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Although canonically GLP1Rs signal through the stimulatory alpha Gs protein, we find that semaglutide utilizes both Gs- and Gq-signaling pathways in GLP1Rs in the area postrema (AP)the primary site of semaglutide action in the brainto differentially regulate neuronal activation across distinct neuronal clusters

Shows distinct binding dynamics versus native amylin and salmon calcitonin, with cryoEM data indicating unique conformational effects on CTR/RAMP complexes that may underlie its robust and durable anorectic activity

After ceasing, the rebound rate of weight gain was much greater for the medication group than placebo