N-terminally modified GLP1R agonists drive G protein bias via extracellular loop 3 displacement.

This is a structural and mechanistic study combining cryo-EM, cell signaling assays, and diet-induced obese mice, not a clinical investigation. Semaglutide appears mainly as an acetylated variant used to probe biased GLP-1 receptor signaling, so the relevance is molecular rather than protocol-level. The findings are associated with a clearer picture of how modifications change receptor signaling and trafficking. Of interest to readers following the mechanistic and next-generation-molecule angle rather than human outcomes.