INJURY REPAIR
3-Phase Recovery
12 week structured protocol
BPC-157
Restores angiogenesis and perfusion. Activates VEGFR2-Akt-eNOS signaling, accelerates fibroblast migration and upregulates Type I/III collagen.
TB-500
Regulates actin dynamics for efficient cell migration and proper spatial organization. Reduces adhesions between tissue planes.
GHK-Cu
Regulates matrix metalloproteinases to break down disorganized collagen while upregulating organized synthesis. Orchestrates transition from reactive scar tissue to functional matrix.
KPV
Directly blocks NF-κB—the master transcription factor orchestrating inflammatory gene expression—with precision and without systemic immunosuppression.
NAD+
Powers cellular energy systems driving all tissue regeneration. Fuels metabolic processes behind collagen production, DNA repair, and cellular turnover—giving cells the energy reserves needed to execute healing.
Angiogenesis stops, fibroblasts go dormant—tissue can't get nutrients or healing signals
Overactive immune response creates heat, swelling, pain—blocks tissue from rebuilding
Disorganized collagen forms scar tissue—weak, inflexible, prone to re-injury
Cells can't move to injury site, tissue planes stick together, mobility restricted
Restarts perfusion and cellular activation through VEGFR2-Akt-eNOS signaling
Calms inflammation without suppressing repair by directly blocking NF-κB
Optimizes collagen architecture by regulating matrix metalloproteinases
Enables cell migration and tissue organization by regulating actin dynamics
- Active malignancy or proliferative retinopathy → avoid BPC-157 & TB-500 (angiogenic)
- Wilson's disease → avoid GHK-Cu
- Pregnancy / breastfeeding → insufficient safety data