Retatrutide + cagrilintide (10Mg)

Retatrutide — Triple Receptor Agonist

Retatrutide simultaneously activates:

• GLP-1 receptors > appetite suppression, gastric slowing

• GIP receptors > metabolic effiency, insulin sensitivity modulation

• Glucagon receptors> increased energy expenditure, fat oxidation

Its defining feature is that it does not only reduce food intake, but also actively increases metabolic throughput, particularly via hepatic and mitochondrial pathways.

Cagrilintide — Long-Acting Amylin Analogue

Cagrilintide is a synthetic analogue of amylin, a hormone co-secreted with insulin that governs meal termination and post-meal satiety. Its core actions include:

• Early satiety signaling

• Prolonged fullness after meals

• Reduced meal size and eating frequency

• Brainstem-mediated gastric slowing

Cagrilintide primarily refines how meals end, rather than how hunger begins.

This combination is powerful because each compound acts on different anatomical and neurohormonal layers.

A. Central Nervous System Integration

• Retatrutide acts strongly in the hypothalamus, suppressing hunger drive and food reward while simultaneously activating glucagon-linked energy signaling

• Cagrilintide acts predominantly in the area postrema and brainstem, reinforcing satiety and fullness perception

Together, they:

• Suppress hunger initiation

•  Accelerate satiety onset

• Extend post-meal fullness

• Reduce hedonic and compulsive eating

This results in behavioral appetite silence, not forced restriction.