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Peptijournal · GHK-Cu vs BPC-157 vs TB-500 · https://peptijournal.com/compare?c=ghk-cu,bpc-157,tb-500 · Impreso
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01Protocol
GHK-Cu
- Start
- 1 mg
- Range
- 1–2 mg
- Frequency
- Once daily
- Cycle
- 4–8 weeks
- Vials
- 50 / 100 mg
BPC-157
- Start
- 0.25 mg
- Range
- 0.25–0.5 mg
- Frequency
- Once or twice daily
- Cycle
- 4–8 weeks
- Vials
- 5 / 10 mg
TB-500
- Start
- 2 mg
- Range
- 2–5 mg per week
- Frequency
- 2× weekly (loading), then weekly
- Cycle
- 4–6 week loading, then maintenance
- Vials
- 5 / 10 mg
- Ajuste gradual
- Weeks 1–4: 2–2.5 mg, twice weekly
- Weeks 5+: 2 mg, once weekly
02Quick calculator
GHK-Cu
BPC-157
TB-500
03Mechanism of action
GHK-Cu
GHK (glycyl-L-histidyl-L-lysine) is an endogenous tripeptide found in human plasma, saliva and urine that binds Cu(II) with high affinity. The GHK-Cu complex is studied as a copper-delivery and signaling molecule: in fibroblast cultures it stimulates collagen and glycosaminoglycan synthesis, modulates metalloproteinases and their inhibitors, and gene-expression analyses associate GHK with shifts in many genes linked to tissue remodeling, antioxidant response and inflammation.
BPC-157
BPC-157 is a 15-amino-acid fragment of a protein found in gastric juice. Preclinical studies associate it with increased growth-hormone-receptor expression, angiogenesis pathways (including VEGF-related signalling) and lower inflammatory cytokines. The exact receptor target is not established.
TB-500
TB-500 has been analytically identified as the acetylated thymosin β4 residues 17–23 fragment, Ac-LKKTETQ; some suppliers also use that name for full-length 43-amino-acid thymosin β4. These are not interchangeable. The wound-repair findings below concern full-length thymosin β4, which binds G-actin and participates in cell migration; confirm the sequence of any supplier-labeled product.
04Study endpoints
GHK-Cu
- Increased collagen synthesis in cultured human fibroblasts at nanomolar concentrations (in vitro).
- Enhanced wound contraction, angiogenesis and extracellular-matrix deposition in animal wound models.
- Connectivity Map analyses link GHK to reversal of gene-expression signatures associated with tissue damage and aging.
- Topical cosmetic studies report changes in skin density, elasticity and fine-line measurements.
BPC-157
- A 2025 systematic review found 36 studies: 35 preclinical and 1 clinical.
- Animal models showed improved functional, structural and biomechanical outcomes in muscle, tendon, ligament and bone injuries.
- The only clinical study was a small retrospective series: 7 of 12 patients with chronic knee pain reported relief for more than 6 months.
TB-500
- In a rat full-thickness wound model, thymosin β4 increased re-epithelialisation by 42% at day 4 and up to 61% at day 7 vs saline.
- In the same full-length thymosin β4 study, treated wounds contracted at least 11% more by day 7, with more collagen deposition and new blood vessels.
- Full-length thymosin β4 increased keratinocyte migration 2–3-fold in cell-culture assays; this is not evidence for an arbitrary TB-500-labeled vial.
05Safety & regulatory findings
GHK-Cu
- Used as an ingredient in topical cosmetic products; not approved by the FDA as a drug for any indication.
- Most mechanistic evidence is from cell culture and animal models. Human topical research also includes controlled diabetic-ulcer studies; those formulations and wound-care settings do not establish injectable benefits.
- Plasma GHK levels are reported to decline with age, a basis for its study in aging research.
BPC-157
- Not FDA-approved for any use and listed as prohibited by the World Anti-Doping Agency.
- The cited human evidence does not establish systemic human pharmacokinetics; experimental clearance findings are not a validated human half-life for this research vial.
- Preclinical safety studies reported no organ toxicity, but the 2025 review found no clinical safety data.
TB-500
- Most evidence is on full-length thymosin β4; data on the TB-500 fragment itself is limited.
- Not approved for human use; listed as prohibited by the World Anti-Doping Agency.