Receptor targets explained

Incretin receptors: GLP-1, GIP and glucagon

These sit in the pathways governing insulin response, gastric emptying and appetite signalling after eating. Semaglutide acts on GLP-1 alone; tirzepatide adds GIP; retatrutide adds glucagon on top of both (one receptor against three). Each addition is a different pathway rather than more of the same, which is why receptor count is the organising axis for the incretin class.

Growth hormone: GHRH receptor and the ghrelin receptor

Two independent inputs reach the same output across the growth hormone peptides. GHRH analogues — tesamorelin, CJC-1295, sermorelin — act on the GHRH receptor and amplify the size of a growth hormone pulse. Secretagogues such as ipamorelin act on the ghrelin receptor and trigger a pulse instead.

Because the inputs are independent, the research convention is to combine one of each rather than choose between them (see why CJC-1295 and ipamorelin are combined).

Melanocortin receptors: MC1R, MC3R and MC4R

MC1R sits on melanocytes and drives pigmentation. MC3R and MC4R sit in pathways governing appetite and sexual function. Afamelanotide is MC1R-selective; melanotan II is not, which is the mechanistic reason its reported effects extend well beyond skin (see MC1R-selective vs non-selective).

This family, covered under cosmetic peptides, is the clearest illustration of why selectivity is not a technical footnote — the same molecular class produces entirely different profiles depending on how narrowly it binds.

Where the model does not apply

Not everything in the catalogue is a receptor agonist. NAD+ (covered under mitochondrial peptides) is a coenzyme in cellular energy metabolism rather than a signalling molecule binding a receptor, and GHK-Cu is a copper-binding tripeptide whose activity is tied to the complex it forms. Applying a receptor-selectivity frame to either would misdescribe them.