LL-37
Cathelicidin / hCAP-18 fragment
Human host defense peptide with broad-spectrum antimicrobial and wound-healing properties. Naturally produced by immune cells. Dual antimicrobial plus healing mechanism is unique.
Mechanism of action
Directly disrupts bacterial cell membranes — broad spectrum antimicrobial against bacteria viruses and fungi. Stimulates keratinocyte migration for wound healing. Modulates Toll-like receptor signaling. Angiogenic and chemotactic for immune cells. Naturally produced by neutrophils skin cells and epithelium.
Effects in the body
LL-37 is one of your body's own antimicrobial weapons produced by neutrophils skin cells and epithelium. It kills bacteria through membrane disruption then signals wound repair. The dual antimicrobial and healing mechanism makes it interesting for wound care and antibiotic resistance research.
Pros & cons (from the literature)
- Broad-spectrum antimicrobial against bacterial viral and fungal pathogens
- Wound healing AND immune activation in same molecule
- Naturally human — high theoretical tolerability
- Topical and injectable applications studied
- Research interest in antibiotic resistance context
- RUO status not compoundable in USA
- Can be pro-inflammatory at high doses
- May promote autoimmune reactions in susceptible individuals
- Injectable human data limited
- Manufacturing complexity and cost
Protocol summary (from published research)
Dosing ranges reproduced from published research literature. Not a prescription, not medical advice.
FDA & regulatory status
Evidence base
Extensive preclinical data. Mechanism well characterized. Phase I and II human topical trials for wound care published. Injectable systemic data more limited.
Primary research sources
Peer-reviewed literature referenced throughout this profile is drawn from PubMed, Cell Metabolism, and clinical trial registries cited in the evidence base above.