If a clinician is contemplating the use of iDeglira or iGlarlixi in a T2D patient already on an oral antidiabetic agent who is not meeting HA1c goals, should the oral medication be adjusted in any way, or should it be discontinued?
From a practical perspective, how should we deploy the new ultra-long basal insulins and for which patient populations — T1D and/or T2D — are they best suited? How are these agents titrated?
What is the rationale for deploying more concentrated basal insulins — U200 degludec and U300 insulin glargine — and what advantages do they offer with respect to physiologic glycemic control and hypoglycemia risk?
Based on clinical profiles and metabolic parameters, which patients with T2D are ideally suited for treatment with a fixed ratio, combination of insulin and a GLP-1 RA?
What options and evidence are available to guide us in adding antiglycemic agents to intensify basal insulin therapy? What is the role and rationale for using a fixed ratio insulin-GLP- 1 RA combination formulation?
What are the practical, translational implications of LEADER and how might we explain, mechanistically or physiologically, the reduction in MACE events observed in the liraglutide group?
What were the results of the LEADER trial? How were critical CV risk parameters such as BP, weight and HA1c levels affected? What was the take-away implication of this CV outcomes trial?
How was liraglutide titrated and what dose end point were you trying to achieve? What was the adherence rate to the study medication in the liraglutide arm?
Can you detail the background characteristics of the patient cohorts studied in the LEADER Trial? What percentage of patients was evaluated for primary prevention vs. secondary prevention of cardiovascular events?
What was the rationale and clinical design framework for the LEADER trial? What were the inclusionary and exclusionary criteria and what was the objective of the trial as it relates to the GLP-1 RA liraglutide?