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Whether a given study design benefits from synchronising with that pulse, or deliberately offsetting it, depends on the readout being measured, because the timing affects whether the exogenous GH signal amplifies or dampens the endogenous pulse

The C18 fatty diacid-albumin binding mechanism that extends Semaglutides half-life to one week also modifies its receptor pharmacology in important ways relative to native GLP-1 , the albumin-bound form of Semaglutide that constitutes the pharmacokinetically relevant circulating species interacts with GLP-1R through a receptor engagement profile influenced by the bulky albumin-fatty acid complex, potentially modifying receptor internalisation kinetics, biased signalling between Gs, Gq/11, and beta-arrestin pathways, and the duration and amplitude of downstream signalling relative to native GLP-1 or shorter-acting analogues

And that's another thing we didn't talk about