Where to Buy Peptides Online — LL-37 Mechanism & Research Overview

Research-only educational content. No medical claims. All products at PureTestedPeptides.com are for laboratory, in-vitro, or analytical use only — not for human consumption.


LL-37 10mg vial — Pure Tested Peptides
LL-37 (10 mg) product photo — click to open product page.

LL-37 is the human cathelicidin antimicrobial peptide — a short, positively charged, alpha-helical peptide generated from the hCAP18 precursor. In the lab, it’s famous for two big reasons: (1) it sticks to and destabilizes negatively charged microbial membranes, and (2) it doubles as an immune “tuning” signal (chemotaxis, cytokine shaping, barrier support). Think of LL-37 as a Swiss-army micropeptide: direct microbe pressure + host-defense choreography.

Below we break down how LL-37 works mechanistically (membrane interactions, LPS neutralization, nucleic-acid binding, antibiofilm behavior, and immune receptor cues) in a friendly, plain-English way — while keeping the details researchers care about.

View LL-37 10 mg (Research-Only)

LL-37 at a glance: the mechanism map


Illustration: LL-37 binds microbial membranes (electrostatic), disrupts bilayers, neutralizes LPS, cues immune cells via FPR2, binds DNA/RNA (NETs), and disrupts biofilms. Research-only schematic.
  • Electrostatic docking & bilayer stress: LL-37’s cationic helix targets the anionic surface of bacterial membranes. Enough local crowding → curvature strain → pores/defects.
  • LPS neutralization: Binding to lipid A/core regions of endotoxin can blunt TLR4-triggering in model systems.
  • Immune receptor signaling: LL-37 can serve as a chemotactic cue through FPR2 on epithelial/immune cells, shaping cell trafficking and reactive programs.
  • DNA/RNA interactions: It associates with extracellular nucleic acids (e.g., in neutrophil extracellular traps), stabilizing structures and tuning TLR sensing in vitro.
  • Antibiofilm behavior: By perturbing matrix and cell membranes simultaneously, LL-37 can interfere with mature biofilms in experimental systems.

For deeper background, see the LL-37 product page for literature pointers and the innate-immunity overview.

How LL-37 “does the job”

1) Membrane targeting 101

Microbial outer surfaces are usually more negative than mammalian membranes. LL-37’s positive residues cruise right in, align on the bilayer, and — in enough numbers — make the membrane leaky. Depending on lipid composition and crowding, it’s a mix of toroidal pores, carpet-like destabilization, and transient defects. Net effect: tough day for bacterial homeostasis.

2) Endotoxin buffering

LL-37 can dock into LPS, the big inflammatory trigger from Gram-negative walls. By sequestering LPS, it can reduce TLR4 activation in model systems — handy when the goal is to study immune responses without runaway noise.

3) Immune choreography

LL-37 isn’t just a membrane buster. It’s also a “go here, do this” signal: chemotaxis via FPR2, shaping neutrophil behavior, and helping epithelial barriers keep it together under stress. In vitro, you’ll see changes in ROS, cytokines, and migration.

4) Nucleic-acid binding & NET effects

It binds DNA/RNA like a tiny Velcro strap. In the context of neutrophil extracellular traps (NETs), that can stabilize structures and modulate how TLRs read the room. The specific outcome depends on context (sequence/length, ionic strength, etc.).

5) Biofilm disruption

Biofilms resist a lot of interventions because matrix plus altered physiology = fortress. LL-37 has a two-front effect — perturbing cells and the surrounding matrix — which can help break up established biofilms in bench models.

6) Tissue repair cues

Keratinocytes and fibroblasts “hear” LL-37. In wound models, LL-37 exposure can nudge migration and angiogenic signaling — again, context-specific and dose-dependent, but consistent with a broader host-defense peptide role that’s more conductor than soloist.

GLP3 online: triple-agonist research tools


GLP3-R 20mg — product photo
 GLP3-R (20 mg) is a triple agonist research compound (GLP-1R/GIPR/GCGR) useful when you’re modeling complex energy-balance pathways alongside innate-immunity questions. Open GLP3-R 20 mg.

CJC-1295 with DAC (stable GH-axis stimulus)


CJC-1295 with DAC 5mg — product photo
 CJC-1295 (with DAC) extends systemic exposure through albumin binding — a friendly model when your study design prefers steadier GH/IGF-axis signaling. Open CJC-1295 with DAC 5 mg.

MOTS-c (mitochondrial-encoded micropeptide)


MOTS-c 10mg — product photo
 MOTS-c is tied to the AMPK axis and stress-response signaling. Researchers sometimes profile innate-immunity peptides like LL-37 alongside mitochondrial peptides to map crosstalk between metabolism and defense. Open MOTS-c 10 mg.

SLU-PP-332 (ERR pan-agonist tool)


SLU-PP-332 — product photo
 ERRα/β/γ activation (via SLU-PP-332) is a clean way to light up oxidative-metabolism programs in muscle and other tissues. Pairing this with LL-37 can help tease apart how metabolic tone shifts immune phenotypes in bench models. Open SLU-PP-332.

Methods notes researchers often care about

  • Buffers & salts: Because LL-37 is cationic, ionic strength changes the story (binding and aggregation). Keep your buffer conditions consistent.
  • Surfaces & plastics: Adsorption can quietly drop effective concentration; pre-wetting or carrier proteins (as appropriate to your protocol) can help.
  • Membrane composition: Gram-negative vs Gram-positive vesicles behave differently; tailor lipid mixes to your organism/model.
  • Dose/time windows: LL-37 can flip from immunostimulatory to modulatory depending on dose and cell type; plan a range.

Need a larger catalog view? See All Peptides for Sale.

Disclaimer: All compounds referenced are sold strictly for research, laboratory, or analytical purposes only. Not for human consumption. No statements here are evaluated by the FDA. No disease diagnosis, treatment, or prevention claims are made.