LL-37 — questions, answered plainly.

LL-37 is the C-terminal 37-residue active fragment of the human cathelicidin precursor hCAP-18. It is an endogenous antimicrobial and immunomodulatory peptide expressed by neutrophils, macrophages, and epithelial cells as part of innate host defence.

LL-37's amphipathic α-helical structure disrupts microbial membranes — the standard antimicrobial-peptide mechanism. Beyond membrane disruption, the Fabisiak 2016 review (PMID 27117377) describes immunomodulatory and chemotactic activity via FPR2 signalling and other innate immune pathways.

No. Synthetic LL-37 is not FDA-approved for any indication at the time of writing. Clinical research is investigational; published primary evidence is dominated by in vitro and rodent studies.

Nagaoka et al. 2020 (Int J Mol Sci, PMID 32825174) used a cecal ligation and puncture sepsis model and reported that LL-37 was associated with reduced macrophage pyroptosis, enhanced neutrophil extracellular trap formation, and antimicrobial microvesicle release in treated mice.

Vera-Cruz et al. 2021 (Clin Invest Med, PMID 34600462) is a narrative review framing LL-37's in vitro inhibition of HIV in primary T cells and its potential as a multipurpose prevention technology. This is early-stage research, not established clinical evidence.

Most efficacy data are from in vitro and rodent models. Human pharmacology evidence is limited to small early-phase studies in specific dermatology and infection contexts. Clinical use remains investigational.