Analysis of the principle of dupilumab/dalbitux in the treatment of atopic dermatitis

Dupilumab (dupilumab) is a new treatment drug for immune-mediated diseases, especially in the treatment of atopic dermatitis (AD). Atopic dermatitis is a chronic inflammatory skin disease caused by abnormalities in the immune system. It is often accompanied by severe itching and skin damage, affecting the patient's quality of life. Traditional treatments often rely on topical steroids or immunosuppressants, but these treatments often fail to meet the needs of all patients, especially those with moderate to severe disease.

The therapeutic principle of dupilumab is mainly by inhibiting the signaling of two key cytokines,IL-4 and IL-13. IL-4 and IL-13 are key factors mediating allergic reactions, eosinophil recruitment, and immune system overactivation. In the pathological process of atopic dermatitis, the signaling of IL-4 and IL-13 is abnormally activated, leading to the excessive activation of T cells and B cells, thereby triggering the chronic inflammatory response of the skin and the destruction of the skin barrier function.

By specifically bindingIL-4Rα subunit of IL-4 and IL-13 receptors, dupilumab can effectively inhibit the signaling pathways of these cytokines, thereby reducing the excessive response of the immune system and relieving skin inflammation and itching symptoms. This mechanism makes dupilumab an effective option for the treatment of atopic dermatitis, especially refractory moderate to severe atopic dermatitis.

In clinical application, dupilumab is suitable for adult and pediatric patients aged 6 months and above, especially those who cannot be effectively controlled by topical drugs. It can be used as a monotherapy or in combination with topical corticosteroids. Through this treatment modality, dupilumab can help improve patients’ skin condition, reduce inflammation, relieve itching, and improve quality of life.

Keyword tags: dupilumab, Dupilumab, dalbitux, atopic dermatitis, immunotherapy, IL-4, IL-13, skin inflammation, immune regulation

References：https://www.ema.europa.eu/en/medicines/human/EPAR/dupixent