TB-500 vs GHK-Cu

Both get filed under repair. They act on different tissue, through unrelated chemistry, and the evidence behind them is not of the same kind.

TB-500 is a synthetic 17-amino-acid fragment of thymosin beta-4. Its defining property is sequestering monomeric G-actin, and the associated literature covers cytoskeletal dynamics, cell migration and VEGF-linked angiogenesis. It is preclinical. Human trials of the full thymosin beta-4 protein exist in a small number of specific settings, and those are not trials of this fragment as supplied — a distinction that gets lost in most of what is written about it elsewhere.

GHK-Cu is not a straight peptide at all but a tripeptide-copper complex, Gly-His-Lys coordinated to a copper ion, and the copper is not packaging. The research is dermatological: collagen synthesis and dermal stem-cell signalling, with a body of in-vitro and topical work behind it that has no equivalent on the TB-500 side.

So the decision is tissue and route. A question about connective tissue and vascular response is not a question about dermal matrix, and the two literatures do not transfer.

One thing the table shows by omission: the purity column can be empty for GHK-Cu, because the catalogue does not publish a release specification for it the way it does elsewhere. We would rather show that gap than fill it.

Both are stored at 2–8 °C and supplied for laboratory research only.