Allergic contact dermatitis is driven by an overreaction of the body's immune system to a normally harmless substance resulting in skin inflammation.1 Preclinically, topical administration of the T helper 2 (Th2) hapten fluorescein isothiocyanate (FITC) drives an immunogenic sensitization in mice, and recall challenge on the ear triggers a localized inflammatory contact hypersensitivity. Pharmacological inhibition of the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway has previously demonstrated efficacy in a phase 2 clinical trial in patients with atopic dermatitis (AD) (NCT03011892). Ruxolitinib cream, a topical JAK1/JAK2 inhibitor,2,3 is currently being evaluated in clinical trials for the treatment of mild-to-moderate AD (NCT0311892, NCT03745651, NCT03745638).
Contact hypersensitivity and dermatitis was induced in Balb/C mice via FITC sensitization4 and subsequent recall response. Topical administration of ruxolitinib cream was compared to steroid (betamethasone cream, 0.05%). Efficacy was quantified via inflammatory edema, immune phenotyping, tissue histology, and immune pathway analysis. 
Topical administration of 1.5% ruxolitinib cream (once daily [QD] and twice daily [BID]) dose-dependently reduced inflammatory swelling and lichenification following recall FITC challenge in both acute (p < 0.05) and chronic (p < 0.05) contact dermatitis. Ruxolitinib efficacy was associated with a significant (p < 0.01) dose-dependent reduction in Th2 lymphocytes within the auricular (draining) lymph node. Pathway analysis revealed downregulation of inflammatory mechanisms consistent with JAK1/JAK2 inhibition. 
Ruxolitinib cream was highly effective at inhibiting contact dermatitis in mice, ameliorated pro-inflammatory mechanisms, and reduced skin thickening. Together, the data suggest that ruxolitinib cream may have potential as a therapeutic agent for the treatment of contact dermatitis.

Ruxolitinib cream ameliorates a preclinical model of skin dermatitis via modulation of inflammatory T-cell subsets