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Representing the leading edge of incretin pharmacology research, R (GLP 3) builds on the dual-agonist mechanism of T (GLP 2) by adding glucagon receptor activity enabling investigation into the additive metabolic effects of all three incretin axes simultaneously

The four amino-acid substitutions relative to native GHRH(1-29) are engineered to resist that enzymatic degradation particularly cleavage by dipeptidyl peptidase-4 (DPP-4) at the N-terminus which extends the peptides functional plasma half-life modestly relative to unmodified sermorelin-type fragments

Platelet hyperactivation that occurs during inflammatory states (e.g., T2DM) facilitates the pathogenesis of CVDs (Figure 2C) (65)

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