Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of KPV and LL-37 — mechanism, dosing, side effects, legal status, and pricing.
KPV (Lys-Pro-Val) is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (alpha-MSH residues 11-13), the smallest alpha-MSH fragment retaining anti-inflammatory activity. Research-only; not FDA-approved. Evidence is primarily preclinical with no controlled human trials.
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.
KPV
LL-37
Category
Legal Status
Mechanism
Dose Range
Route
Frequency
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
KPV
LL-37
COA corpus from Disclosed Labs — independently tested batches only.
KPV
89
COAs
99.5%
Avg purity
15
Labs
LL-37
31
COAs
99.2%
Avg purity
8
Labs
Dalmasso et al. (Gastroenterology 2008; PMID 18061177) demonstrated PepT1-mediated uptake of KPV and reduction of DSS- and TNBS-induced colitis in mice. Kannengiesser et al. (Inflammatory Bowel Diseases 2008; PMID 18092346) showed anti-inflammatory effects in two murine colitis models at least partly independent of MC1R signaling. Brzoska et al. (Endocrine Reviews 2008; PMID 18612139) reviewed alpha-MSH and related tripeptides, summarizing NF-kB suppression across cell types. Subsequent preclinical work (largely from the Merlin group at Georgia State) has explored oral nanoparticle and polysaccharide-hydrogel delivery for IBD. No controlled human trials have been published.
Key references
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.
KPV and LL-37 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
Half-life
Side Effects
Contraindications
Lab Testing
Key references
Disclosed Labs