JAK Inhibitors in Atopic Dermatitis
Atopic dermatitis (AD), also known as atopic eczema, is a chronic, pruritic, relapsing inflammatory dermatological condition. The exact cause of the disease is unknown; however, certain factors such as epigenetic, genetic, immunological, and environmental interactions with overlapping skin barrier defects are indicated in its pathogenesis.
Oral Janus kinase (JAK) inhibitors have been approved for use in treating patients with rheumatoid arthritis and other inflammation & immunity disorders. Signaling proteins linked to cytokine receptors activate transcription factors, called signal transducer and activator of transcription (STAT) and modulate the expression of thousands of genes associated with inflammatory processes. JAK inhibition of type 2 cytokine signaling has recently shown pruritic benefit in clinical trials. JAK inhibition is not restricted to systemic administration but has also been developed as a topical treatment option.
• Which clinical trial endpoints would be most impactful for you in assessing a drug’s efficacy for atopic dermatitis (ex. IGA, EASI, SCORAD, pruritus, QOL)?
• In what patient subset or severity would you consider using a JAK inhibitor?
• Would the availability of a topical JAK impact the prescribing trends for topical calcineurin inhibitors or crisaborole?