Given the multiple diabetes- and non-diabetes-focused therapies — statins, SGLT2 inhibitors, antihypertensive agents, etc. — we can use to reduce CV risk in patients with T2D, where do you see liraglutide fitting in based on LEADER?
Since the reduction in non-fatal MI in the LEADER trial was not significant enough to explain the impressive 22% in CV mortality, what factors do you think might have played a role?
What did we learn about the degree of glycemic control achieved with liraglutide in the LEADER trial? And might the differences in glycemic exposure and other metabolic factors explain the reduction on kidney disease?
Can you drill down into the results of LEADER, including primary end points and breakdown of MACE events? What did we learn about the dose of liraglutide required for CV outcome improvement?
What is the foundational importance of the LEADER trial and what makes it different and, perhaps, more significant than previous trials evaluating strategies for CV risk reduction in T2D?
What is the principal take-away from the LEADER trial about the role of liraglutide in patients with T2D and CV risk factors?
What did we learn from the LEADER trial about regimen adherence with once-daily liraglutide?
What did we learn from the reduction in microvascular end points — including those reflecting renal function — reported in the LEADER trial?
What are the significant differences in time points and types of vascular benefits seen in LEADER using a GLP-1 RA vs the EMPA-REG trial which evaluated an SGLT2 inhibitor?
Given the positive results of LEADER, can you speculate on the likely mechanisms that explain the CV risk reduction that was observed?
In your view, what impact should, and will, the LEADER trial have on clinical management of patients with T2D, especially those at risk for cardiovascular disease?
What metabolic and hemodynamic parameters were affected most significantly in LEADER and what new information did we learn about the safety profile of liraglutide?