Cagrilintide

Product Overview

Cagrilintide is a structurally modified amylin analog with enhanced stability and prolonged biological activity compared to native amylin. It achieves dual-receptor activation at calcitonin and amylin receptors through a bypass binding mode distinct from other existing DACRAs. Clinical trials show significant weight loss of 11.8% compared to 2.3% with placebo after 68 weeks, with promising results both alone and in combination with semaglutide.

Mechanism of Action

Cagrilintide mimics the naturally occurring hormone amylin, co-secreted with insulin after meals. Structural modifications overcome native amylin's tendency to form amyloid fibrils and its short half-life. It activates Gs signaling pathways through calcitonin receptors (CTR) and amylin receptors (AMY1R), crossing the blood-brain barrier to directly target satiety neurons.

Key Benefits

Appetite Control — Rapidly crosses the blood-brain barrier and activates calcitonin and amylin receptors in key brain regions. Causes genuine neurochemical changes in the hunger set point, reducing cravings for sweet and salty foods while increasing the feeling of fullness.

Post-Meal Glucose Management — Mimics the natural post-meal hormone pattern to significantly reduce post-meal glucagon secretion, directly contributing to lower blood glucose levels.

Delayed Gastric Emptying — Inhibits smooth muscle contractions in the stomach and partially relaxes the pylorus, providing sustained fullness, prolonged nutrient absorption, and stabilized post-meal blood glucose levels.

References

1. Enebo LB, et al. Safety, tolerability, pharmacokinetics of cagrilintide with semaglutide for weight management. *Lancet.* 2021;397:1736–1748.
2. Gadde KM, et al. Obesity: pathophysiology and management. *J Am Coll Cardiol.* 2018;71:69–84.
3. Zhao F, et al. Structural insights into multiplexed pharmacological actions of tirzepatide at the GIP, GLP-1 or glucagon receptors. *Nat Commun.* 2022;13:1057.