LL-37 (Human Cathelicidin Antimicrobial Peptide)
Also Known AshCAP-18 · CAMP · Human Cathelicidin · FALL-39 · Cathelicidin antimicrobial peptide
The only human cathelicidin antimicrobial peptide, derived by proteolytic cleavage of the 18 kDa precursor protein hCAP-18 by proteinase 3 in neutrophil granules. Named for its N-terminal Leu-Leu dipeptide and 37-residue length. Expressed in neutrophils, epithelial cells, macrophages, and other cell types. First characterized in the mid-1990s.
Leu-Leu-Gly-Asp-Phe-Phe-Arg-Lys-Ser-Lys-Glu-Lys-Ile-Gly-Lys-Glu-Phe-Lys-Arg-Ile-Val-Gln-Arg-Ile-Lys-Asp-Phe-Leu-Arg-Asn-Leu-Val-Pro-Arg-Thr-Glu-SerHow LL-37 Works
Membrane Disruption (Direct Antimicrobial)
LL-37 adopts an amphipathic alpha-helical conformation in membrane environments. The cationic face interacts electrostatically with negatively charged bacterial membranes (LPS in Gram-negatives, lipoteichoic acid in Gram-positives), while the hydrophobic face inserts into the lipid bilayer. This creates transmembrane pores or carpet-like disruption, leading to osmotic lysis. Selectivity for bacterial over mammalian membranes is driven by the charge difference (bacterial membranes are more anionic).
Chemotactic & Immunomodulatory Signaling
LL-37 activates formyl peptide receptor-like 1 (FPRL1/FPR2), a G-protein-coupled receptor on neutrophils, monocytes, and T-cells, driving chemotaxis of immune cells to infection sites. It also modulates TLR signaling — LL-37 binds extracellular DNA and RNA, facilitating endosomal TLR9 and TLR7/8 activation while dampening surface TLR4 signaling from LPS.
Anti-Biofilm Activity
LL-37 disrupts bacterial biofilms at sub-inhibitory concentrations by reducing initial bacterial attachment, stimulating twitching motility (in Pseudomonas aeruginosa), and interfering with quorum sensing signaling. This anti-biofilm activity is mechanistically distinct from its direct antimicrobial action and occurs at concentrations below those needed for planktonic killing.
Wound Healing & Angiogenesis
LL-37 promotes wound healing through EGFR transactivation (via metalloprotease-mediated HB-EGF shedding) and direct VEGF-mediated angiogenesis via FPRL1. It stimulates epithelial cell migration and proliferation in wound models and promotes neovascularization at wound sites.
Published Research
Antimicrobial Defense
StrongLL-37 shows broad-spectrum activity against Gram-positive and Gram-negative bacteria, fungi (Candida spp.), and enveloped viruses. MIC values typically range from 1-32 micromolar depending on organism and assay conditions. Importantly, bacterial resistance development to LL-37 is rare compared to conventional antibiotics, as the membrane-targeting mechanism requires fundamental changes in membrane composition.
Biofilm Infections
ModerateClinically, biofilms cause >60% of chronic infections. LL-37 shows unique anti-biofilm activity at sub-MIC concentrations against P. aeruginosa, S. aureus, and other biofilm-forming pathogens. Mechanisms include prevention of initial attachment, disruption of established matrix, and interference with quorum sensing. Clinical relevance for chronic wound, implant, and pulmonary infections.
Innate Immune Regulation
ModerateLL-37 bridges innate and adaptive immunity through chemokine-like activity (FPRL1-mediated immune cell recruitment), modulation of dendritic cell differentiation, and regulation of TLR signaling. Deficiency states (morbus Kostmann, specific granule deficiency) are associated with increased infection susceptibility, validating its non-redundant immune role.
Wound Repair
ModerateLL-37 is upregulated in wound fluid and at wound margins. It promotes re-epithelialization through EGFR transactivation and angiogenesis through FPRL1-VEGF signaling. In diabetic wound models (where endogenous LL-37 expression is impaired), exogenous LL-37 application restores healing trajectory.
Autoimmunity (Psoriasis, Rosacea)
StrongLL-37 is overexpressed in psoriatic lesions where it forms complexes with self-DNA, activating plasmacytoid dendritic cells via TLR9 and driving IFN-alpha production — a key pathogenic step in psoriasis. In rosacea, aberrant cathelicidin processing produces inflammatory peptide fragments. This dual role — protective in infection, pathogenic in autoimmunity — illustrates the complexity of host defense peptide biology.
Safety Profile
LL-37 is an endogenous human peptide expressed constitutively and inductively at epithelial surfaces. At physiological concentrations, it is selective for microbial membranes over host cell membranes. At supraphysiological concentrations (>25 micromolar), cytotoxicity to mammalian cells can occur due to loss of membrane selectivity. Topical and local administration routes minimize systemic exposure. The role in autoimmune pathology (psoriasis, rosacea) reflects dysregulated expression rather than inherent toxicity. No human clinical trial data for exogenous LL-37 administration is available from completed studies.
Handling & Storage
LL-37 is a 37-residue amphipathic peptide that readily adsorbs to plastic and glass surfaces. Use low-binding microcentrifuge tubes and pipette tips. Reconstitute with sterile water or bacteriostatic water. Store lyophilized at -20°C. Reconstituted solutions at 2-8°C, use within 14 days. The peptide can aggregate at high concentrations — keep working solutions dilute.
Peer-Reviewed Literature
- 1
A comprehensive summary of LL-37, the factotum human cathelicidin peptide
Vandamme D, Lanber B, Vergote I, Bhatt T.
- 2
Human host defense peptide LL-37 prevents bacterial biofilm formation
Overhage J, Campisano A, Bains M, et al.
- 3
Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide
Lande R, Gregorio J, Facchinetti V, et al.
- 4
The cathelicidin anti-microbial peptide LL-37 is involved in re-epithelialization of human skin wounds and is lacking in chronic ulcer epithelium
Heilborn JD, Nilsson MF, Kratz G, et al.
- 5
An angiogenic role for the human peptide antibiotic LL-37/hCAP-18
Koczulla R, von Degenfeld G, Kupatt C, et al.
LL-37 FAQ
What is LL-37?
LL-37 is the only human cathelicidin antimicrobial peptide — a 37-amino-acid, amphipathic, alpha-helical peptide produced by neutrophils, epithelial cells, and macrophages. It has broad-spectrum antimicrobial activity, anti-biofilm properties, and immunomodulatory functions that bridge innate and adaptive immunity.
How does LL-37 kill bacteria?
LL-37 adopts an alpha-helical structure that inserts into negatively charged bacterial membranes, forming pores or carpet-like disruptions that cause osmotic lysis. Selectivity for bacterial over mammalian membranes is driven by the greater negative charge density of bacterial membrane phospholipids compared to the neutral (zwitterionic) mammalian cell surface.
Why is LL-37 relevant to biofilm infections?
LL-37 disrupts biofilms at concentrations below those needed to kill planktonic bacteria. It prevents initial bacterial attachment, stimulates bacterial motility (reducing sessile growth), and interferes with quorum sensing. This is clinically relevant because biofilms cause >60% of chronic infections and are resistant to conventional antibiotics.
Is LL-37 involved in autoimmune conditions?
Yes. In psoriasis, overexpressed LL-37 binds self-DNA released from damaged keratinocytes, forming complexes that activate plasmacytoid dendritic cells via TLR9, triggering IFN-alpha production and driving the inflammatory cascade. This illustrates that host defense peptides can be pathogenic when dysregulated.
How should LL-37 be handled?
LL-37 adsorbs readily to standard plastic and glass surfaces — use low-binding tubes and tips. Store lyophilized at -20°C. Reconstitute with sterile or bacteriostatic water; keep reconstituted solution at 2-8°C and use within 14 days. Avoid high concentration stocks as LL-37 can self-aggregate.
LL-37 Products
All compounds 99%+ purity, verified by Janoshik Analytical. GMP-manufactured lyophilized powder.
LL-37
5mgYour body's natural antibiotic — destroys bacteria, viruses, and fungi on contact, breaks up stubborn biofilms, and accelerates wound healing.
- Broad-spectrum antimicrobial — kills bacteria, viruses, and fungi
- Accelerates wound healing and tissue repair
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Disclaimer: This monograph is provided for educational and research purposes only. G26x Peptides products are sold exclusively as research chemicals. They are not intended for human consumption, therapeutic use, or as dietary supplements. All research should be conducted in compliance with applicable laws and institutional review board protocols. Information presented here is sourced from published peer-reviewed literature and does not constitute medical advice.