Yay-Z1 said:
Could yall be confusing Cagri with Pramlintide
Here's something I wrote. Does it answer your question?
Cagrilintide retains the three proline substitutions that pramlintide made to human amylin to make it resistant to fibrillation, but it has four more improvements:
While pramlintide has a short half-life and must be dosed multiple times per day, researchers created a long-acting version that allows once-weekly dosing by adding a long fatty acid chain to the pramlintide molecule. The fatty acid allows cagrilintide to bind to albumin (a protein in the blood). When bound to albumin, cagrilintide is cleared from the body more slowly.
Researchers made cagrilintide resistant to a chemical reaction called deamination, which can break down the molecule, by replacing the asparagine amino acid (Asn) at position 14 with glutamic acid (Glu). Note: deamiNation is a distinctly different process from deamiDation (the latter leading to fibrillation).
They also made cagrilintide more soluble, meaning it dissolves more easily in water, by replacing valine (Val) with arginine (Arg) at position 17.
While pramlintide is a single-hormone agonist for amylin receptors, cagrilintide is a dual-hormone agonist for both amylin and calcitonin receptors. This is due to proline (Pro) being replaced by Tyrosine (Tyr) at position 37.
Those are the only four changes made to pramlintide to create cagrilintide. One important thing to note is that none of the changes made pramlintide more resistant to fibrillation or more stable at a higher pH. This means that any research on the pH requirements or fibrillation of pramlintide will also apply to cagrilintide.