Dupilumab is approved for severe uncontrolled atopic dermatitis and add-on therapy for severe asthma with eosinophilic phenotype. Its mechanism is:

• A Monoclonal antibody blocking IgE binding to its high-affinity receptor FceRI on mast cells
• B Monoclonal antibody directed against IL-5, reducing eosinophil survival
• C Monoclonal antibody blocking TSLP, preventing innate lymphoid cell activation
• D Monoclonal antibody blocking the shared IL-4 receptor alpha subunit (IL-4Rα), thereby inhibiting both IL-4 and IL-13 signalling simultaneously ✓

Explanation

Dupilumab is a fully human monoclonal antibody targeting the IL-4Rα (IL-4 receptor alpha) subunit. This subunit is shared between the type I IL-4 receptor (IL-4Rα + γc chain) and the type II IL-4/IL-13 receptor (IL-4Rα + IL-13Rα1). By blocking IL-4Rα, dupilumab simultaneously inhibits both IL-4 and IL-13 signalling — two key Th2 cytokines responsible for IgE production, B-cell class switching, eosinophil recruitment, and epithelial barrier dysfunction. This broad Th2 blockade explains dupilumab's efficacy in atopic dermatitis, asthma, eosinophilic esophagitis, and chronic rhinosinusitis with nasal polyps.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.