Research summary

LL-37 research

StatusNot FDA-approvedNCAANot listed

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.
  • As a cationic peptide it kills microbes by disrupting their membranes and biofilms, and it promotes keratinocyte migration and angiogenesis at wound sites.
  • It is not FDA-approved. Note: vitamin D upregulates the body's own LL-37, a well-established biological link.

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.

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

  • Refrigerate at 2–8°C and protect from light.

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

  • MRSA biofilm eradication (2019, in vitro, CDC biofilm reactor): >4-log reduction, outperforming conventional antibiotics and silver nanoparticles against S. aureus biofilms.

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.

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