Activates incretin signaling to potentiate glucose-dependent insulin secretion, delay gastric emptying, and reduce appetite.

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Mediates GIP-dependent insulin secretion; co-agonism with GLP-1R is thought to enhance weight loss and glycemic control.

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Activation increases hepatic glucose output and energy expenditure; biased/co-agonist approaches aim to preserve lipid oxidation and satiety without hyperglycemia.

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Amylin receptor activation reduces food intake via central satiety signaling and slows gastric emptying.

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Inhibits endocrine secretion and cell proliferation; relevant for several peptide therapeutics outside the metabolic space.

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