Remogliflozin etabonate

Remogliflozin etabonate (GSK189075) is an orally active, selective and low-affinity sodium glucose cotransporter (SGLT2) inhibitor with Ki values of 1.95 μM, 2.14 μM, 43.1 μM, 8.57 μM for hSGLT2, rSGLT2, hSGLT1, rSGLT1, respectively. Remogliflozin etabonate is a prodrug based on benzylpyrazole glucoside and is metabolized to its active form, Remogliflozin, in the body. Remogliflozin etabonate exhibits antidiabetic efficacy in rodent models[1].

Research Areas >> Metabolic Disease

Signaling Pathways >> Membrane Transporter/Ion Channel >> SGLT

hSGLT1:43.1 μM (Ki)

rSGLT1:8.57 μM (Ki)

hSGLT2:1.95 μM (Ki)

rSGLT2:2.14 μM (Ki)

Remogliflozin etabonate (GSK189075; 10 or 30 mg/kg; orally; twice daily for 6 weeks) significantly reduced both the FPG and GHb levels in a dosedependent manner[1]. Remogliflozin etabonate (3, 10, 30 mg/kg; orally) increases urinary glucose excretion in a dose-dependent manner. Remogliflozin etabonate dose-dependently inhibits the increase in plasma glucose after glucose loading and decreases the plasma insulin in normal rats[1]. Remogliflozin etabonate (1-10 mg/kg; orally) decreases the blood glucose and reduces the AUC0–6 h for blood glucose in a dose-dependent manner[1]. Remogliflozin etabonate (high-fat diet containing 0.01, 0.03, or 0.1% remogliflozin etabonate for 8 weeks) reduces the levels of plasma glucose, plasma insulin, and GHb in a dose-dependent manner, and it suppresses the development of hypertriglyceridemia in male GK rats (6 weeks of age)[1]. Animal Model: db/db mice at the age of 8 weeks[1] Dosage: 10 or 30 mg/kg Administration: Orally; twice daily for 6 weeks Result: Significantly reduced both the fasting plasma glucose (FPG) and glycated hemoglobin (GHb) levels in a dosedependent manner. Reduced both urine volume and urinary glucose excretion with ameliorated the hyperglycemia.

[1]. Yoshikazu Fujimori, et al. Remogliflozin Etabonate, in a Novel Category of Selective Low-Affinity Sodium Glucose Cotransporter (SGLT2) Inhibitors, Exhibits Antidiabetic Efficacy in Rodent Models. J Pharmacol Exp Ther. 2008 Oct;327(1):268-76.