LL-37What the studies show

Q: What kind of evidence exists for LL-37 (cathelicidin)?

Mixed evidence. Decades of lab-dish and mouse work plus one 34-patient topical wound trial; nothing on injected LL-37 in people, and solid evidence that excess LL-37 drives rosacea and psoriasis.

The body's own antibiotic peptide, made in skin and white blood cells, which kills microbes in a dish and also drives rosacea and psoriasis.

5 min read · Mixed evidence · Updated November 2026

In short

Name: LL-37 (cathelicidin)
Evidence: Mixed evidence
Bottom line: Decades of lab-dish and mouse work plus one 34-patient topical wound trial; nothing on injected LL-37 in people, and solid evidence that excess LL-37 drives rosacea and psoriasis.

Before you read this

This guide explains what published studies found. That is all it is.

It is not medical advice and it is not instructions for using anything. Where a dose appears, we are reporting what a named study gave the people or animals in it — a fact about the study, not an instruction to you.

The compounds here are not approved by the FDA for use in people and are sold for laboratory research only. A study tells you what happened to the subjects in it; it does not tell you what would happen to you. Talk to a doctor first.

What it is

LL-37 is a 37-amino-acid peptide and the only member of the cathelicidin family that humans make; the name comes from the two leucines at its start and its length ¹. The body stores it as a longer, inactive protein called hCAP18 inside neutrophils and in the lining cells of skin, gut and airways, and an enzyme snips LL-37 off when it is needed ¹. It is a true antimicrobial: in a dish it punches holes in bacterial membranes and kills a broad range of bacteria, and it also pulls immune cells toward a site of injury and nudges skin cells to multiply and move ¹. One of the more striking findings is where its supply comes from. In 2005 researchers showed that the cathelicidin gene is a direct target of the vitamin D receptor, and that active vitamin D strongly turns the gene on in immune cells ² — a plausible link between vitamin D and resistance to infection.

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Wounds

In 2003 a Swedish group looked for LL-37 in human skin wounds and found it at the healing edge, made by the skin cells moving in to close the gap; in chronic venous ulcers that had failed to heal, the same cells had none. When they blocked LL-37 with antibodies in pieces of human skin kept alive in the lab, re-epithelialisation slowed ³. That made the peptide a candidate for the ulcers that lack it.

The same researchers took it to a trial. In 2014, 34 patients with hard-to-heal venous leg ulcers had either LL-37 in a gel, at one of three strengths, or a placebo gel applied to the ulcer over four weeks. The two lower strengths healed faster than placebo; the highest did not, and the authors noted that the effect did not rise with dose ⁴. It remains the only randomized trial of LL-37 in people.

The other edge

The same molecule turns up on the wrong side in two common skin diseases. In rosacea, skin contains more cathelicidin than normal and more of the enzyme that cuts it, producing abnormal fragments; when a 2007 study injected those fragments into mouse skin, the mice developed rosacea-like redness and inflammation, and blocking the enzyme prevented it ⁵. In psoriasis, LL-37 binds the DNA that leaks from damaged cells and turns it into a trigger: the complex activates plasmacytoid dendritic cells to pour out interferon, which drives the disease ⁶.

So LL-37 is not simply "good". At the right place and amount it kills microbes and helps skin close; in excess or in the wrong form it inflames. In a dish, at higher concentrations, it damages human cells as well as bacterial ones ¹.

In people

Beyond the 34-patient ulcer trial, there is no published study of LL-37 given to people by any route, and no injected or systemic form has been tested. It is not an approved medicine anywhere. The body makes it constantly, and a great deal is known about what it does in cells and in mice, but the question of what happens when extra LL-37 is added to a person has been answered only for a gel on a leg ulcer.

That is partly by design. Because LL-37 damages human cells at higher concentrations in a dish, and because the rosacea and psoriasis work shows it can tip toward inflammation, the clinical work built on it has stayed local — a gel on a wound, where the amount and the place are controlled — rather than anything that circulates through the body ¹.

What these studies are, and aren't

Mixed evidence. Decades of lab-dish and mouse work plus one 34-patient topical wound trial; nothing on injected LL-37 in people, and solid evidence that excess LL-37 drives rosacea and psoriasis.