Peptide Library

Appears to promote blood-vessel formation and tissue repair — mostly shown in rodents.

Profile in production — references being resolved.

Binds actin to regulate cell movement, supporting wound closure and reduced scarring.

Carries copper into cells and shifts gene expression toward repair.

Dampens inflammatory signalling (NF-κB) inside immune and gut-lining cells, partly by being carried into cells through the PepT1 transporter, without the pigmentation effects of full α-MSH

Activates the "innate repair receptor" (a pairing of the EPO receptor with the β-common receptor CD131) that is switched on in injured tissue, producing EPO's tissue-protective effects without stimulating red blood cell production

Punches holes in bacterial membranes directly and acts as an immune signal — recruiting white cells, binding bacterial endotoxin, promoting wound closure and new blood vessels

Buffers acid in muscle, scavenges reactive oxygen species and reactive aldehydes, chelates metals, and blocks the formation of advanced glycation end-products (AGEs) that stiffen and damage proteins

Slows the division of blood-forming stem cells and dampens TGF-β-driven scarring; broken down by ACE, so ACE inhibitors raise its level several-fold

Acts locally in the gut lining to stop tight junctions between cells from loosening, so fewer gluten fragments and other large molecules slip through

Activates GC-C receptors on the surface of the intestinal lining, raising cGMP, which drives chloride and bicarbonate (and therefore water) into the gut lumen to soften stool and speed transit, while cGMP leaking from the cells quietens…

Activates guanylate cyclase-C on the gut lining, raising cGMP, which pushes chloride and water into the bowel and softens stool; cGMP also damps visceral pain nerves

Released by duodenal S cells when acid arrives; tells the pancreas to pour out bicarbonate-rich fluid and the stomach to release gastrin in people with gastrinoma — the basis of its diagnostic uses

Released by duodenal I cells after a fatty or protein-rich meal; contracts the gallbladder, drives pancreatic enzyme secretion, slows stomach emptying and signals fullness to the brain via the vagus nerve

Mimics the gut hormone GLP-2: thickens and lengthens the intestinal lining, increases blood flow and nutrient absorption, and slows transit — so people with very short bowels absorb more from what they eat and need less intravenous feeding

Activates the GLP-2 receptor in the gut to increase villus height, mucosal surface area and nutrient absorption, so people on intravenous nutrition can reduce it

Activates the intestinal GLP-2 receptor to expand absorptive mucosal surface, reducing the intravenous nutrition and fluid people with short bowel syndrome need