LL-37 Guide: What It Is and How It Works

Why an immune peptide is suddenly everywhere

Stubborn wounds. Recurring skin infections. A gut that won’t bounce back after antibiotics. These are the real-world puzzles pushing scientists to revisit our built-in defenses.

Meet LL-37, a 37–amino acid antimicrobial peptide your body makes to fend off microbes and jump-start repair. It first drew attention in wound healing and infection defense, and early studies now explore benefits for skin, sinuses, and tissue recovery.

Curious how a native molecule became a lab focus, and what that could mean in practice?

Meet the body’s cathelicidin

LL-37 is the only human cathelicidin. Think of cathelicidins as first responders that can puncture microbial membranes and coordinate early immune signals. Your cells produce a larger precursor (hCAP18) that is cleaved into the active LL-37 fragment in epithelial tissues and by white blood cells.

Research-grade LL-37 is made synthetically via solid-phase peptide synthesis, typically as a sterile acetate salt for topical or local research use. Access varies by jurisdiction and is generally limited to research settings.

If your body already makes it, what happens when we add more from the outside?

From membranes to messengers: the mechanism

LL-37 works in two modes. First, it directly disrupts microbial membranes across a range of bacteria, some fungi, and certain enveloped viruses in lab studies. Second, it acts as a signal that shapes repair and inflammation. It engages receptors like FPR2/ALX on immune and endothelial cells and can influence purinergic pathways such as P2X7. Through these routes it recruits immune cells, neutralizes bacterial endotoxin (LPS), and helps trigger factors that support re-epithelialization and new vessel growth.

In everyday terms, after a scrape, LL-37 helps skin cells crawl to close the gap while drawing in cleanup crews. In the nose or lungs, it can stiffen mucosal defenses, though sensitive airways may feel irritated at high levels. In a chronic wound, it can nudge a stuck inflammatory phase toward actual tissue repair when microbes are part of the delay.

Context is everything. At balanced levels, LL-37 coordinates defense and repair; at high, persistent levels, it can amplify inflammation or pair with self-DNA to overactivate immunity, a pattern linked to psoriasis in research. So how is it being tested in humans so far?

How it’s used in research settings

There is no FDA-approved dosing standard for LL-37. Human studies have centered on topical and local applications for skin or mucosal conditions, with small early-phase trials suggesting feasibility and local tolerability. Systemic use is still investigational and lacks robust controlled data.

Routes explored

• Topical gels or creams for hard-to-heal skin ulcers, aiming for local antimicrobial and pro-repair effects
• Intralesional (local) injections to concentrate exposure in a wound or lesion while limiting systemic spread
• Intranasal or inhaled routes in mucosal immunity research, where airway sensitivity is a consideration
• Subcutaneous or intravenous routes remain exploratory with no consensus on safe or effective systemic dosing
• Oral delivery is not favored because peptides are degraded in the gut

You may hear about “cycles” or peptide “stacks.” There is no validated cycling schedule, and combinations have little controlled evidence beyond standard wound care. That makes safety the next logical question, right?

Safety snapshot: risks, unknowns, red flags

Short-term local use has looked tolerable in small studies, but long-term or systemic safety has not been well characterized. What can go wrong? At the application site, some people feel burning, redness, swelling, or pain. On mucosal surfaces like sinuses or airways, higher concentrations can irritate. Because LL-37 boosts signaling, it may worsen conditions where innate immunity is already revved up. At very high local doses, what harms microbes can also stress human cells. And by exerting broad antimicrobial pressure, it can shift the local microbiome, which may help in infected wounds but could unbalance healthy flora elsewhere.

Extra caution is reasonable in pregnancy and lactation (no data), active autoimmune or autoinflammatory disease such as psoriasis (risk of immune overactivation), chronic airway disease like asthma (sensitivity is possible), active cancer (context-dependent preclinical effects), and in children (limited data).

For local use, the “monitoring lab” is the tissue itself: Is the wound shrinking? Is there irritation? Are cultures moving in the right direction? For any systemic exposure in research, clinicians often track a basic safety panel and inflammation trends while anchoring decisions to the underlying condition. What else should you know before chasing access?

Where LL-37 fits among peptides

Peptides aren’t one thing. LL-37 lives in the antimicrobial and immune-modulating corner, where it blends pathogen control with repair signaling. By contrast, TB-500 (a thymosin beta-4 fragment) emphasizes cell migration through actin dynamics. BPC-157 shows pro-angiogenic and mucosal effects in preclinical models. GHK-Cu shines in dermatology for collagen and elastin support. Mechanistic pairing sounds attractive — for example, an antimicrobial signal with a matrix-remodeling signal in an infected, nonhealing wound — but this remains hypothesis space with few controlled head-to-head or combination trials.

Want the less glamorous, more effective reminder? Standard wound care still does the heavy lifting: debridement, off-loading, and glycemic control when relevant. Ready for the regulatory fine print?

Regulatory reality check

LL-37 is not FDA-approved for any indication. In the U.S., it is treated as a research-use chemical. It is excluded from routine compounding bulks lists, which limits legitimate pharmacy access and places more burden on verifying quality and provenance.

Quality controls that matter

• Verified identity and purity (HPLC, mass spectrometry)
• Low endotoxin levels for anything applied to tissue or blood
• GMP-grade manufacturing, documented chain of custody, and appropriate storage

Athletes should note WADA’s S0 category. Any pharmacological agent not approved for human use is prohibited in and out of competition, which captures LL-37. Given the early science and tight regulations, how do you track whether anything is actually helping?

Biomarkers to watch

LL-37’s footprint is immune and tissue-centric, not endocrine. The focus is on safety, inflammation, infection control, and functional healing.

Practical markers clinicians consider

• CBC with differential to watch neutrophils, eosinophils, and infection dynamics
• CRP or hs-CRP to track systemic inflammation trends
• Liver enzymes and creatinine for general safety with any investigational systemic exposure
• Microbiology from wounds or sinuses (culture or PCR) to confirm infection control when relevant
• Wound dimensions, photo documentation, or perfusion assessments when blood flow matters

Bringing it all together

LL-37 is a native human defense peptide with a dual personality. It can puncture microbes and choreograph early repair, which maps to outcomes people care about: cleaner wounds, faster re-epithelialization, stronger barriers. The most encouraging human data are small and local. Systemic use remains an open question, and it is not FDA-approved.

The throughline is balance. Too little signal, and healing stalls. Too much for too long, and irritation or misdirected inflammation shows up. That is why personalization, measurement, and evidence-first thinking beat one-size-fits-all protocols.

If you want precision, start with the terrain. At Superpower, we combine a single panel spanning 100-plus biomarkers with clinical context so you can see inflammation, micronutrient status, metabolic health, and whether peptide strategies even make sense for your goals.

Because the real win isn’t chasing the newest peptide. It’s knowing what your body needs to heal well and stay strong. Ready to see your biology in high definition?