A 37-amino-acid antimicrobial peptide your skin and white blood cells already make. Human trials tested it mainly as an ulcer cream.
Also called Cathelicidin LL-37, Human cathelicidin antimicrobial peptide, CAMP, hCAP18 (precursor), Ropocamptide
LL-37 is a 37-amino-acid peptide the body makes on its own. White blood cells and skin and airway lining cells store it as a larger precursor, hCAP18, and cut LL-37 free when they meet bacteria or an injury. It punches holes in bacterial membranes, pulls immune cells to the site, and helps new blood vessels form. Vitamin D switches the gene on directly, which is why vitamin D status comes up in LL-37 discussions.
Unlike most peptides sold online, LL-37 has been through real placebo-controlled trials, but only as a topical treatment for chronic leg and foot ulcers. A 34-person trial in 2014 looked promising at the two lower strengths. The larger 148-person follow-up, HEAL LL-37, found no healing benefit over placebo in the full group. A 25-person diabetic foot ulcer trial in 2023 showed more granulation tissue but no significant difference in wound shrinkage. Nobody has published a trial of injected LL-37 for immunity, infection or longevity, which is how it is marketed.
Too much LL-37 is part of several skin diseases. People with rosacea carry abnormally high levels and abnormally processed forms of it in facial skin, and in psoriasis LL-37 binds the body's own DNA and sets off an immune attack. In a melanoma trial where it was injected into tumors, one patient developed multiple wart-like skin growths. It is not approved anywhere and is not a legal US compounding ingredient as of October 2026.
What it binds to, and what happens inside the body after that, step by step.
LL-37 is positively charged and folds into a helix that sticks to and breaks the negatively charged membranes of bacteria. At the same time it signals human cells through the formyl peptide receptor FPRL1 and other receptors, drawing in immune cells and stimulating endothelial cells to form new vessels. The same DNA-binding stickiness that helps it trap microbes lets it carry the body's own DNA into immune cells, which drives inflammation in psoriasis.
Human results and animal results are kept apart below. A result in rats tells you a mechanism is plausible. It does not tell you what happens in a person.
Three placebo-controlled trials tested LL-37 as a topical treatment for chronic ulcers. The first small trial showed faster healing at the two lower strengths, the larger phase 2b trial showed no benefit in the full group, and a small diabetic foot trial improved granulation but not wound size. There are no human trials of injected LL-37 for infection, immunity or aging, and human biology studies tie excess LL-37 to rosacea and psoriasis.
148 adults with venous leg ulcers, median ulcer duration 20.3 months, plus compression
No significant healing improvement with LL-37 over placebo in the full study group; a post hoc look suggested benefit only in ulcers of 10 cm2 or more.
Read the study34 adults with venous leg ulcers, first-in-human dose-ranging trial
Mean ulcer area fell 68% and 50% at the two lower strengths, healing rate was about 6-fold placebo at the lowest; the highest strength did no better than placebo.
Read the study25 adults with uninfected or mildly infected diabetic foot ulcers in Jakarta (13 LL-37, 12 placebo)
Granulation index was higher with LL-37 at every visit, but wound area shrinkage at day 28 and bacterial counts did not differ significantly.
Read the study1 patient with stage IIIC melanoma in a phase 1 intratumoral LL-37 trial
After 8 weekly injections she developed multiple wart-like and blistering skin lesions with atypical squamous growth; they cleared within 2 months of stopping.
Read the studyFacial skin from people with and without rosacea, plus mouse injection experiments
Rosacea skin held abnormally high cathelicidin levels and abnormal fragments; injecting those fragments into mouse skin caused inflammation.
Read the studyHuman psoriasis skin and human immune cells
LL-37 bound to the body's own DNA activated TLR9 and interferon production in dendritic cells, identified as a driver of psoriasis.
Read the studyChick chorioallantoic membrane, rabbit hind-limb ischemia, knockout mice
LL-37 grew new vessels through FPRL1, and mice lacking the mouse version had fewer vessels in healing wounds.
Read the studyThese are questions the published research has not answered.
No product containing LL-37 is approved as a medicine by the FDA.
No approved LL-37 drug exists anywhere. Promore Pharma developed it as ropocamptide, a topical treatment for venous leg ulcers; its phase 2b trial missed its primary endpoint in 2021, and no phase 3 trial has been registered. No active LL-37 drug trial was found on ClinicalTrials.gov as of October 2026. WADA does not name LL-37, but S0 bans pharmacological substances without current approval for human therapeutic use.
No human half-life has been published for LL-37, so we do not draw a clearance curve. Half-lives quoted online for it are usually estimates from animal data.
This table records the doses that trials and approved labels used, with the source for each row. It is a record of research, not a recommendation, and it is open to free members.
Which symptoms are expected and which mean stop and get help: side effects and red flags.
Tap a claim to see what the studies found.
LL-37 kills bacteria in a dish and is part of normal immune defense, but no human trial has given injected LL-37 to prevent or treat infection.
A 34-person trial looked good, but the 148-person phase 2b trial found no benefit over placebo in the full group, and a small diabetic foot trial improved granulation but not wound size.
Excess or abnormally processed LL-37 is part of how rosacea and psoriasis develop, and intratumoral injections produced atypical skin growths in one melanoma patient.
These claims rest on test-tube work with bacteria. No human study has tested LL-37 for Lyme disease or chronic biofilm infections.
The active form of vitamin D directly switches on the CAMP gene that makes LL-37 in human immune and skin cells. This is a cell-level finding; how much a supplement changes LL-37 in a given person varies.
These pairings come up often. Almost none have been tested together in a trial, and the evidence note on each says so plainly.
Paired in clinic protocols for chronic infections on the idea that LL-37 kills microbes directly while thymosin alpha-1 boosts T-cell response.
EvidenceNo study has tested the combination, and injected LL-37 has no human efficacy data for any infection.
No product-specific published stability data. Research suppliers and peptide practice call for frozen, dry, dark storage.
No published data for injectable solutions. Clinical trial formulations were made for topical use. LL-37 is broken down by proteases in wound fluid, so contamination shortens its life.
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