Categories
Repair & Regeneration
Compounds studied for wound healing, tissue repair, and musculoskeletal recovery.
This category collects compounds whose primary research signal is on the biology of tissue repair — angiogenesis, extracellular-matrix remodelling, tendon and ligament healing, gut-lining integrity, and related processes. Most human evidence in this area is early or animal-derived.
Popular research blends often combine several agents in this category. Blends are noted separately on the site so their evidence base does not inherit strength from any single component.
Educational content only. If you have a musculoskeletal or wound-care question about your own body, contact a qualified clinician.
Compounds in this category
7 compounds in this category
Aura
Repair & RegenerationResearch BlendPreclinical EvidenceA three-component research blend combining GHK-Cu 50 mg, BPC-157 10 mg and KPV 10 mg in a single lyophilized vial (70 mg total). The three components address distinct but complementary layers of tissue repair: GHK-Cu modulates the expression of thousands of genes involved in ECM remodelling, collagen and elastin synthesis, angiogenesis and scarless healing; BPC-157 supports VEGF-driven angiogenesis, fibroblast migration and collagen production at the repair site; and KPV suppresses the NF-κB inflammatory pathway that would otherwise antagonise the ECM and vascular repair activities of the other two components. At the reference reconstitution (5 mL bacteriostatic water → 10 mg/mL GHK-Cu + 2 mg/mL BPC-157 + 2 mg/mL KPV) and 0.2 mL injection volume, all three components fall within their individually-established therapeutic ranges — a distinguishing feature of Aura relative to other multi-component repair blends. No blend-specific FDA authorisation exists; the individual components have their own regulatory profiles (see the component compound pages).
Learn moreBPC-157
Repair & RegenerationEarly Human EvidenceA synthetic 15-amino-acid fragment corresponding to a portion of a protein found in human gastric juice. Preclinical work — almost all of it from Sikiric's laboratory at the University of Zagreb — describes broad tissue-protective effects across gut, tendon, muscle, bone, brain, and vascular endpoints, with proposed mechanisms centred on VEGF-mediated angiogenesis, fibroblast migration, and modulation of the nitric oxide system. The compound has no approved indication in any jurisdiction and no completed phase-2 or phase-3 randomised trial in humans.
Learn moreBPC-157 / TB-500 Blend
Repair & RegenerationResearch BlendPreclinical EvidenceA two-component tissue-repair research blend combining BPC-157 and TB-500 in a 1:1 ratio, supplied as either a 5/5 mg (10 mg total) or 10/10 mg (20 mg total) lyophilized vial. The mechanistic rationale is direct: BPC-157 addresses the vascular supply and fibroblast recruitment side of tissue repair through VEGF-driven angiogenesis and NO-mediated signalling; TB-500 addresses the cellular migration side through actin polymerisation dynamics that enable repair cells and stem cells to reach injury sites. Together the two address the two most commonly rate-limiting layers of tissue repair — vascular supply and cellular movement — in a single reconstitution. Simpler than running the two peptides in parallel from separate vials.
Learn moreGHK-Cu
Repair & RegenerationModerate Human EvidenceAn endogenous copper-binding tripeptide (glycyl-L-histidyl-L-lysine complexed with copper(II)) first isolated from human plasma in 1973. GHK-Cu has the broadest gene-expression footprint characterised for any small research peptide — genome-wide microarray studies catalogue approximately 4200 human genes significantly modulated at physiological concentrations. Mechanistically, GHK-Cu functions as a copper-delivery vehicle: the tripeptide chelates and delivers copper into cells, where copper acts as an essential cofactor for enzymes involved in extracellular matrix synthesis, angiogenesis, antioxidant defense, and DNA repair. Approved and marketed for topical cosmetic use in many jurisdictions; not FDA-approved for systemic therapeutic indications.
Learn moreGlow
Repair & RegenerationResearch BlendPreclinical EvidenceA three-component research blend combining GHK-Cu 50 mg, BPC-157 10 mg and TB-500 10 mg in a single lyophilized vial (70 mg total). Structural repair with skin rejuvenation: GHK-Cu at the gene-expression / ECM signalling layer, BPC-157 at the vascular / fibroblast layer, and TB-500 at the cellular migration and cytoskeletal-remodelling layer. The mechanism story is complementary rather than redundant — each component addresses a distinct rate-limiting step in tissue repair. Relative to Aura, Glow substitutes TB-500 for KPV, trading inflammatory-environment control for cellular-migration capacity. The trade-off worth being honest about: at the 0.2 mL reference injection, TB-500 is delivered at maintenance levels rather than acute-injury loading levels. No FDA blend authorisation exists; the individual components have their own regulatory profiles.
Learn moreKlow
Repair & RegenerationResearch BlendPreclinical EvidenceA four-component research blend that combines all three peptide families addressed by the other repair blends plus the anti-inflammatory KPV component. Composition: GHK-Cu 50 mg + TB-500 10 mg + BPC-157 10 mg + KPV 10 mg = 80 mg total. The mechanism story covers all four rate-limiting layers of tissue repair: GHK-Cu at the gene-level ECM signalling layer, TB-500 at the cellular migration and cytoskeletal remodelling layer, BPC-157 at the vascular supply and fibroblast layer, and KPV at the inflammatory-environment control layer. In effect, Klow is Glow plus KPV — adding NF-κB pathway suppression to the three mechanistic components of Glow — and Aura plus TB-500 — adding cellular migration to the three components of Aura. It is the most comprehensive of the repair blends when all four components are available and the intended use warrants their combined effect.
Learn moreTB-500
Repair & RegenerationEarly Human EvidenceA 17-amino-acid synthetic peptide corresponding to the N-terminal actin-binding region of thymosin β4 — a 43-amino-acid endogenous protein. TB-500 is NOT thymosin β4 itself. Popular sources routinely treat the two as interchangeable; they are not. The mechanistic hypothesis is that the actin-sequestering region of Tβ4 alone recapitulates a subset of the parent protein's cell-migration and wound-healing effects. Human evidence for TB-500 specifically is essentially absent. The compound originated in equine veterinary use and is on the WADA prohibited list.
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