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I think most people think about these processes in terms of a single, ideal bound conformation of the peptide to the receptor as the basis for signalling, says Gellman, but Im increasingly suspecting that certain modes of dynamics are critical for signalling. He is now trying to design this structural variability into his hybridtides to see if this will improve on the performance of GLP-1 drugs

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559 These predictions inform rational design of combination therapies that strategically exploit compensatory relationships rather than acting blindly upon isolated mechanisms

The biggest biological difference: Semaglutide acts through GLP-1 activity, while tirzepatide acts through both GIP and GLP-1 activity

it is the explanation for almost every feature of the drugs