Nicholas A. Di Prospero

TL;DR: There is a growing body of evidence to suggest that impaired mitochondrial function may affect key cellular processes, thereby altering synaptic functioning and contributing to the atrophic changes that underlie the deteriorating long-term course of these illnesses.

TL;DR: The studies in diabetic CETP-ApoB100 transgenic mice recapitulate many of the changes in circulating lipids found with SGLT2 inhibition therapy in humans and suggest that the increased LDL cholesterol found with this therapy is because of reduced clearance of LDL from the circulation and greater lipolysis of triglyceride-rich lipoproteins.

TL;DR: Results from the preclinical and clinical studies led canagliflozin to be the first‐in‐class SGLT2 inhibitor approved in the United States, and support canag liflozin as a safe and effective therapeutic option across a broad range of patients with T2DM.

TL;DR: Coadministration of canagliflozin with rifampin, probenecid, and cyclosporine A was well-tolerated and could necessitate an appropriate monitoring of glycemic control.

TL;DR: Plasma canagliflozin exposures were dose‐proportional as the 90% CI of the slope of the regression line for dose‐normalized AUC∞ and Cmax fell entirely within the prespecified limits of −0.124 to 0.124; no clinically significant safety issues were noted, and canag liflozin was generally well‐tolerated.