LL-37

The only cathelicidin the human body makes. White blood cells and skin cells release it to fight infection and signal the immune system; it is cut from the precursor hCAP18 at sites of infection.

Its positively charged helix binds and disrupts negatively charged bacterial membranes and endotoxins, and it acts on some viruses and fungi. It also recruits immune cells and can either damp or amplify inflammation. In wound models it promotes skin-cell migration and new blood vessels; vitamin D, UVB light and butyrate increase the body's own production.

Human research is all topical, on chronic wounds. A 34-patient phase I/II trial in venous leg ulcers reported faster healing at the lowest gel strength, but a 144-patient phase IIb trial found no significant difference overall, with benefit only in large wounds in an unplanned analysis. A small diabetic foot ulcer trial improved granulation but not wound area. In lab and animal work, excess LL-37 is part of the disease process in psoriasis and rosacea, and it appears to promote some cancers while inhibiting others. No human safety or pharmacokinetic data outside topical use were found.

Trials reported local wound reactions (mainly at the highest strength) and one mild irritant dermatitis, with no treatment-related serious events in the phase IIb trial. FDA's compounding review cited immunogenicity, harm to male reproduction in nonclinical studies, and possible tumor promotion. It is toxic to many human cell types in the lab at concentrations close to its antimicrobial levels.

Not FDA-approved for any use. FDA removed it from compounding Category 2 in April 2026 but did not place it in Category 1, so it has no compounding pathway; it is reportedly scheduled for FDA advisory committee review by early 2027. Not named on the WADA list, but as an unapproved substance it likely falls under S0.