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Explore  /  LL-37 (Cathelicidin)
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LL-37 (Cathelicidin)

A
lead outcome
Endogenous antimicrobial defense
grades vary by outcome ↓
Peptide
also called — LL-37 · cathelicidin (the human cathelicidin) · the C-terminal active fragment of hCAP18 (gene CAMP)
(defensive:) antimicrobialwound healingangiogenesis(pathological when dysregulated:) rosacea / psoriasis / lupus inflammation(gray-market pitch:) healing / anti-infective / skin

The double-edged sword of innate immunity — a natural antibiotic that, dysregulated, drives inflammatory disease. LL-37 is unusual in this register: it's sold as a healing/antimicrobial peptide, yet its largest and strongest evidence base is about its role in causing skin disease (rosacea, psoriasis

In brief

LL-37 is the body's own broad-spectrum antimicrobial peptide — the only human cathelicidin — a 37-amino-acid innate-immune effector made by skin and immune cells, switched on by vitamin D and injury, and activated by protease cleavage. It genuinely kills microbes (by disrupting their membranes) and supports wound healing and angiogenesis. But its defining feature is a dual role: it's also an "alarmin," and when its expression or processing goes wrong, it becomes a driver of inflammatory and autoimmune disease — it generates the inflammatory fragments of rosacea, breaks tolerance to self-DNA in psoriasis (via TLR9), and feeds lupus. That's the paradox for a register: LL-37 is sold as a healing/antimicrobial peptide, but its largest, most rigorous evidence base is about how it causes skin disease when dysregulated. As an exogenous therapeutic it's preclinical with no approvals, and administering a pro-inflammatory alarmin — particularly to anyone prone to rosacea or psoriasis — could plausibly do the opposite of healing. A fascinating, important molecule; a genuinely double-edged one; not a validated therapy.

Legal standing, by region
European Union
not an approved drug

not an approved drug; investigational. Not an approved cosmetic ingredient (an injectable pro-inflammatory alarmin is not a topical cosmetic). No compounding pathway.

Evidence, by outcome

An honest grade per outcome — drawn from the evidence, not any catalogue. Hype and undemonstrated marketing claims grade low.

OutcomeEvidence base · effectGrade
Endogenous antimicrobial defense
This grades LL-37's natural role — NOT a demonstrated benefit of taking exogenous LL-37
Extensive: potent broad-spectrum membrane-disrupting killing; surges in wounds
A
Exogenous wound healing / antimicrobial therapy (the marketed use)
No approved product; no human trials establishing efficacy or safety of exogenous use
Preclinical / early; angiogenic & pro-healing in models
D
Role in rosacea (as a cause)
This is evidence it drives disease — a reason for caution, not a therapeutic credential
Strong: abnormal processing → pro-inflammatory fragments → erythema/telangiectasia
A
Role in psoriasis / lupus (as a cause)
Again: robust evidence of harm/pathogenic role, underscoring the risk of exogenous use
Strong: LL-37+self-DNA→TLR9→break self-tolerance; T-cell autoantigen; NET/IFN in SLE
A
Safety of exogenous administration
It's a pro-inflammatory alarmin; plausible to trigger/worsen inflammatory-autoimmune skin disease; contraindicated intuition for rosacea/psoriasis-prone users
Not established in humans

Identity the only human cathelicidin — a 37-amino-acid, cationic, amphipathic α-helical peptide that is a core effector of innate immunity. It's produced as an inactive precursor (hCAP18) by keratinocytes, neutrophils and other cells, then cleaved by proteases (kallikreins KLK5/KLK7) into the active LL-37. Its production is induced by vitamin D (UV light → vitamin D → cathelicidin — one reason facial skin is a hotspot) and by an alternative ER-stress pathway. It sits in the skin's chemical barrier — the first line of defense against microbes. ## Mechanism (as proposed) LL-37 is cationic and amphipathic, so it's drawn to negatively-charged microbial membranes, which it inserts into and disrupts, killing bacteria rapidly and broadly (its antimicrobial face). But the same peptide is a host immunomodulator/"alarmin": it chemoattracts immune cells, promotes angiogenesis and wound repair, and — critically — binds host nucleic acids (self-DNA/RNA) and ferries them into immune cells, where they activate Toll-like receptors (notably TLR9). In healthy skin this is controlled; when cathelicidin is over-expressed (psoriasis) or mis-processed into inflammatory fragments (rosacea) or released in NETs (lupus), it breaks immune tolerance and ignites chronic inflammation/autoimmunity. So LL-37's healing and harming functions are two faces of one molecule — which is exactly why exogenous use is not a simple "healing peptide" proposition.

Sources — 4 cited
01Reinholz M, Ruzicka T, Schauber J. Cathelicidin LL-37: an antimicrobial peptide with a role in inflammatory skin disease. Ann Dermatol. 2012 (dual role; rosacea/psoriasis/AD; vitamin D & ER-stress induction).
02Lande R, et al. Cationic antimicrobial peptides in psoriatic skin cooperate to break innate tolerance to self-DNA. (LL-37 + self-DNA → TLR9/pDC); LL-37 as psoriasis T-cell autoantigen.
03Yamasaki K, Di Nardo A, Gallo RL, et al. — cathelicidin processing (KLK5/KLK7) and pro-inflammatory fragments in rosacea.
04Reviews: innate immunity & cathelicidin in inflammatory skin disease (PMC3904447); LL-37 as a "double-edged sword" (host defense vs disease). (Exogenous therapeutic use preclinical; no human approvals as of 2026.)
Review status
Not yet reviewed

A credentialed reviewer (PharmD / PhD / MD) will be named before this entry is finalised. Until then, treat it as a working draft. Last updated July 2026 (watch: engineered LL-37 analogs/fragments that dissociate antimicrobial from pro-inflammatory activity — the field's key therapeutic goal).

Grades reflect the published evidence, not our interest. No dosing, reconstitution, or administration is published for research compounds — that restraint is deliberate.

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LL-37 (cathelicidin) — the double-edged antimicrobial peptide: healer, and driver of rosacea/psoriasis · Vallydia