Apex Research Reference
LL-37
Cathelicidin Antimicrobial Peptide — Human hCAP18 Fragment
ANTIMICROBIAL IMMUNOMODULATORY WOUND HEALING ANTI-BIOFILM ENDOGENOUS
01 — Identity

What Is LL-37?

1995
CHARACTERIZED
37 AA
AMINO ACIDS
Cathelicidin
PEPTIDE CLASS
Endogenous
ORIGIN
Origin
The only human cathelicidin. Cleaved from the C-terminus of hCAP18 (human cationic antimicrobial protein 18) by protease 3. Produced by neutrophils, macrophages, mast cells, NK cells, and epithelial cells at sites of infection and inflammation.
Chemical Class
37-amino acid cationic amphipathic alpha-helical peptide. The "LL" designation refers to the two leucine residues at the N-terminus.
Primary Use
Broad-spectrum antimicrobial, anti-biofilm, wound healing acceleration, immune modulation. First-line innate immune defense peptide.
Administration
Subcutaneous injection for systemic effects. Topical spray or gel for wound healing. Intranasal for respiratory applications.
LL-37 kills microorganisms by disrupting the integrity of microbial cell membranes — it inserts into the lipid bilayer and causes membrane depolarization and lysis. Critically, this mechanism targets bacterial membranes (negatively charged) over mammalian cell membranes (zwitterionic) — giving it broad antimicrobial activity with selectivity for pathogens over host cells.
02 — Research History

Discovery & Research Timeline

1980s
Cathelicidin family identified in mammalian neutrophils. Multiple species found to express cathelicidins as innate immune defense peptides. The human version (hCAP18) is identified as a neutrophil granule protein.
1995
Gudmundsson et al. fully characterize LL-37 as the C-terminal cleavage product of hCAP18. The 37-amino acid sequence and its broad-spectrum antimicrobial activity are documented. LL-37 confirmed as the only human cathelicidin peptide.
2003
Pivotal research demonstrates LL-37 disrupts and penetrates established bacterial biofilms — particularly Pseudomonas aeruginosa. Biofilm disruption is a critical advance since biofilms protect chronic wound bacteria from antibiotics.
2005
Wound healing studies show LL-37 stimulates keratinocyte migration and proliferation, promotes re-epithelialization, and induces angiogenesis. VEGF upregulation confirmed as a mechanism of LL-37-driven wound repair.
2012
Anti-cancer research reveals LL-37 selectively induces apoptosis in certain cancer cell lines (colon, lung, breast) while sparing normal epithelial cells. The mechanism involves mitochondrial membrane disruption in cancer cells.
2016–Present
Autoimmune research links LL-37 to lupus pathogenesis (anti-LL-37 antibodies found in SLE patients) and identifies immunomodulatory roles in psoriasis and rosacea. Research peptide community adopts LL-37 for wound healing, infection, and immune support protocols.
03 — Primary Benefits

Documented Effects

01
Broad-Spectrum Antimicrobial
Kills gram-positive bacteria, gram-negative bacteria, fungi, enveloped viruses, and some protozoa by disrupting membrane integrity. Effective against both antibiotic-sensitive and antibiotic-resistant strains including MRSA.
02
Anti-Biofilm Activity
Penetrates and disrupts established bacterial biofilms — the protective matrix that makes chronic wound infections resistant to antibiotics. LL-37 is one of the few agents capable of penetrating mature P. aeruginosa biofilms.
03
Wound Healing Acceleration
Stimulates keratinocyte migration and proliferation for re-epithelialization. Upregulates VEGF for angiogenesis. Reduces biofilm burden at wound sites. One of the most potent peptides for chronic wound resolution.
04
Immune Modulation
Acts as a bidirectional immune regulator — pro-inflammatory at infection sites (recruits neutrophils and monocytes) and anti-inflammatory in non-infected tissue (reduces excessive cytokine production). Balances rather than simply stimulates immunity.
05
Respiratory Protection
Highly expressed in lung epithelium and airway secretions. Reduces bacterial burden in upper and lower respiratory infections. Studied in cystic fibrosis, COPD, and COVID-19 contexts for innate airway defense enhancement.
06
Anti-Cancer Activity
Selectively induces apoptosis in cancer cell lines (colon, lung, breast, ovarian) while sparing normal cells. Mechanism differs from chemotherapy — mitochondrial membrane disruption rather than DNA damage.
07
Angiogenesis Promotion
Promotes formation of new blood vessels via VEGF, FGF2, and direct endothelial cell stimulation. Relevant for wound healing, ischemic tissue repair, and recovery from vascular injury.
04 — Reconstitution

Mixing & Storage

▸ Standard Reconstitution — 5mg Vial
5mg vial + 300 units BAC water = 16.7 mcg per unit on insulin syringe
5,000 mcg total per vial · Refrigerate after reconstitution · Use within 4–6 weeks · Protect from light
LL-37 can also be used topically. For wound healing applications, dissolve in sterile saline at 50–100 mcg/mL and apply directly to wound bed. For injectable use, standard BAC water reconstitution applies. Some protocols combine topical + injectable for systemic + local effect.
UNRECONSTITUTED
Refrigerate at 2–8°C. Protect from light and humidity. Stable for shipping at room temp short-term.
RECONSTITUTED
Refrigerate at 2–8°C. Use within 4–6 weeks. Protect from light. Do not freeze liquid solution.
05 — Dosing Protocol

Dose Levels & Unit Draws

LevelDoseSyringe DrawDescription
LOW
100mcg
6 units on insulin syringe		 6u Immunomodulatory and general immune support dose. Conservative starting point. Assess tolerance — some users experience temporary redness at injection site.
STANDARD
250–500mcg
15–30 units on insulin syringe		 15–30u Therapeutic dose for active infection support, wound healing, and anti-biofilm protocols. Daily SC injection for systemic effect.
HIGH
500–1000mcg
30–60 units on insulin syringe		 30–60u Intensive antimicrobial or chronic wound healing protocol. Higher doses may cause increased injection site inflammation — manage with rotating sites.
For topical wound healing: dissolve reconstituted LL-37 to a concentration of 50–100 mcg/mL in sterile saline. Apply to clean wound bed 1–2× daily under dressing. Can be combined with systemic SC injection for dual-route delivery in chronic wounds or persistent infections.
06 — Timing & Frequency

When & How Often

VariableRecommendationWhy
Frequency Daily (acute) / Every other day (maintenance) Active infection or wound healing: daily SC injection. Immune support maintenance: every other day is adequate given the immunomodulatory mechanism.
Time of Day AM preferred Innate immune activity is highest in the morning. AM dosing aligns with natural immune rhythm. Not a hard requirement.
Fasted vs Fed Either acceptable LL-37 mechanism is not dependent on metabolic state. Food intake does not significantly affect efficacy.
Injection Site Rotate sites — abdomen, thigh, arm LL-37 can cause local inflammation at the injection site (part of its mechanism). Rotating sites prevents site-specific inflammation accumulation.
Topical Application 1–2× daily directly to wound For wound healing protocols, topical application delivers LL-37 directly to the wound bed for local antimicrobial + healing effect. Can be combined with systemic SC dosing.
07 — Biomarker Monitoring

Lab Tests & Optimal Ranges

▸ Immune Function
BiomarkerLab TestClinical RangeOptimal Range
WBC Differential
Immune cell baseline		 CBC with differential CLINICALWBC 4.5–11.0 × 10³/µL OPTIMALWBC 4.5–6.0; neutrophil 50–65%
hsCRP High-Sensitivity CRP CLINICAL<3.0 mg/L OPTIMAL<0.5 mg/L
IL-6 Serum IL-6 CLINICAL<7.0 pg/mL OPTIMAL<1.5 pg/mL
IL-10
Anti-inflammatory cytokine		 Serum IL-10 CLINICAL<9.1 pg/mL OPTIMALStable or rising with treatment
▸ Safety Panel
BiomarkerLab TestClinical RangeOptimal Range
AST / ALT CMP CLINICALAST 10–40 / ALT 7–56 U/L OPTIMALAST <26 / ALT <26 U/L
Creatinine / eGFR CMP CLINICALCreat 0.7–1.3 / eGFR >60 OPTIMALeGFR >90
CBC Complete Blood Count CLINICALStandard ranges OPTIMALMid-range; WBC 4.5–6.0
⚠ LL-37 is not FDA-approved for injectable use. Most research is in vitro and animal models. Human pharmacokinetic data for injectable LL-37 is limited. At infection sites LL-37 may cause transient local inflammation — this is part of its mechanism (innate immune recruitment) and is expected. Topical use for wound care has a strong clinical research base and is considered lower risk than systemic injection.
08 — Cycle Protocol

Cycle Length, Frequency & Timing

ACUTE INFECTION / WOUND
4–8 Weeks
Daily SC injection at 250–500mcg for active infection or wound healing protocol. Continue until resolution then taper.
IMMUNE SUPPORT
8–12 Weeks
Every-other-day dosing at 100–250mcg for immune modulation and chronic inflammation support. 4-week break between cycles.
PROTOCOL SUMMARY
4–12 wk
CYCLE LENGTH
Daily
ACUTE FREQ
EOD
MAINTENANCE FREQ
AM
TIMING
SC / Topical
ROUTE
4 wk
BREAK