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Moreover, DPP4 acts as a physiological substrate for glucosedependent insulinotropic polypeptide (GIP), which is another incretin hormone, and its levels rise in response to the inhibition of DPP4 activity [51, 110]

Critical reanalysis of the mechanisms underlying the cardiorenal benefits of SGLT2 inhibitors and reaffirmation of the nutrient deprivation signaling/autophagy hypothesis

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Recently, several efforts have been focused on the development of ML models for peptide 21,22 and small-molecule 23,24 design, demonstrating the success of these approaches in de novo prediction of functional molecules

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This route however appears to be largely ignored and probably will continue to be ignored, since the strategy so far has been to simply create agonists which are structurally designed to be resistant to DPP-4 (In fact, most modifications to extend the half-life of GLP1R/GIPR/GR agonists so far, do so by making the drugs resistant to DPP-4 )