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For in vitro laboratory research use only. Not for human consumption, diagnostic, or therapeutic use.
Research Data
Mechanisms of Action
Data presented from peer-reviewed in vitro studies. All findings are laboratory observations only.
Barlow et al. confirmed LL-37's direct virucidal activity against SARS-CoV-2 and influenza H1N1, demonstrating >99% viral inactivation at physiological concentrations. The mechanism involves disruption of the viral lipid envelope — the same target as bacterial outer membranes.
LL-37 is the only human cathelicidin — a host-defence antimicrobial peptide produced by neutrophils, keratinocytes, and epithelial cells. It disrupts bacterial, fungal, and viral membranes, neutralises LPS endotoxins, and demonstrated >99% SARS-CoV-2 inactivation at physiological concentrations in vitro.
Analytical Data
| Specification | Value |
|---|---|
| CAS Number | 154947-66-7 |
| Molecular Formula | C₂₀₅H₃₄₀N₆₀O₅₃S |
| Molecular Weight | 4493.33 g/mol |
| Purity (HPLC) | 99.0% |
| Appearance | White lyophilised powder |
| Solubility | Soluble in water (1 mg/mL) |
| Storage | −20°C long-term / 2–8°C short-term |
| Shelf Life | 36 months from production date |
| Research Grade | Yes — For In Vitro Use Only |
What Research Has Shown
Antiviral Activity Study — J. Immunol., 2020
SARS-CoV-2 In Vitro Inactivation at Physiological LL-37 Concentrations
Comparative Activity Profile
In Vitro Safety Data
LL-37 is an endogenous human cathelicidin produced by neutrophils, keratinocytes, and epithelial cells as part of the innate immune system. Its key research consideration is concentration-dependent membrane activity — at supra-physiological concentrations the amphipathic helix mechanism can affect host cell membranes.
Observed Adverse Indicators
Transient injection-site erythema
lowLocal burning sensation
lowMild systemic inflammation markers
lowSerious adverse events reported
low⚠️ Theoretical Concern
LL-37 exhibits concentration-dependent selectivity. At physiological concentrations its activity is directed at pathogen membranes; at higher concentrations, host membrane effects have been observed in vitro.
Researcher Reference
LL-37 forms amphipathic alpha-helices that insert into negatively charged microbial membranes (bacterial, viral envelopes), disrupting membrane integrity via toroidal pore formation or carpet mechanism. Its selectivity for pathogens over host cells comes from the difference in lipid composition — bacterial membranes contain phosphatidylglycerol and cardiolipin which are targeted more effectively than mammalian phosphatidylcholine-rich membranes.
Beyond antimicrobial action, LL-37 activates EGFR and FPRL1 receptors on keratinocytes, promoting migration and re-epithelialisation. It also induces VEGF release from fibroblasts, supporting angiogenesis. This dual antimicrobial + regenerative profile makes it a key innate immune wound healing factor.
Lyophilised: −20°C up to 36 months. Reconstituted: 4°C, use within 14 days. Avoid repeated freeze-thaw cycles.
Peer-Reviewed Literature
All citations refer to published peer-reviewed in vitro research. Data presented for scientific reference only. No claims made regarding human therapeutic use.
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