LL-37 (Human Cathelicidin): Research, Mechanism & Current Evidence
The only human cathelicidin, studied as a natural antimicrobial and immune signalling peptide.
Also known as human cathelicidin · hCAP18 · CAMP gene product · Human Cathelicidin
What is LL-37?
LL-37 is the only cathelicidin peptide humans produce. It is cut from a longer precursor protein called hCAP18 and is found in skin, airway lining, sweat and immune cells.
Its name comes from its structure: 37 amino acids beginning with two leucines.
What is LL-37 researched for?
Antimicrobial activity against bacteria, fungi and enveloped viruses, including drug-resistant organisms.
Wound healing, especially chronic wounds where LL-37 levels are found to be low.
Its dual role in inflammation, where it appears protective in some conditions and to worsen others such as psoriasis and rosacea.
- 68% ulcer area reduction demonstrated with 0.5mg/mL concentration in clinical trials.
- Enhanced granulation tissue formation and wound closure.
- Accelerated healing demonstrated in animal models.
- Boosts natural immune defenses against pathogens.
- Active against MRSA and multi-drug resistant bacteria with >4 log reduction in biofilms.
- Balances immune responses without causing immunosuppression.
- Stimulates skin cell growth and regeneration.
- Promotes new blood vessel formation for tissue repair.
- Supports collagen production for wound healing.
How does LL-37 work?
Most antibiotics interfere with a specific bacterial process. LL-37 works physically instead: it is positively charged and attaches to the negatively charged surface of bacterial membranes, disrupting them. That makes resistance harder to develop.
It also acts as a signal to the immune system, recruiting immune cells and influencing inflammatory responses — which is why its effects are not uniformly beneficial.
What does the research show?
Antimicrobial activity is well established in laboratory conditions. A small randomised trial of topical LL-37 in hard-to-heal venous leg ulcers reported improved healing at low concentrations.
Its involvement in psoriasis pathology is well documented, and is a genuine counterweight to the wound-healing findings.
Limitations of the current evidence
It is broken down quickly in the body and can damage human cells at higher concentrations, which limits systemic use.
Because it drives inflammation as well as resolving it, more is not straightforwardly better.
References
Venous Leg Ulcer Trial - Grönberg et al. Wound Repair and Regeneration
2014
68% ulcer area reduction demonstrated at optimal doses in chronic venous leg ulcers.
Melanoma Phase I Trial
2015
Intratumoral LL-37 in melanoma patients demonstrated safety and immune stimulation (NCT02225366).
Controlled clinical trial
MRSA Biofilm Study - Noore et al.
PLOS ONE · 2019
>4 log reduction in MRSA biofilms compared to conventional antibiotics.
Structural Analysis
Wang et al. · Journal of Biological Chemistry · 2008
NMR spectroscopy determining 3D structure of LL-37.