Source comparison
LL-37 BPC-157 for Chronic Infection: Protocol Comparison
This table compares LL-37 and BPC-157 across mechanism, typical research dosing, half-life, and clinical application context. The final column provides a professional assessment of each peptide's role in infection protocols. LL-37 Membrane disruption via catio
This comparison does not assign a generated winner or score.
- This table compares LL-37 and BPC-157 across mechanism, typical research dosing, half-life, and clinical application context. The final column provides a professional assessment of each peptide's role in infection protocols.
- LL-37
- Membrane disruption via cationic pore formation; immune cell recruitment via FPRL1 binding
- 2–10 μg/mL (in vitro); topical formulations 50–200 μg/mL
- 4–6 hours (plasma); tissue retention longer
- Biofilm infections, MRSA, diabetic ulcers, post-surgical wounds
- Direct antimicrobial without resistance risk; immune modulation critical for chronic infection clearance
- BPC-157
- VEGF upregulation; angiogenesis; collagen synthesis; MMP modulation
- 10 μg/kg daily (animal models); human equivalents not established
- Unknown; gastric peptide likely short plasma half-life
- Hypoxic wounds, ischemic tissue, tendon/ligament repair, gastric ulcers
- Addresses vascular insufficiency that sustains chronic infection; not antimicrobial itself
- Combination Protocol
- LL-37 kills pathogens and recruits immune cells; BPC-157 restores tissue architecture and perfusion
- Sequential or concurrent administration depending on infection stage
- N/A (combination protocols not standardised)
- Recurrent soft tissue infections, non-healing wounds with biofilm colonisation
- Mechanistically complementary but lacks Phase III human trial data; investigational use only