Portal hypertension and liver lesions in chronically alcohol drinking rats prevented and reversed by stable gastric pentadecapeptide BPC 157 (PL-10
GHK-Cu Peptide & Barrier Integrity (Preclinical Research) In a mouse model of DSS-induced ulcerative colitis, researchers observed that GHK-Cu influenced cellular signaling pathways related to barrier integrity, including: Tight junction protein expression SIRT1/STAT3 signaling pathways While this study was preclinical and not cosmetic-focused, it reinforced something researchers have long suspected: GHK-Cu interacts with fundamental cellular repair processes, not just surface-level skin processes [1]
The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice. Endocrinology 142(12):51825189
TB-500 (derived from Thymosin Beta-4) Often promoted to: accelerate muscle recovery reduce inflammation improve flexibility However, current evidence is largely limited to animal and laboratory studies, and strong human clinical trial evidence is lacking

Thus, we suggest that one single application of the NO-synthase (NOS) blocker N(G)-nitro-L-arginine methyl ester (L-NAME) may induce retinal ischemia in rats, and that the stable pentadecapeptide BPC 157 may be the therapy, since it may interact with the NO-system and may counteract various adverse effects of L-NAME application (see Wu et al., 2020) [i.e., activation of the VEGFR2-Akt-eNOS signaling pathway without the need of other known ligands or shear stress ( In the previous eye research studies, BPC 157 counteracts atropine-mydriasis, but it also opposes an immediate and hour-lasting miotic effect of L-NAME in rats and guinea pigs, and participates in pupil control potentially via NO-mediated and cholinergic mechanisms ( This may be essential for the effective counteraction of the damaging effect of the retrobulbar L-NAME application
After reconstitution: the peptide is dissolved in bacteriostatic water and must be refrigerated