In the obesity landscape, glucagoon-like peptide-1 (GLP-1) agonists dominate the weight loss market. Amylin agonists work differently from GLP-1s but may be able to induce similar weight loss with fewer adverse events. My client wanted to understand the molecular differences between various amylin assets and their hypothetical impacts on the efficacy / adverse event profile.

Project’s key research questions/topics include:
(1) Describe the medical literature as it pertains to Amylin for obesity specifically – e.g. years researching, articles on Amylin published, clinical trials, or other types of experience – please specify.

(2) Comment on the differences between cagrilintide, petrelintide, amycretin and any other amylin agonists?

(3) Describe the theoretical physiologies of the various subsets within amylin receptors (calcitonin, AMY1R, AMY2R, AMY3R).

(4) Comment on whether the pH of the assets differ, and whether these could have material impacts on the drug profile?

(5) Comment on the solubility of cagrilintide and other amylin assets, as well as the corresponding impacts on the drug profile (e.g. half-life)?

Despite the similarities between GLP-1 and Amylin agonists (e.g. both molecular classes slow gastric emptying, decrease glucagon, and inhibit food intake), there are important distinctions between the central and/or peripheral pathways that mediate their effects on hyperglycemia and energy balance.