LL-37 Peptide Protocol Guide - Dosing, Reconstitution & Safety

LL-37 is the only cathelicidin antimicrobial peptide made by humans. It comes from a larger protein called hCAP-18 and helps the body respond to microbes, inflammation, and wound repair. In the research-peptide market, it is usually sold as a freeze-dried powder that is reconstituted before subcutaneous injection.

There is an important gap to understand before planning anything. The human clinical trials for LL-37 delivered it as a gel applied directly onto a leg ulcer, not as an injection. The daily subcutaneous protocol common in the research community is community-derived, not trial-validated.

LL-37 has two very different dosing contexts. The clinical-trial picture is topical and measured as a concentration on the wound. The research-community picture is a subcutaneous injection measured in micrograms. They are not interchangeable, so this section keeps them on separate tabs.

Reconstitution turns the dry powder into a measurable liquid. The key math is simple: vial size divided by BAC water gives the concentration, and dose divided by concentration gives the draw volume. On a U-100 syringe, 1 mL equals 100 units.

Example: a 5 mg vial plus 2 mL of BAC water gives 2.5 mg/mL (2,500 mcg/mL). A 250 mcg dose is 0.10 mL, which is 10 units on a U-100 syringe. A 10 mg vial plus 2 mL gives 5 mg/mL, so 250 mcg becomes 0.05 mL, or 5 units.

This chart summarizes the commonly reported subQ LL-37 ranges from the dosing section above.

In plain terms, LL-37 does two jobs. First, it pokes holes in the outer membranes of bacteria, some fungi, and some viruses, which can kill them directly. Second, it acts as a signal that calls immune cells to a site and shapes how much inflammation happens there.

The peptide carries a strong positive charge and folds into an amphipathic alpha-helix, which lets it bind negatively charged microbial membranes and disrupt them. Beyond that, it binds bacterial endotoxin (LPS), acts through receptors such as FPR2 and scavenger receptors, recruits cells, blocks biofilm formation, and supports new blood vessels and skin regrowth in wounds.

That last point matters. The same signaling that helps wounds can, in the wrong context, push inflammation. LL-37 complexed with self-DNA or self-RNA is a documented driver of immune activation in psoriasis and lupus, which is why LL-37 is not simply a 'clean' immune booster.

Because LL-37 can amplify inflammation, the literature points to a few groups that may need extra caution. This is educational context, not a medical screening tool.

In the topical wound trials, LL-37 was well tolerated and the studies reported it as safe when applied locally with compression therapy. That safety finding is for the gel on skin, not for daily injection.

Community and clinic reports of subcutaneous use most often describe local injection-site reactions: redness, swelling, itching, or a burning sensation. This is consistent with LL-37's biology, since it can trigger mast cells to release histamine, which produces warmth, redness, and itching near the injection site.

Slower injection and a lower starting amount are commonly suggested to reduce local reactions. Persistent or spreading reactions are a stop signal.

The only human timeline data comes from the wound trials. There, twice-weekly topical LL-37 improved healing rates over a 4-week (first-in-man) and 13-week (Phase IIb) treatment window, with the strongest effect in large, long-standing ulcers.

For injectable community use, there is no validated timeline because it has not been studied in human trials. Any promised week-by-week result should be treated as unsupported. For research planning, the practical focus is monitoring the injection site, tracking skin or inflammatory changes, and stopping if reactions build.

Human evidence for LL-37 is real but narrow. Two randomized, placebo-controlled trials tested a topical LL-37 gel on hard-to-heal venous leg ulcers, both run by the developer Promore Pharma under the drug name ropocamptide.

Everything else is preclinical or mechanistic: antimicrobial action, anti-biofilm activity, immune signaling, and disease-association work in psoriasis, lupus, and rosacea. Popular research-community claims about systemic infection control, gut health, or Lyme disease do not have human-trial support for injected LL-37.

As of July 2026, LL-37 is not FDA-approved for any indication. The synthetic drug version, ropocamptide, developed by Promore Pharma in Sweden, completed a Phase IIb topical wound-healing trial and is described by the company as being prepared for a future Phase III program. It has not received marketing authorization.

The LL-37 sold as a research peptide is a research-use-only product, not an approved medicine. It is not the same formulation as the topical drug candidate studied in trials.

In research-community discussion, LL-37 is often grouped with recovery and immune peptides, but its profile is distinct. BPC-157 and TB-500 are discussed for soft-tissue recovery and are not antimicrobial. KPV is discussed as an anti-inflammatory fragment. LL-37 is unusual because it is a direct antimicrobial and immune-signaling peptide with a genuine double edge: it can both fight microbes and amplify inflammation.