Wound healing / re-epithelialization
Heilborn 2003 showed that LL-37 expression is upregulated at the leading edge of healing acute wounds but absent in chronic ulcer epithelium, suggesting endogenous deficit drives non-healing. Carretero 2008 demonstrated that recombinant LL-37 transferred via adenovirus accelerated re-epithelialization in ob/ob diabetic mice. A Phase 2 venous ulcer trial of synthetic LL-37 was reported but cleanly indexing the primary publication remains a verification challenge.
1 human study · 6 animal studies
Key findings & citations
- LL-37 strongly expressed at acute wound edges; absent in chronic ulcer epithelium.
- Adenoviral LL-37 transfer accelerated re-epithelialization in diabetic mouse wounds.
- Phase 2 venous leg ulcer trial of synthetic LL-37 reported clinical benefit at intermediate doses.
Our take
Mechanism is solid, the clinical trial program never reached approval. Reasonable as adjunct in non-healing wounds where standard care fails, but data is thin.