Evidence at a glance
What the research says about LL-37
The LL-37 evidence base cited here is 7 sources — 4 preclinical, 2 review. Critically, that evidence is almost entirely preclinical (animal and in-vitro) — no human clinical trials are cited, so efficacy and safety in people remain unproven. Regulatory status: Not FDA-approved.
Summary
Key takeaways
- LL-37 is the only human cathelicidin antimicrobial peptide — a 37-amino-acid cationic peptide (~4,493 Da) cleaved from the hCAP18 precursor, with broad-spectrum activity against bacteria, viruses, and fungi plus wound-healing and immune-modulating effects.
- The strongest research interest is TOPICAL wound healing: a first-in-man RCT in chronic venous leg ulcers reported ~68% ulcer-area reduction at 0.5 mg/mL, and it eradicates MRSA biofilms in vitro better than some conventional antibiotics.
- As a cationic peptide it kills microbes by disrupting their membranes and biofilms, and it promotes keratinocyte migration and angiogenesis at wound sites.
Overview
LL-37 is the human body's own broad-spectrum antimicrobial peptide and a key part of innate immunity. Research interest centers on using it topically to clear infection and accelerate healing in chronic, hard-to-heal wounds — venous leg ulcers, diabetic foot ulcers, pressure ulcers, and burns — where its antimicrobial and pro-healing actions combine.
It is investigational and not FDA-approved; everything below is research context rather than medical guidance.
What Is LL-37?
LL-37 is a 37-amino-acid cationic peptide (~4,493 Da), named for its two leading leucines (LL) and its length. It is the active fragment cleaved from hCAP18, the only cathelicidin produced in humans, and is expressed by neutrophils, epithelial cells, and other tissues as a first line of antimicrobial defense.
Its positive charge is functional: it lets the peptide bind and disrupt the negatively-charged membranes of bacteria (and the matrix of biofilms), which is the basis for its antimicrobial breadth.
How It Works
LL-37 works on two fronts. As a direct antimicrobial, its cationic structure disrupts microbial membranes and biofilms, killing bacteria, viruses, and fungi — including drug-resistant strains. As a wound-healing and immune modulator, it promotes keratinocyte migration (re-epithelialization), stimulates angiogenesis (new blood vessels), and signals immune cells to the wound. Applied topically, it acts locally at the wound bed without meaningful systemic exposure.
Dosing (topical, research-reported)
Research use is topical and wound-specific; there is no approved dosing. Figures below reflect trial/research protocols.
- Chronic venous ulcers: ~0.5 mg/mL topical gel, ~twice weekly
- Diabetic foot ulcers: ~0.5–1.6 mg/mL topical cream, daily
- Acute wounds: ~1.6 mg/mL once daily; pressure ulcers ~0.5–1.0 mg/mL in a hydrogel
- Applied to clean, debrided wounds under a sterile dressing; continued until healing
Concentration matters and isn't simply 'more is better' — the venous-ulcer trial found the best healing at the LOWER 0.5 mg/mL dose, with diminishing benefit at higher concentrations.
Pharmacokinetics
Human pharmacokinetic data for LL-37 is limited, and it is used topically rather than for sustained systemic levels. Note: some sources circulate identical short PK figures (e.g. ~3-minute peak, ~30-minute half-life) for both LL-37 and the unrelated tripeptide KPV — given their very different sizes (a 37-mer vs a 3-mer), those shared numbers look like a template default rather than measured values and should not be cited without primary confirmation.
Application & Storage
- Apply a thin layer of the sterile gel/cream to a cleaned, debrided wound and cover with a sterile dressing; change daily to twice weekly per protocol.
- Refrigerate at 2–8°C and protect from light.
- Use a sterile, clinical-grade formulation (verified 0.5–1.6 mg/mL, appropriate pH); avoid homemade/DIY preparations — sterility on an open wound is critical.
Side Effects & Safety
Used topically on clean/debrided wounds, with monitoring for infection or delayed healing and discontinuation on any hypersensitivity reaction. Sterile technique is essential because the target is an open wound. Systemic safety data is limited, which is part of why the research focus has stayed topical.
Key Studies
- Venous leg ulcer RCT (2014, first-in-man, 34 participants): topical LL-37 produced ~68% ulcer-area reduction at 0.5 mg/mL with markedly faster healing kinetics.
- MRSA biofilm eradication (2019, in vitro, CDC biofilm reactor): >4-log reduction, outperforming conventional antibiotics and silver nanoparticles against S. aureus biofilms.
- Multidrug-resistant bacteria (2017, clinical isolates): broad-spectrum activity (MIC ~1–256 µg/mL) including resistant strains.
Legal & Status
LL-37 is not FDA-approved and is sold as a research chemical for laboratory use only, not intended for human consumption.
Citations
7 peer-reviewed sources
All citations link to the original source (PubMed, journal site, or regulatory filing). Independent research database — no vendor influence on what's cited.
Preclinical4 sources
The Cathelicidin Anti-Microbial Peptide LL-37 Is Involved in Re-Epithelialization of Human Skin Wounds and Is Lacking in Chronic Ulcer Epithelium
Induction of Keratinocyte Migration via Transactivation of the EGFR by the Antimicrobial Peptide LL-37
In Vitro and In Vivo Wound Healing-Promoting Activities of Human Cathelicidin LL-37
Cathelicidin Antimicrobial Peptide LL-37 in Psoriasis Enables Keratinocyte Reactivity against TLR9 Ligands
Review2 sources
Database1 source
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