Shop Metabolic

The triple agonist. One 39-residue molecule pulling the GIP, GLP-1 and glucagon receptors at the same time, built on a GIP backbone with an exendin-4 tail.

Almost nothing on this shelf ever finished. This one went the entire distance, cleared an FDA approval in 2010, and it was built in Montreal.

Another one with no amino acids in it, sitting in the peptide aisle under false pretences. Cation mass 159.21, which is roughly a tenth of the smallest actual peptide we stock.

Your pancreas sends two signals every time you eat, not one. Almost nobody outside the field has heard of the second one. Cagrilintide is a long-acting copy of it.

For twenty years GIP was the incretin receptor nobody wanted, written off as the one that was not earning its place in the system. Tirzepatide was built to pull it on purpose, and the field had to go back and re-read its own literature.

The trial read out and it did not work. So rather than shelve the compound, somebody changed what it was for a living. That is the whole story and it is why you can buy it.

Cut six amino acids off the front of a peptide and it got roughly ten thousand times more active. That result, from 1987, is the reason this entire shelf exists.

Every dual agonist on this shelf was designed by somebody. This one is based on a molecule your own gut has been making the whole time.

Nearly everything written about this compound is actually about a different molecule. Sorting out which is which is most of the work of understanding it.

Most compounds are built to talk to a cell. This one was built to find an address and take the building down. That difference is the entire reason to be careful with it.

Two different satiety signalling systems in one vial. Which sounds simple until you try to work out which half any given result belongs to.

The original incretin, exactly as your gut makes it, no edits. Plasma half-life about one minute, which is why every famous analogue exists and why this one is strictly a reference material.