What are the PK/PD properties for GLP-1 RAs and how do these differences affect their clinical roles? And specifically, how do long- vs. short-acting GLP-1 RAs affect PPG vs FPG?
What are the physiologic properties of incretin system-targeting agents?
What do we know about dosing as it might impact CV outcomes, for liraglutide in the LEADER Trial, and how does this compare to what we learned from SGLT2 inhibitor-based CV outcomes trials?
What are the translational implications of the LEADER trial based on the results reported at ADA 2016?
Can you review for us the design and rationale of the LEADER trial?
How do make sense of the results and designs of the various cardiovascular outcome trials, including the LEADER trial, in patients with T2D and what do you believe is the take home message?
What are the important developments at ADA 2016 as far as GLP-1 RAs?
How would specific basal insulin-GLP-1 RA combination agents be used in specific patient populations with T2D? Are there trials that shed light on this?
From a clinical perspective, who are the ideal patient candidates for the fixed ratio, combination formulations, i.e. glargine insulin plus lixisenatide vs. degludec insulin plus liraglutide?
Why is the combination of basal insulin and a GLP-1 RA logical from the standpoint of mechanistic complementarity?
What is the rationale for combining basal insulin plus GLP-1 RA into a fixed ratio formulation? How does this strategy impact pan-glycemic—FPG and PPG—control and other metabolic target goals and risk factors?
What incretin-targeted therapies are available to modulate the incretin hormones and what are the clinical differences among the available options?