LL-37
Also known as: Cathelicidin LL-37 · hCAP-18 cleaved peptide · CAP18(104-140)
Phase 2 chronic wound trial data (Grönberg 2014); in vitro cancer-cell-line stimulation findings flagged as open question; no major clinical AE signal; no regulatory approvals.
Rating per Panya's data-first method, not regulator endorsement. The mechanism, dose, and risk sections below carry the underlying data.
LL-37 is a 37-residue endogenous antimicrobial peptide cleaved from the human cathelicidin precursor (hCAP-18). Active against gram-positive and gram-negative bacteria, fungi, and several enveloped viruses; under research for chronic wound healing, biofilm-resistant infections, and oral disease.
Last reviewed · Panya.health editorial
Panya scores vendors against an 11-signal rubric. Vendors at or above 70 out of 100 are routable; below 70 are documented but get no Panya affiliate link. For prescription peptides like Mounjaro and Wegovy, Panya routes today through licensed clinicians. For research peptides like LL-37, vendor scorecards land in a follow-up sprint after legal review and payment processor selection. Until then, the page surfaces commonly-mentioned vendor names so adults can do their own diligence. We do not yet earn commission on any LL-37 vendor.
Not medical advice. LL-37 is not approved for human medical use in most jurisdictions. The data below is what users do; it is not what regulators have validated. You decide your risk profile.
What it does, and how
LL-37 is the only human cathelicidin, encoded by the CAMP gene and cleaved from the hCAP-18 precursor by proteinase 3 in neutrophils and other cells. Studies demonstrate three primary mechanisms: direct disruption of microbial membranes through carpet-like and toroidal-pore models documented by NMR and AFM (Henzler-Wildman 2003, Sochacki 2011); modulation of innate immune signalling through formyl peptide receptor 2 (FPR2) and other receptors with both pro- and anti-inflammatory effects depending on context (Wuerth 2017); and chemotactic activity for neutrophils, monocytes, and T-cells in inflamed tissue (De Yang 2000). Activity spectrum tested in vitro: gram-positive cocci including S. aureus and MRSA, gram-negative rods including P. aeruginosa and E. coli, several Candida species, and enveloped viruses including HSV-1, RSV, and influenza A (Tripathi 2013, Currie 2016). Concentration thresholds for direct kill range 1 to 50 µg/mL depending on organism and assay conditions.
Typical practice
Published clinical trials use the following ranges. Topical chronic-wound trials: 1 to 10 µg/mL gel formulation applied twice daily for 4 to 8 weeks; phase 2 venous leg ulcer trial dosed 0.5 to 1.6 mg of LL-37 per application (Grönberg 2014). Diabetic foot ulcer pilots: similar topical concentrations. Dental periodontal pockets in research: local microgram-level applications. Community subcutaneous-injection protocols documented in user logs run 100 to 500 µg per dose, daily or every-other-day, for 2- to 6-week courses; these protocols do not have trial validation. Reconstitution typical: 5 mg vial in 2 to 5 mL bacteriostatic water. Half-life in serum is short (minutes to a few hours depending on protease environment), which is one reason topical and depot formulations dominate the trial literature.
The dosing above is community practice, not a regulator-validated protocol. Trial-validated dosing for LL-37 in humans does not exist for most use cases listed.
Risks and contraindications
Adverse events reported in clinical trials are mostly local: injection-site or application-site irritation, transient erythema, occasional pruritus. Systemic adverse events have not been a primary signal in the topical-application phase 2 work. In vitro and animal data report two areas worth knowing about: at high concentrations LL-37 has shown pro-inflammatory and cytotoxic effects on host cells in some assay conditions (the same membrane-disrupting mechanism that kills microbes can damage mammalian cells above threshold concentrations); LL-37 promotes proliferation in some cancer cell lines (ovarian, lung, breast) in vitro and is upregulated in several human tumours (von Haussen 2008, Heilborn 2005), which has produced an open question in the literature about whether exogenous LL-37 administration could affect tumour biology in humans (no clinical data either direction). No trial data exists in pregnancy, lactation, or paediatric cohorts. Drug interactions have not been formally characterised.
Where this stands legally
FDA has not approved LL-37 as a drug. Sold as a research peptide. PMX-30063 (Brilacidin), a synthetic mimetic of LL-37 / defensin chemistry, has progressed in FDA-regulated trials for oral mucositis and ABSSSI; LL-37 itself has not.
MHRA has no LL-37 product registration. Topical LL-37 has been studied in UK and Swedish dermatology research settings under research-product manufacturing.
EMA has no LL-37 marketing authorisation. Phase 2 venous leg ulcer trial work has been conducted in Sweden and Germany under research-medicines provisions.
TGA has no LL-37 product on the ARTG. Compounded research preparations available through specialist pharmacies under physician oversight.
Thai FDA has not registered LL-37 as a drug. Sold through research-peptide vendors and used at some Bangkok dermatology and integrative-medicine clinics for chronic wound and biofilm contexts; physician oversight varies.
HSA has no LL-37 product registration. Research-grade material accessible through licensed research channels.
No Vietnam Drug Administration registration. Research-peptide channels supply the limited community use; HCMC dermatology clinics occasionally compound topical preparations.
The Hancock and Sørensen labs in Vancouver and Copenhagen have published most of the foundational LL-37 mechanistic and clinical work; Swedish dermatology research has driven the chronic-wound trial track.
Where users say they source it
Names below are sourced from community discussion. None are currently scored against the Panya 11-signal rubric. Panya does not earn commission on any of these. You can search them yourself; treat the list as a starting point for your own diligence, not an endorsement.
- International research-peptide suppliers with COA per lot covering peptide identity by HPLC and mass-specPending Panya 11-signal audit
- Topical research formulation pharmacies (US compounding pharmacies, Swedish research pharmacies)Pending Panya 11-signal audit
- Dermatology clinics compounding topical LL-37 for chronic wound contexts (case-by-case, physician-led)Pending Panya 11-signal audit
Full vendor scorecards for LL-37 land in a follow-up sprint after lawyer review and payment processor selection. We will not route users to any vendor that scores below 70 on the rubric.
Papers worth reading directly
- Grönberg A, Mahlapuu M, Ståhle M 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 →
- Vandamme D, Landuyt B, Luyten W, Schoofs L. (2012) A comprehensive summary of LL-37, the factotum human cathelicidin peptide. Cell Immunol →
- von Haussen J, Koczulla R, Shaykhiev R et al. (2008) The host defence peptide LL-37/hCAP-18 is a growth factor for lung cancer cells. Lung Cancer →
- Heilborn JD, Nilsson MF, Jimenez CI et al. (2005) Antimicrobial protein hCAP18/LL-37 is highly expressed in breast cancer and is a putative growth factor for epithelial cells. Int J Cancer →
- Tripathi S, Tecle T, Verma A et al. (2013) The human cathelicidin LL-37 inhibits influenza A viruses through a mechanism distinct from that of surfactant protein D or defensins. J Gen Virol →
Adjacent reading
Track LL-37 in your peptide journal.
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