Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of LL-37 and Vilon — mechanism, dosing, side effects, legal status, and pricing.
LL-37 is the only human cathelicidin antimicrobial peptide — a 37-amino-acid peptide (starting with two leucines) cleaved from the hCAP-18 precursor. It has broad-spectrum antimicrobial activity and immunomodulatory roles, but is also implicated in the pathogenesis of autoimmune and inflammatory skin diseases including psoriasis, rosacea, and lupus. Not FDA-approved; research-use only.
Vilon is a synthetic dipeptide (Lys-Glu / KE) from the Khavinson bioregulator series, originally derived from thymus extracts and studied in Russian preclinical models as an immunomodulator and geroprotector. Not FDA-approved; all published evidence originates from a single research group.
LL-37
Vilon
Category
Legal Status
Mechanism
Dose Range
Route
Frequency
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
LL-37
Vilon
COA corpus from Disclosed Labs — independently tested batches only.
LL-37
31
COAs
99.2%
Avg purity
8
Labs
Vilon
11
COAs
99.7%
Avg purity
6
Labs
LL-37 was characterized in the mid-1990s as the processed antimicrobial product of hCAP-18 (Gudmundsson et al., 1996). Dürr et al. (2006, Biochim Biophys Acta, PMID 16716248) provided a foundational review of its structure and activity as the sole human cathelicidin. Overhage et al. (2008, Infection and Immunity, PMID 18591225) showed LL-37 prevents Pseudomonas aeruginosa biofilm formation at 0.5 µg/mL — far below its MIC. A randomized, placebo-controlled Phase 1/2 trial (Grönberg et al., 2014, Wound Repair and Regeneration, PMID 25041740) found topical LL-37 safely accelerated healing of hard-to-heal venous leg ulcers at low doses. Its dual role in autoimmunity is well established: Lande et al. (2014, Nature Communications, PMID 25470744) identified LL-37 as a T-cell autoantigen in two-thirds of moderate-to-severe plaque psoriasis patients. No FDA approval exists for any indication. Injectable grey-market protocols for Lyme, biofilm, or mold illness lack controlled clinical evidence and carry theoretical autoimmune risk given LL-37's role in psoriasis, lupus, and rosacea pathogenesis.
Key references
Evidence is limited to Khavinson-group preclinical work. Khavinson & Anisimov (Dokl Biol Sci, 2000; PMID 10944717) reported that Vilon (L-Lys-L-Glu) inhibited spontaneous tumor growth and extended lifespan in CBA mice. A small Russian report on Vilon as an adjuvant in elderly colorectal-cancer patients (Kuznik et al., 2005; PMID 16075684) is non-randomized and unreplicated. No Western-framework clinical trials, pharmacokinetic, or dose-response studies have been published.
Key references
LL-37 and Vilon are both in the Immune category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Dosing Notes
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