The only human cathelicidin, a 37-amino-acid antimicrobial and immune-signalling peptide. Extensively studied as a molecule; barely studied as a therapy.
LL-37 is part of the innate immune system — the fast, non-specific defence that acts before antibodies get involved. It kills bacteria by punching holes in their membranes, which is hard for bacteria to develop resistance against. It also has a second role as a signal, recruiting immune cells to a site of injury and influencing wound healing and inflammation. Its therapeutic development has repeatedly stalled because at concentrations that kill bacteria it also damages human cells.
The 37-residue C-terminal cleavage product of human cationic antimicrobial protein 18 (hCAP18), the sole human cathelicidin, encoded by CAMP. Amphipathic alpha-helical structure enables electrostatic association with anionic bacterial membranes and permeabilisation via carpet or toroidal pore mechanisms. Beyond direct microbicidal activity it acts as a chemoattractant via FPR2, neutralises LPS, modulates TLR signalling, and promotes angiogenesis and re-epithelialisation. Vitamin D response elements in the CAMP promoter link vitamin D status to expression. Clinical evaluation is limited to small topical trials, notably in venous leg ulcers; systemic development has been constrained by cytotoxicity and rapid proteolysis.
Research areas
Community-specified data
Source note: 50 days on, 4 weeks off. Take in AM
Not medical guidance. These third-party figures have not been independently verified, clinically reviewed, or endorsed by DB Peptide. They may be inaccurate or unsafe and should not replace product labelling or advice from a qualified clinician.
Every protocol below is reproduced from a published study or approved labelling, with its source named. These are records of what was studied — not recommendations, and not a suggestion that any of them is appropriate for any person.
| Protocol as reported | Source |
|---|---|
| Topical LL-37 at 0.5, 1.6 or 3.2 mg/ml applied twice weekly for 4 weeks to hard-to-heal venous leg ulcersThe lower doses showed better healing; the highest did not, consistent with concentration-dependent cytotoxicity. | Grönberg et al., Wound Repair and Regeneration 2014 |
Small phase 1/2 topical trials in venous leg ulcers. No systemic clinical programme.
Both, depending on context. It supports wound healing and clears pathogens, but elevated LL-37 in skin is a documented driver of rosacea, and complexed with self-DNA it triggers the interferon response implicated in psoriasis. It is a genuinely double-edged molecule.
Treatment with LL-37 is safe and effective in enhancing healing of hard-to-heal venous leg ulcers: a randomized, placebo-controlled clinical trial
The human antimicrobial peptide LL-37: a pluripotent peptide with multiple functions
Cathelicidin anti-microbial peptide LL-37 in psoriasis enables keratinocyte reactivity against nucleic acids
Medical disclaimer
This page is for informational and research purposes only. Nothing here constitutes medical advice. The compounds discussed are research chemicals. Consult a qualified clinician before starting any protocol.
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