Atopic dermatitis (AD) is a common inflammatory dermatologic disease clinically 
characterized by intense itch, recurrent eczematous lesions, and a chronic or 
relapsing disease course. Mild-to-moderate AD can be controlled by using 
moisturizers and topical immunomodulators such as topical corticosteroids and 
calcineurin inhibitors. If topical therapies fail, phototherapy and systemic 
immunosuppressant therapies, such as ciclosporin, methotrexate, and 
azathioprine, can be considered. However, relapse and side effects could still 
occur. The pathogenesis of AD involves epidermal barrier dysfunction, skin 
microbiome abnormalities, and cutaneous inflammation. Inflammatory mediators, 
such as interleukin (IL)-4, IL-13, IL-31, IL-33, IL-17, IL-23, and thymic 
stromal lymphopoietin, are involved in AD development. Therefore, a series of 
biological agents targeting these cytokines are promising approaches for 
treating AD. Dupilumab is the first biological agent approved for the treatment 
of AD in patients aged 6 years and older in the United States. Tralokinumab, 
lebrikizumab, and nemolizumab have also been confirmed to have significant 
efficacy against AD in phase III or IIb clinical trials. Also, fezakinumab was 
effective in severe AD patients in a phase IIa trial. However, phase II trials 
of ustekinumab, tezepelumab, etokimab, secukinumab, and omalizumab have failed 
to meet their primary endpoints. Phase II trials of GBR 830 and KHK 4083 are 
ongoing. In general, further studies are needed to explore new therapeutic 
targets and improve the efficacy of biological agents.