LL-37

Cathelicidin, hCAP18 C-terminal fragment, CAP-18 (37-residue peptide), human cathelicidin antimicrobial peptide

Recovery, repair & tissue

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Summary

Class: Naturally occurring 37-amino-acid antimicrobial peptide; the active fragment cut from the human cathelicidin precursor hCAP18. Supplied synthetically for research
Mechanism: Punches holes in bacterial membranes directly and acts as an immune signal — recruiting white cells, binding bacterial endotoxin, promoting wound closure and new blood vessels
Routes studied: Topical (human venous leg ulcer trial); intratracheal, intraperitoneal, intravenous and topical in animals; extensive in-vitro work. Community: subcutaneous injection, topical, nasal
Dose range reported: Human topical trial: 0.5 mg/ml and 1.6 mg/ml applied to ulcers twice weekly for 4 weeks; a 3.2 mg/ml arm was not better. Animal: variable, often mg/kg. Community subcutaneous: 50–100 µg/day, sometimes split, typically short courses. No validated systemic human dose
Half-life: Minutes in plasma — rapidly degraded by proteases and bound by serum proteins. Normal blood levels of the precursor are in the tens of ng/ml
Storage: Lyophilised: refrigerate or freeze, protect from light. Reconstituted: refrigerate; it is a cationic peptide that sticks to plastic and degrades, so community practice is short storage
Regulatory status: Not approved for any indication. See region table

Doses are as reported in studies or by the community — never recommendations.

1What it is

LL-37 is a peptide your own body makes. It is the only cathelicidin-family antimicrobial peptide in humans, produced by neutrophils, skin cells, gut and lung lining cells and others. The precursor, hCAP18, is cut by an enzyme to release the 37-amino-acid active peptide, named for its first two leucine residues. Vitamin D strongly increases its production, which is one of the proposed links between vitamin D status and infection risk.

It is part of innate immunity — the fast, non-specific defence that acts before antibodies exist. Low cathelicidin levels are associated with conditions such as atopic dermatitis and some infections; excessive levels are implicated in rosacea and psoriasis. That double edge is important when reading research on giving extra.

The published human evidence is a single small trial of topical LL-37 on chronic leg ulcers. Injection in humans has not been studied.

2How it's thought to work

Direct antimicrobial action. the peptide is positively charged and forms a helix that inserts into negatively charged bacterial membranes, disrupting them. Active against Gram-positive and Gram-negative bacteria, some fungi and enveloped viruses, and against biofilms (Dürr 2006 review).

Endotoxin binding. neutralises lipopolysaccharide (LPS), the toxic component of Gram-negative bacteria, reducing septic-shock-type signalling in models.

Immune signalling. chemoattracts neutrophils, monocytes and T cells via the FPRL1 receptor; modulates cytokine release in both directions depending on context.

Wound repair. promotes re-epithelialisation and through EGFR transactivation and other pathways (Koczulla 2003; Heilborn 2003).

Pro-inflammatory potential. LL-37 complexed with self-DNA activates plasmacytoid dendritic cells, a mechanism implicated in psoriasis (Lande 2007). Higher doses are cytotoxic to human cells in vitro.

Inserts into bacterial membranes and opens holes in them, binds bacterial endotoxin, and calls white blood cells to the site.Schematic — not to scale

3What the research shows

Chronic venous leg ulcers (topical)

A Phase 1/2 randomised, placebo-controlled first-in-human trial (n=34) of topical LL-37 applied to hard-to-heal venous leg ulcers reported significantly faster healing at the two lower concentrations over 4 weeks, with no safety signals; the highest concentration showed no benefit (Grönberg 2014, Wound Repair Regen). Small, short, single study. A larger follow-up has been reported in abstract form †. [2]

Antimicrobial activity including biofilms

Extensive in-vitro data against Pseudomonas aeruginosa, Staphylococcus aureus (including MRSA) and others, with biofilm inhibition at concentrations below those that kill free-floating bacteria (Overhage 2008, Infect Immun). Resistance development appears slower than with conventional antibiotics . [5]

Infection and sepsis models

Rodent studies report protection in models of lung infection, peritonitis and endotoxaemia, often attributed to LPS neutralisation rather than direct killing. Some models show worsened inflammation at high doses.

Graded C/D

Wound healing and angiogenesis

Mouse and ex-vivo human skin models show faster closure and increased vascularisation (Koczulla 2003, J Clin Invest; Heilborn 2003, J Invest Dermatol). Delivery of the LL-37 gene also improved wound healing in diabetic mice (Steinstraesser 2014). [3][4]

Graded B/C

Role in disease (observational, not treatment)

Human observational work associates low LL-37 with atopic dermatitis and infection susceptibility, and high LL-37 with rosacea, psoriasis and some autoimmune processes. This is about endogenous levels and does not show that giving the peptide is helpful or harmful.

Systemic injection in humans

None published. Community use for "chronic infections", Lyme, SIBO or biofilms rests on in-vitro data and anecdote.

4Reported side effects and interactions

Literature-reported

topical use in the ulcer trial was well tolerated; no systemic effects detected. , LL-37 is toxic to human cells at concentrations not far above its antimicrobial range, and high doses in animal models can increase inflammation. There is no human safety data for injection.

Community-reported

injection-site pain, redness and swelling are very common and sometimes pronounced; fatigue, flu-like symptoms, headache and "die-off" sensations are reported (these are interpreted by members in various ways and have no established cause). Some report worsened skin inflammation.

Theoretical. LL-37 is implicated in psoriasis and rosacea pathology, autoimmunity (via self-DNA complexes), and in some cancers as a growth factor (e.g. ovarian, lung) while being protective in others (e.g. colon). Giving extra to anyone with an autoimmune or inflammatory skin condition, or an active malignancy, is an untested risk. Antibodies to a self-peptide given by injection are a theoretical concern.

Interactions. none established. Activity is reduced by serum proteins and high salt in vitro. Vitamin D raises endogenous production.

Markers researchers commonly monitor

Marker	Why it's watched
CBC with differential	LL-37 recruits and activates neutrophils and monocytes; white-cell shifts are the most plausible systemic signal.
CRP and ESR	LL-37 can be pro- or anti-inflammatory depending on dose and context; a rise would flag the former.
Vitamin D (25-OH)	the main physiological regulator of endogenous cathelicidin; low levels are the usual reason endogenous LL-37 is low.
Skin examination	flare of psoriasis- or rosacea-like inflammation is the most specific theoretical adverse effect.
Antinuclear antibodies	only in the context of a theoretical autoimmune concern; no evidence yet that exogenous LL-37 triggers autoimmunity.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Typically supplied in 5 mg vials. LL-37 is a sticky cationic peptide that adsorbs to plastic surfaces and aggregates; community practice is to with , use low-binding or glass containers where possible, avoid shaking, and keep storage short. Topical preparations in the trial used a gel vehicle.

Open in calculator, pre-loaded →

6Commonly studied alongside

Thymosin alpha-1 (community "immune" pairing; no combined study), KPV, BPC-157. In laboratory work, with conventional antibiotics for synergy against biofilms.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Placed in Category 2 of the FDA's 2023 compounding bulk-substances list, restricting compounding
European Union	Not authorised. A topical formulation has been in clinical development in Sweden †
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered
Sport	Not specifically named by WADA; as a non-approved substance it falls under S0 †

8Open questions

Does injected LL-37 survive long enough in blood to do anything, given its minute-scale and protein binding?
Where is the line between the antimicrobial and the pro-inflammatory/cytotoxic dose in humans?
Would systemic use trigger psoriasis-type autoimmunity in susceptible people?

9References

1Dürr UHN, Sudheendra US, Ramamoorthy A (2006). LL-37, the only human member of the cathelicidin family of antimicrobial peptides. Biochim Biophys Acta. PubMed · DOI
2Grönberg A et al. (2014). Treatment with LL-37 is safe and effective in enhancing healing of hard-to-heal venous leg ulcers: a randomized, placebo-controlled clinical trial. Wound Repair Regen. PubMed · DOI
3Koczulla R et al. (2003). An angiogenic role for the human peptide antibiotic LL-37/hCAP-18. J Clin Invest. PubMed · DOI
4Heilborn JD et al. (2003). The cathelicidin anti-microbial peptide LL-37 is involved in re-epithelialization of human skin wounds and is lacking in chronic ulcer epithelium. J Invest Dermatol. PubMed · DOI
5Overhage J et al. (2008). Human host defense peptide LL-37 prevents bacterial biofilm formation. Infect Immun. PubMed · DOI
6Lande R et al. (2007). Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide. Nature. PubMed · DOI
7Vandamme D et al. (2012). A comprehensive summary of LL-37, the factotum human cathelicidin peptide. Cell Immunol. PubMed · DOI
8FDA (2023). Bulk drug substances for compounding — LL-37 category 2 listing. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

25 Oct 2026Profile published — awaiting medical review

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