Overview
LL-37 is classified as a antimicrobial peptide peptide. Broad-spectrum antimicrobial, anti-biofilm, wound healing, immune modulation, anti-inflammatory.
The only human cathelicidin antimicrobial peptide. LL-37 is a 37-amino acid cationic peptide that directly disrupts microbial membranes (bacteria, viruses, fungi) and neutralizes bacterial endotoxins (LPS). Beyond direct antimicrobial action, LL-37 modulates innate immunity by chemoattracting neutrophils, monocytes, and T-cells to infection sites. Promotes wound healing via EGFR-mediated keratinocyte migration and angiogenesis. Demonstrates potent anti-biofilm properties against resistant organisms.
Also known as: Cathelicidin, CAP-18, hCAP-18
Category
Antimicrobial Peptide
Half-Life
4h
Route
SubQ
FDA Status
Not Approved
How Does LL-37 Work?
The only human cathelicidin antimicrobial peptide. LL-37 is a 37-amino acid cationic peptide that directly disrupts microbial membranes (bacteria, viruses, fungi) and neutralizes bacterial endotoxins (LPS). Beyond direct antimicrobial action, LL-37 modulates innate immunity by chemoattracting neutrophils, monocytes, and T-cells to infection sites. Promotes wound healing via EGFR-mediated keratinocyte migration and angiogenesis. Demonstrates potent anti-biofilm properties against resistant organisms.
At the molecular level, LL-37 operates through pathways characteristic of the Antimicrobial Peptide class, interacting with target receptors and downstream signaling cascades to produce its observed effects.
Published Research
The following studies are indexed from PubMed and peer-reviewed journals:
[1]LL-37 broad-spectrum antimicrobial and immunomodulatory effects
Comprehensive review of LL-37's dual antimicrobial and immunomodulatory functions, including membrane disruption, chemotaxis, cytokine regulation, and wound healing promotion.
Evidence: moderate[2]LL-37 anti-biofilm activity against resistant pathogens
Overhage et al.: LL-37 inhibits biofilm formation by Pseudomonas aeruginosa at sub-MIC concentrations, affecting bacterial attachment, migration, and quorum sensing.
Evidence: preclinical[3]LL-37 promotes wound healing via EGFR transactivation
Tokumaru et al.: LL-37 promotes wound re-epithelialization by stimulating keratinocyte migration through EGFR transactivation, providing mechanistic basis for wound-healing applications.
Evidence: preclinical[4]Cathelicidin deficiency increases susceptibility to infection
Chromek et al.: Studies in CAMP-knockout models demonstrate that cathelicidin deficiency significantly increases susceptibility to urinary tract and skin infections, validating LL-37's critical role in host defense.
Evidence: preclinical[5]LL-37 in chronic inflammatory conditions and immune regulation
Kahlenberg et al.: Review of LL-37's role in autoimmune and chronic inflammatory conditions including psoriasis, lupus, and rosacea. LL-37 acts as a danger signal activating dendritic cells and driving type I interferon production.
Evidence: moderateSafety Profile
Endogenous human peptide with well-characterized biology. Cytotoxic to eukaryotic cells at high concentrations (>25mcg/mL). Concentration-dependent effects: low doses immunomodulatory, high doses cytotoxic. Growing research interest in CIRS/mold illness protocols. Not FDA-approved as a therapeutic.
| Side Effect | Incidence | Severity |
|---|---|---|
| Injection site reaction (redness, swelling) | ~15% of users | mild |
| Flu-like symptoms (immune activation) | ~10% of users | mild |
| Mild fever | ~5% of users | mild |
| Fatigue | ~8% of users | mild |
Sourcing LL-37 for Research
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Full Research Profile
LL-37 — dosing, interactions, timelines & more
Comprehensive compound profile with sourcing information, stacking synergies, and outcome timelines.