LL-37 is the only known human cathelicidin antimicrobial peptide — the C-terminal 37-amino acid fragment of the hCAP-18 precursor (human cationic antimicrobial protein 18, encoded by the CAMP gene). It is produced primarily by neutrophils, epithelial cells, mast cells, and NK cells, and serves as a first-line innate immune defence molecule with a remarkably broad biological profile: direct membrane-disrupting antimicrobial activity against bacteria, viruses, and fungi; TLR4 and LPS antagonism/modulation (endotoxin neutralisation); angiogenesis promotion; wound healing; and anti-biofilm activity. Its dual role as antimicrobial and immunomodulator makes it the central research tool for innate immunity, wound healing, and skin defence biology.
4493.3 g/mol
Molecular weight
Cathelicidin
Only human cathelicidin — hCAP-18 derived
Broad-spectrum
Antibacterial, antiviral, antifungal activity
Immunomodulatory
TLR4 modulation, angiogenesis, wound healing
≥99%
Purity — HPLC verified
LL-37 — Specifications
LL-37 — specifications
Property
Value
CAS Number
154947-66-7
Molecular Formula
C₂₀₅H₃₄₀N₆₀O₅₃
Molecular Weight
4493.3 g/mol
Half-life
Minutes (plasma); tissue activity longer
Class
Human cathelicidin antimicrobial peptide (CAMP)
Purity
≥99% HPLC verified
COA
Janoshik independent third-party
⚙️
Mechanism of Action — LL-37
LL-37 has multiple simultaneous mechanisms — no single receptor:
Antimicrobial (membrane disruption): Amphipathic α-helical structure → electrostatic interaction with negatively charged bacterial membranes → carpet/toroidal pore model → membrane disruption. Effective against Gram+, Gram−, mycobacteria, fungi, enveloped viruses
P2X7 purinergic receptor: LL-37 acts as allosteric modulator → NLRP3 inflammasome activation in macrophages
LL-37 in skin defence — the psoriasis paradox
In normal skin, LL-37 is low-level — a first-line defence. In psoriasis, keratinocytes overexpress LL-37, which complexes with self-DNA → activates plasmacytoid dendritic cell TLR9 → type I interferon production → T-cell-mediated inflammation. This is why LL-37 is simultaneously a defence molecule and a driver of inflammatory skin disease. Studying LL-37 dose-response and context-dependence (antimicrobial vs autoimmune-promoting) is a major active research area in dermatology and innate immunity.
Key Research Studies & Clinical Data
Key LL-37 research
Study
Model/Context
Key finding
Zanetti et al. 2004 (review, JLB)
Human cathelicidin biology
LL-37 comprehensive mechanism review — foundational reference for the field
Lau et al. 2018 (FASEB)
Wound healing, LL-37 topical
LL-37 accelerated wound closure via VEGF/angiogenesis in diabetic mouse model
Dominguez-Villar et al. 2021 (Sci Immunol)
COVID-19 lung LL-37
Reduced LL-37 in COVID-19 lungs correlated with worse outcomes — antiviral role
Research Protocols — LL-37
Protocol 1: Antimicrobial MIC determination
LL-37 serial dilution (0.5–32 µg/mL) in 96-well broth microdilution against S. aureus, P. aeruginosa, E. coli, C. albicans, MRSA. MIC/MBC determination per CLSI guidelines. Membrane integrity control: SYTOX green uptake (flow cytometry), inner membrane disruption (β-galactosidase leakage in E. coli).
LL-37 is the only human cathelicidin antimicrobial peptide — the C-terminal fragment of hCAP-18, expressed in neutrophils and epithelial cells. It kills bacteria, fungi, and viruses through membrane disruption, neutralises LPS, promotes angiogenesis and wound healing, and modulates TLR signalling.
How does LL-37 kill bacteria?
LL-37 forms an amphipathic alpha-helix that electrostatically attracts to the negatively charged outer membrane of bacteria (Gram+ and Gram−). It then disrupts the membrane through a carpet or toroidal pore mechanism — causing membrane depolarisation and cell lysis. Unlike antibiotics, this physical mechanism makes resistance development much more difficult.
Why does LL-37 both fight infection and drive inflammation in psoriasis?
In psoriasis, overproduced LL-37 forms complexes with self-DNA, which activates plasmacytoid dendritic cell TLR9 — triggering type I interferon production and initiating T-cell-mediated autoimmune inflammation. This is context-dependent: low LL-37 is antimicrobial; high LL-37 in psoriatic skin activates innate immune pathways. Studying this dose-dependence requires both in vitro and in vivo models.
What research models use LL-37?
Key models include: MIC/MBC antimicrobial assays against MRSA and Gram-negative pathogens; LPS endotoxin neutralisation and sepsis models; wound healing (diabetic mouse punch biopsy); IMQ psoriasis model; lung infection (P. aeruginosa); and antiviral studies (HSV, influenza, SARS-CoV-2 in vitro).
What formats does QSC supply LL-37 in?
QSC supplies LL-37 as 5mg lyophilised vials in 10-vial kits (50mg total), ≥99% purity HPLC verified with Janoshik COA. Ships from domestic QSC warehouses in USA, EU, UK, Canada, and Australia.
Research Use Only: All QSC compounds are sold strictly for laboratory research purposes. Not for human use. Not approved by the FDA or equivalent regulatory bodies for human administration. All purchases confirm research intent and compliance with applicable local regulations.
