Healing and angiogenesis

The healing-and-angiogenesis class is the area of peptide pharmacology where mechanistic plausibility runs furthest ahead of human clinical evidence — and where the practitioner-protocol layer has built the most elaborate self-experimentation framework on top of an evidence base that is overwhelmingly rodent. Three molecules in this corpus interface with tissue repair through angiogenesis-coupled mechanisms: BPC-157 acts through the VEGFR2-eNOS-NO axis and tendon-fibroblast migration, TB-500 (thymosin β4) acts through actin sequestration and cell-migration regulation, and GHK-Cu acts through copper-dependent fibroblast collagen and elastin synthesis with dermal fibroblast effects.

This dossier surveys what each molecule actually does in the published literature, where the rodent-to-human translation gap sits for each, and which of the practitioner protocols and stack rationales survive contact with the evidence.

The most important framing for the class as a whole is honesty about evidence depth. Each peptide page on this list is explicit about the gap between mechanism and outcome data. The claim that BPC-157, TB-500, or GHK-Cu accelerates human tissue repair at biohacker-doses for biohacker-indications is supported by mechanistic plausibility, by extensive rodent data, by ophthalmic-development clinical trials in adjacent indications, and by practitioner observation — but not by the kind of large-cohort placebo-controlled human trials that would make the claims clinically established. The peptide pages are written accordingly; the dossier is the same.