Ipragliflozin - CAS 761423-87-4
Catalog number: 761423-87-4
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C21H21FO5S
Molecular Weight:
404.45
COA:
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Targets:
SGLT
Description:
Ipragliflozin is a highly potent and selective SGLT2 inhibitor and has little and NO potency for SGLT1/3/4/5/6.
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Purity:
>98%
Synonyms:
ASP-1941
MSDS:
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1.Ipragliflozin effectively reduced visceral fat in Japanese patients with type 2 diabetes under adequate diet therapy.
Yamamoto C1, Miyoshi H, Ono K, Sugawara H, Kameda R, Ichiyama M, Yamamoto K, Nomoto H, Nakamura A, Atsumi T. Endocr J. 2016 Apr 6. [Epub ahead of print]
To investigate if Ipragliflozin, a novel sodium-glucose co-transporter 2 inhibitor, alters body composition and to identify variables associated with reductions in visceral adipose tissue in Japanese patients with type 2 diabetes mellitus. This prospective observational study enrolled Japanese participants with type 2 diabetes mellitus. Subjects were administered Ipragliflozin (50 mg/day) once daily for 16 weeks. Body composition, visceral adipose tissue volume and plasma variables were measured at 0, 8, and 16-weeks. The subjects' lifestyle habits including diet and exercise were evaluated at baseline and 16 weeks. The primary endpoint was defined as the decrease of visceral adipose tissue mass. Twenty-four of 26 enrolled participants completed the study. The visceral adipose tissue decreased significantly (110 ± 33 to 101 ± 36 cm2, p = 0.005) as well as other parameters for metabolic insufficiency including hemoglobin A1c. Seventy-one % of the total body weight reduction (-2.
2.Effect of ipragliflozin, an SGLT2 inhibitor, on progression of diabetic microvascular complications in spontaneously diabetic Torii fatty rats.
Takakura S1, Toyoshi T2, Hayashizaki Y3, Takasu T3. Life Sci. 2016 Feb 15;147:125-31. doi: 10.1016/j.lfs.2016.01.042. Epub 2016 Jan 29.
AIMS: We investigated the effect of the selective sodium-dependent glucose cotransporter 2 inhibitor ipragliflozin on the simultaneous progression of diabetic microvascular complications of retinopathy, nephropathy and neuropathy in individual Spontaneously Diabetic Torii (SDT) fatty rats.
3.Ipragliflozin, a sodium-glucose cotransporter 2 inhibitor, ameliorates the development of liver fibrosis in diabetic Otsuka Long-Evans Tokushima fatty rats.
Nishimura N1, Kitade M2, Noguchi R1, Namisaki T1, Moriya K1, Takeda K1, Okura Y1, Aihara Y1, Douhara A1, Kawaratani H1, Asada K1, Yoshiji H1. J Gastroenterol. 2016 Mar 29. [Epub ahead of print]
BACKGROUND: It is widely understood that insulin resistance (IR) critically correlates with the development of liver fibrosis in several types of chronic liver injuries. Several experiments have proved that anti-IR treatment can alleviate liver fibrosis. Sodium-glucose cotransporter 2 (SGLT2) inhibitors comprise a new class of antidiabetic agents that inhibit glucose reabsorption in the renal proximal tubules, improving IR. The aim of this study was to elucidate the effect of an SGLT2 inhibitor on the development of liver fibrosis using obese diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats and their littermate nondiabetic Long-Evans Tokushima Otsuka (LETO) rats.
4.Ipragliflozin as an Initial Therapy in Drug Naïve Subjects with Type 2 Diabetes.
Kutoh E1, Wada A2, Murayama T1, Hirate M1. Drug Res (Stuttg). 2016 Apr 7. [Epub ahead of print]
Objectives: The aim of this study is to investigate ipragliflozin as an initial type 2 diabetes (T2DM) drug. Methods: Ipragliflozin 25-50 mg/day monotherapy was performed with drug naïve subjects with T2DM (n=31). As a comparator, 12.5-25 mg/day alogliptin monotherapy was undertaken (n=32). At 3 months, levels of metabolic parameters were compared with those at baseline. Findings: 4 subjects discontinued ipragliflozin due to intolerance or adverse events, while none dropped out with alogliptin. At 3 months, similar decreases of HbA1c levels were observed with these 2 drugs (10.21-8.31%, p<0.00001, with ipragliflozin, and 10.08-8.25%, p<0.00001, with alogliptin), however fasting blood glucose (FBG) levels decreased with significant inter-group differences (- 23.5% with iprgliflozin and - 10.8% with alogliptin). While similar increases of homeostasis model assessment (HOMA)-B levels were observed with these 2 drugs, HOMA-R levels significantly decreased only with ipragliflozin (-19.
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CAS 761423-87-4 Ipragliflozin

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