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IMMUNEPEPTIDE PROFILE

LL-37

Also known as Cathelicidin, hCAP-18 fragment

LL-37 is the only human cathelicidin antimicrobial peptide, a 37-amino-acid peptide cleaved from the precursor protein hCAP-18. It is produced by immune cells (neutrophils, macrophages), epithelial cells, and keratinocytes as part of the innate immune response. It has broad-spectrum antimicrobial activity against bacteria, viruses, and fungi, and plays a role in wound healing and immune modulation.

Last updated April 10, 2026

TL;DR

Quick summary

LL-37 is the only human cathelicidin antimicrobial peptide, a 37-amino acid fragment of hCAP-18 with broad-spectrum activity against bacteria, viruses, and fungi. It modulates innate immunity, promotes wound healing, and is closely linked to vitamin D status.

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Overview

LL-37 is the only human cathelicidin antimicrobial peptide, a 37-amino-acid peptide cleaved from the precursor protein hCAP-18. It is produced by immune cells (neutrophils, macrophages), epithelial cells, and keratinocytes as part of the innate immune response. It has broad-spectrum antimicrobial activity against bacteria, viruses, and fungi, and plays a role in wound healing and immune modulation.

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Mechanism of action

LL-37 has a helical amphipathic structure that allows it to insert into and disrupt microbial cell membranes, creating pores and causing lysis. Beyond direct antimicrobial action, it modulates the immune response by recruiting immune cells (chemotaxis), promoting wound healing, inhibiting biofilm formation, neutralizing bacterial endotoxins (LPS), and modulating TLR signaling. Vitamin D regulates LL-37 expression, linking vitamin D deficiency to increased infection susceptibility.

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Dosing protocols

PurposeRouteDosageFrequency
immune supportsubcutaneous50100 mcgdaily

Dosing information is for educational purposes only. Consult a qualified healthcare professional before using any peptide.

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Research summary

Extensive research on innate immunity. Studies show broad-spectrum activity against MRSA, E. coli, Pseudomonas, Candida, and enveloped viruses including influenza and HIV. Anti-biofilm activity demonstrated against surgical implant infections. Wound healing promotion through angiogenesis and re-epithelialization. Phase I/II clinical trials for chronic leg ulcers showed improved healing. Vitamin D supplementation increases LL-37 levels — a key finding linking vitamin D to immune function.[1][2][3][4][5]

📄This section cites 5 peer-reviewed sources. View all references →
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Evidence grading

Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.

moderate
Broad-spectrum antimicrobial activityDurr Biochim Biophys Acta 2006 + Bucki 2010 review; extensive in vitro and animal data vs MRSA, Pseudomonas, Candida
preliminary
Chronic wound healing promotionPhase I/II trials in chronic leg ulcers cited in research summary; small controlled studies with limited follow-up
moderate
Vitamin D-mediated immune functionMultiple observational and interventional studies showing vitamin D upregulates LL-37 gene expression; established mechanism
preliminary
Anti-biofilm activityIn vitro studies on surgical implant biofilm models; no completed human biofilm eradication trials
preliminary
Macrophage phagocytosis enhancementWan et al. J Leukoc Biol 2014: in vitro human macrophage assays; mechanism confirmed, translation untested

Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data

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Side effects

Injection site reactions
Redness/swelling
Mild fever (rare, immune activation)

Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.

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Common stacks

Peptides commonly paired with LL-37 for synergistic effects.

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Sourcing & access

Research compound

LL-37 is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).

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Frequently asked questions

LL-37 is a 37-amino acid antimicrobial peptide cleaved from the precursor protein hCAP-18. It is produced by immune cells and epithelial cells as part of the innate immune response and has broad-spectrum activity against bacteria (including MRSA), viruses, and fungi.

LL-37 has an amphipathic helical structure that inserts into and disrupts microbial cell membranes. Beyond direct antimicrobial action, it recruits immune cells, promotes wound healing through angiogenesis, inhibits biofilm formation, and neutralizes bacterial endotoxins.

Reported side effects include injection site reactions, redness or swelling, and rare mild fever attributed to immune activation. LL-37 is not FDA-approved and is available only as a research peptide, so its long-term safety profile in humans is not formally characterized outside small Phase I and II chronic wound healing trials.

Vitamin D directly regulates LL-37 gene expression through the vitamin D receptor, which binds response elements in the cathelicidin gene promoter. Supplementation measurably increases endogenous LL-37 levels, and this pathway is the core mechanism linking vitamin D deficiency to increased susceptibility to bacterial, viral, and fungal infections.

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Research references

  1. LL-37, the only human member of the cathelicidin family of antimicrobial peptidesDürr UHN, Sudheendra US, Ramamoorthy ABiochim Biophys Acta, 2006PubMed
  2. Cathelicidin LL-37: a multitask antimicrobial peptideBucki R, Leszczyńska K, Namiot A, et al.Arch Immunol Ther Exp (Warsz), 2010Review
  3. Therapeutic Potential of Cathelicidin Peptide LL-37, an Antimicrobial Agent, in a Murine Sepsis ModelZhang Z, Shively JEFront Immunol, 2020PubMed
  4. The Human Cathelicidin Antimicrobial Peptide LL-37 and Mimics are Potential Anticancer DrugsKuroda K, Okumura K, Isogai H, et al.Front Oncol, 2015PubMed
  5. Antimicrobial peptide LL-37 promotes bacterial phagocytosis by human macrophagesWan M, van der Does AM, Tang X, et al.J Leukoc Biol, 2014PubMed
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