Atopic dermatitis is a complex disease displaying a heterogeneous clinical presentation, which may involve many overlapping factors in its pathogenesis.

Recent advancements have given a better understanding of the molecular basis of atopic dermatitis allowing its categorization into different phenotypes. 

Emerging treatments utilizes the action of specific molecules concerned with eczema’s pathophysiology. 

Advancements in targeted, endotype-specific therapies will help to personalize the treatment of atopic dermatitis. However, the targeted medicines in atopic dermatitis are still at a very early stage compared to other diseases.

Dupilumab is the first approved biological preparation and is a human antibody that binds to the alpha subunit of interleukin (IL)-4 and IL-13 receptors. 

Drugs like: 

• Anti-IL-13 antibodies, e.g., Tralokinumab and Lebrikizumab;
• Anti-IL-31 receptor antibody, e.g., Nemolizumab;
• Anti-IL-22 antibody, e.g., Fezakinumab;
• IgG1 anti-IL monoclonal antibody, e.g., 33-Etokimab and  
• Anti-thymic stromal lymphopoietin antibody (anti-TSLP), e.g., Tezepelumab

are in-pipeline which will further assist in patient-centered medicine. Selection among many drugs would allow picking an appropriate one for patients relying on the appearance of a filaggrin mutation or the dominant immunotypes of Th2, Th17 or Th22. 

Janus kinase inhibitors, like Abrocitinib, Baricitinib, Upadacitinib, Tofacitinib, Ruxolitinib and Delgocitinib, are of great interest as they inhibit the JAK-STAT pathway, and hinder the transmission of information to the cell nucleus, causing a decrease in the production of many proinflammatory cytokines. 

Newer therapies will surely improve the skin barrier function and restore the immune balance in patients with atopic dermatitis. 

Source: Sroka-Tomaszewska J, Trzeciak M. Molecular mechanisms of atopic dermatitis pathogenesis. Int J Mol Sci. 2021;22(8):4130.