Type 2 diabetes mellitus (T2DM) is a growing and serious global health problem. Pharmacological inhibition of the sodium–glucose cotransporter-2 (SGLT2) increases urinary glucose excretion, decreasing plasma glucose levels in an insulin-independent manner. PF-04971729 is a potent and selective SGLT2 inhibitor with IC50 value of 0.877 nM for h-SGLT2 and it has a 2000-fold increase in selectivity for human SGLT2 over SGLT1 in vitro. Diseases or conditions that can be ameliorated by inhibition of SGLT2 with PF-04971729 include: Type II diabetes, diabetic nephropathy, insulin resistance syndrome, hyperglycemia, hyperinsulinemia, hyperlipidemia, impaired glucose tolerance, obesity (including weight control or weight maintenance), hypertension and reducing the level of blood glucose. PF-04971729 can also be used for treating analogous diseases or conditions in animals. PF-04971729 is rapidly absorbed in preclinical species after oral administration, and it is characterized by low clearance and a moderate steady-state distribution volume. PF-04971729 is well absorbed in humans and eliminated largely via glucuronidation. PF-04971729 improved glycemic control, body weight and blood pressure in 328 patients with T2DM suboptimally controlled on metformin, and was well-tolerated[3].
Ertugliflozin/埃格列净 细胞实验
Cell Line
Concentration
Treated Time
Description
References
C2C12 cells
10 μM
Under hyperglycemic conditions, Ertugliflozin significantly increased the viability of C2C12 cells and inhibited hyperglycemia-induced cell death.
Acta Pharmacol Sin. 2023 Jun;44(6):1161-1174
BV-2 microglia
10 or 20 µM
24 hours
To evaluate the effect of Ertugliflozin on high glucose-induced inflammatory toxicity. Results showed that Ertugliflozin did not significantly inhibit BV-2 microglial proliferation or protect cells from high glucose-induced cytotoxicity.
Biomedicines. 2023 Dec 22;12(1):36
human-umbilical-vein endothelial cells (HUVECs)
100 µM
Investigate the effects of Ertugliflozin on mitochondrial oxidative phosphorylation and glucose uptake. Results showed no significant effect on OCR at 100 µM.
Int J Mol Sci. 2022 Jul 19;23(14):7966
human-umbilical-vein endothelial cells (HUVECs)
10 µM
Investigate the effects of Ertugliflozin on mitochondrial oxidative phosphorylation and glucose uptake. Results showed no significant effect on OCR at 10 µM.
Evaluate the effects of Ertugliflozin on mitochondrial function, high-energy phosphates, and genes encoding mitochondrial proteins, preventing myocardial hypertrophy and diastolic dysfunction
J Am Heart Assoc. 2021 Jul 6;10(13):e019995
Mice
Gαq-overexpressing mice
Oral
0.5 mg/g chow
16 weeks
ERTU treatment prevented cardiac hypertrophy, dilation, contractile dysfunction, myocyte apoptosis, and interstitial fibrosis in Gαq mice, and improved mitochondrial function.
J Mol Cell Cardiol Plus. 2025 Apr 9;12:100296
C57BL/6J mice
High fat, high sucrose (HFHS) diet-induced diabetic cardiomyopathy (DCMP) model
Dietary administration
0.5 mg/g of diet
One month duration
ERTU decreased myocardial intracellular sodium levels, improved energetics and contractile function
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