This 2016 study—“Novel Insight into the Role of Antimicrobial (Host Defense) Peptides/Proteins in Human Skin Diseases”—in particular details how Brilacidin, modeled after defensins, could possibly be developed as a topical agent for a variety of skin disorders, such as Eczema, Acne Vulgaris, Acne Inversa (Hidradenitis Suppurativa), given its role in the cutaneous adaptive immune response, including:
· Regulation of inflammation
· Induction of cell proliferation and differentiation
· Regulation of cytokine/chemokine production
· Facilitation of cell migration
· Promotion of wound healing
· Regulation of barriers
Brilacidin’s low level of systemic absorption when topically administered (as revealed in its use in Ulcerative Proctitis/Ulcerative Proctosigmoiditis and Oral Mucositis, currently in mid-stage clinical trials), while remaining efficacious, further reinforces its therapeutic potential in treating skin diseases. Additional pre-clinical research is underway to determine Brilacidin’s role in regulating IL-17, a central driver most inflammatory diseases, including many skin diseases.
Of note: Brilacidin may be especially effective in treating atopic dermatitis or eczema (a review of novel treatments).
The human skin microbiome is influenced by bacterial infection in a complex manner. It has been hypothesized that increased susceptibility of people with atopic dermatitis to S. aureus infections, which is significantly over-expressed in this skin condition, may arise from the impaired expression of Host Defense Proteins (HDPs). And unlike Crisaborole, which was acquired in 2016 by Pfizer for $5.2 billion, Brilacidin, is highly active against S. aureus. Brilacidin might show another distinct advantage in that the drug candidate exhibits a strong inhibitory effect on IL-1, whereas Crisaborole shows no such activity. (IL-1 is linked to the pathogenesis of numerous diseases, including rheumatic disease and eczema.)
More information on Brilacidin’s potential application in treating dermatology indications can be found here (pdf).