Emerging Topical and Systemic Agents in Atopic Dermatitis

Atopic dermatitis is a systemic disease with cutaneous manifestations, treat it as such by targeting Th2 mediated inflammation early in the process to address multiple atopic diseases at once.

Dupilimab approved for both atopic dermatitis and prurigo nodularis, binds to and inhibits IL-4 receptor alpha subunit, therefore interfering with IL-4 and IL-13 cytokine expression. Tralokinumab selectively binds to IL-13 and inhibits IL-13 induced release of pro-inflammatory cytokines, with reduced incidence of conjunctivitis compared to Dupilimab.

Topical and oral JAK-inhibitors provide quick onset itch relief via inhibition of Th cell differentiation, thus inhibiting the inflammatory cytokine cascade that drives pruritis in atopic dermatitis.

IL-31 is a key immune cytokine involved in the pathogenesis of neurogenic itch.