NameIpragliflozinSynonymsIpragliflozinIpragliflozin impuityIpragliflozinL-ProlineIpragliflozin (ASP1
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| Adı | Ipragliflozin |
| Eşanlamlar | Ipragliflozin Ipragliflozin impuity IpragliflozinL-Proline Ipragliflozin (ASP1941) (1S)-1,5-Anhydro-1-C-[3-[(1-benzothiophen-2-yl)methyl]-4-fluorophenyl]-D-glucitol Ipragliflozin, (1S)-1,5-Anhydro-1-C-[3-[(1-benzothiophen-2-yl)Methyl]-4-fluorophenyl]-D-glucitol |
| CAS'ın | 761423-87-4 |
| Moleküler Formül | C21H21FO5S |
| Molar Kütlesi | 404.45 |
| Yoğunluk | 1.452 |
| Erime noktası | 155-157°C |
| Boling Point | 628.8±55.0 °C(Predicted) |
| Çözünürlük | DMSO'da 10 mM |
| Görüntü | Sabit |
| Renk | Beyaz-Beyaz |
| pKa | 13.27±0.70(Predicted) |
| Depolama Koşulları | Dondurucu |
| In vitro çalışma | Ipragliflozin at nanomolar concentrations inhibited the activity of SGLT2 of mouse, rat and human origin in a concentration-dependent manner. Furthermore, ipragliflozin does not inhibit human SGLT4 and SGLT5(IC50>1,000 nM). ipragliflozin also did not inhibit certain GLUT subtypes such as GLUT1 and GLUT4(IC50>1,000 nM) in mouse 3T3-L1, rat L6, human Caco-2 and HepG2 cells. Ipragliflozin does not interact with various receptors, ion channels, transporters, such as adrenergic receptors (α1, α2, β), muscarinic receptors (such as M1, M2), angiotensin (AT1 and AT2), calcium channels (L-type and N-type), potassium channels (KATP and SKCa), sodium channels (site 2), intestinal secretin (CCKA and CCKB), dopamine (such as D1, D2), endothelin (ETA and ETB), gamma-aminobutyric acid (GABAA and GABAB), glutamate (AMPA, kainate and NMDA), serotonin (5-HT1, 5HT2B, and transporter), histamine (H1, H2, and H3) and neurokinin (NK1, NK2, and NK3),IC50>3000 nM. Ipragliflozin is not affected by the beta-glucosidase in the intestinal tract of mice, and maintains homeostasis. |
| In vivo çalışma | A single oral dose of 0.01-10 mg/kg of ipragliflozin induced urinary glucose excretion in normal and KK-Ay (type 2 diabetes model) mice. Single administration of ipragliflozin(0.1, 0.3 and 1 mg/kg) dose-dependently reduced blood glucose levels in KK-Ay and STZ rats. A single intravenous dose of 0.3 mg/kg or an oral dose of 1 mg/kg of ipragliflozin in rats was found to have a good bioavailability of about 71.7%. In normal mice, Ipragliflozin, after oral administration, has a good pharmacokinetic profile with a dose-dependent increase in urinary glucose excretion and sustained efficacy for 12 hours. In a model of diabetes, a single administration of ipragliflozin resulted in a dose-dependent, sustained Antihyperglycemic effect. The risk of hypoglycemia is low. One hour after oral administration of ipragliflozin(3 mg/kg) to normal mice, the plasma concentration reached a maximum and then gradually decreased. At 8 hours after administration, the blood concentration was still in a detectable state. In pharmacokinetic studies in mice, ipragliflozin has good oral biological activity, high drug concentrations that can be maintained in the body for a long time. The bioavailability of ipragliflozin in rats and monkeys was 71.7-90.7% and 74.5-75.3%, respectively. |
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