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Amylin/Calcitonin Receptor Agonism (cagrilintide) Delays gastric emptying, reduces postprandial glucagon, and strongly promotes satiety Modulates appetite-regulating centers in the hindbrain, hypothalamus, and brain reward circuits, directly influencing food intake and choice May transiently activate the renin-angiotensin-aldosterone system with dose escalation, but without blood pressure or electrolyte derangements GLP-1 Receptor Agonism (semaglutide) Stimulates glucose-dependent insulin secretion and suppresses glucagon release to improve glycemic control Reduces appetite and ad libitum energy intake, with central effects on GLP-1R-expressing nuclei in hypothalamus and brainstem Delays gastric emptying and increases satiety, contributing to progressive bodyweight loss Pharmacokinetic Profile Route of Administration Subcutaneous Dosing Frequency Once weekly Route of Administration : Subcutaneous Injection Dosing Frequency: Once weekly Half -life: Cagrilintide: 7-8 days

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All timelines beyond 12 weeks in this article are extrapolations based on the mechanism of action and user reports, not clinical evidence

Amylin works through different brain regions than GLP-1, particularly the area postrema and hindbrain, to enhance satiety signaling and suppress glucagon