In contrast, UACR and eGFR did not change significantly in patients with eGFR < 90. In addition, analysis of the relationship between the amount of change in UACR and blood pressure at 24 weeks revealed a significant positive correlation between UACR and SBP values, independently of the presence of diabetic nephropathy. CONCLUSIONS: Our results indicate that Ipragliflozin may facilitate HbA1c control and body weight reduction. Furthermore, our results also raise the possibility that Ipragliflozin significantly reduces urinary albumin levels and improves glomerular hyperfiltration in a subset of patients with type 2 diabetes.
Amelioration of fatty liver index in patients with type 2 diabetes on ipragliflozin: an association with glucose-lowering effects.[Pubmed:27980239]
Endocr J. 2017 Mar 31;64(3):363-367.
In this study, we investigated the ameliorating effects of Ipragliflozin on fatty liver in patients with type 2 diabetes. The factors that influenced the amelioration of fatty liver were also examined. Analysis included data of 21 Japanese patients with type 2 diabetes obtained from our prospective observational study. After obtaining patients' informed consent, once-daily Ipragliflozin (50 mg/day) was given for 16 weeks. In addition to several clinical parameters, body composition was also compared before and after 16 weeks of treatment. The extent of fatty liver was estimated using a fatty liver index (FLI). After 16 weeks, FLI significantly decreased, from 70.1 +/- 19.4 to 60.3 +/- 25.5 (p = 0.0009) as well as levels of fasting plasma glucose (FPG), HbA1c, body weight, visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and fat mass. To reveal the factors influencing the FLI changes observed on Ipragliflozin treatment, correlations between changes in FLI and several other measured parameters were examined. Changes in FPG (correlation coefficient = 0.4683, p = 0.0323) and HbA1c (correlation coefficient = 0.4383, p = 0.0469) showed significant positive correlations with changes in FLI. On the other hand, no correlations of changes in FLI were observed with body weight, VAT, SAT nor fat mass. In conclusion, Ipragliflozin ameliorated FLI in Japanese patients with type 2 diabetes. Improvement in FLI was associated with that of glucose intolerance.
Functional imaging of pharmacological action of SGLT2 inhibitor ipragliflozin via PET imaging using (11)C-MDG.[Pubmed:28116097]
Pharmacol Res Perspect. 2016 Jul 1;4(4):e00244.
Sodium-dependent glucose cotransporter 2 (SGLT2) is a pharmacological target of type 2 diabetes mellitus. The aim of this study was to noninvasively visualize the pharmacological action of a selective SGLT2 inhibitor Ipragliflozin in the kidney using positron emission tomography (PET) imaging with (11)C-methyl-d-glucoside ((11)C-MDG), an SGLT-specific radio-labeled substrate. PET imaging with (11)C-MDG in vehicle-treated rats demonstrated that intravenously injected (11)C-MDG substantially accumulated in the renal cortex, reflecting that the compound was reabsorbed by SGLTs. In contrast, Ipragliflozin-treated rats showed significantly lower uptake of (11)C-MDG in renal cortex in a dose-related manner, suggesting that Ipragliflozin inhibited the renal reabsorption of (11)C-MDG. This method of visualizing the mode of action of an SGLT2 inhibitor in vivo has demonstrated the drug's mechanism in reducing renal glucose reabsorption in kidney in living animals.
