Topical doxycycline monohydrate hydrogel 1% targeting proteases/PAR2 pathway is a novel therapeutic for atopic dermatitis. Issue 12 (15th October 2020)

• Record Type: Journal Article
• Authors: Bohannon, Mary; Liu, Mingjin; Nadeau, Peter; Talton, Judy; Gibson, Daniel; Datta, Susmita; Schultz, Gregory; Talton, James; De Benedetto, Anna
• Is Part Of: Experimental dermatology. Volume 29:Issue 12(2020)
• Page Start: 1171
• Page End: 1175
• Publication Date: 2020-10-15
• Subjects: atopic dermatitis -- clinical trial -- doxycycline -- KLK5 -- proteases -- skin barrier; Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.14201
• Languages: English
• ISSNs: 0906-6705

Abstract

Abstract: Atopic Dermatitis (AD) is characterized by skin barrier disruption and an aberrant immune response. Doxycycline is tetracycline antibiotics broadly used systemically to treat inflammatory dermatologic conditions. Several studies have shown doxycycline has anti‐inflammatory and pro‐healing properties, mainly by blocking tissue proteolytic activity. It is our hypothesis that daily application of a novel doxycycline topical formulation in AD subjects will reduce severity of the disease, by blocking cutaneous proteases activity and restoring skin barrier function and inflammation. To test this hypothesis, we performed a proof of concept, open‐label clinical study. Subjects enrolled in the study (n = 15) applied NanoDOX ® Hydrogel 1% daily for 4 weeks on a chosen eczematous area. Investigational drug was well tolerated, and no local or systemic adverse events due to investigational drug were reported. Notably, a significant clinical improvement was observed based on a modified Eczema Area & Severity Index (EASI) score of the treated area from start of treatment to 14 and 28 days post‐treatment ( P < .001). A significant improvement of pruritus was also observed ( P = .02). This proof of concept clinical trial is first to explore the impact of a non‐systemic doxycycline treatment on AD patients. Our results provide evidence to investigate novel AD treatment strategies targeting cutaneous proteases activity.