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MOA: Mechanism of Action

AFRS IS CONSIDERED A SEVERE
MANIFESTATION OF TYPE 2
INFLAMMATION1

AFRS IS CONSIDERED A SEVERE
MANIFESTATION OF TYPE 2
INFLAMMATION1

IL-4 and IL-13 signaling are two of the key and central drivers of underlying type 2 inflammation in AFRS2-4

ONLY DUPIXENT DIRECTLY INHIBITS IL-4 AND IL-13 SIGNALING TO ADDRESS TWO OF THE KEY AND CENTRAL DRIVERS OF TYPE 2 INFLAMMATION2-4,*

*The mechanism of dupilumab action has not been definitively established.2

DUPIXENT TARGETS TWO OF THE KEY AND CENTRAL DRIVERS OF TYPE 2 INFLAMMATION—IL-4 AND IL-13 SIGNALING2-4,*

DUPIXENT inhibits IL-4 and IL-13 signaling by specifically binding to the IL-4 receptor alpha (IL-4Rα) subunit.2,* Blocking IL-4Rα with DUPIXENT inhibits
IL-4– and IL-13–induced inflammatory responses and lowers total IgE in the blood of patients with AFRS, thereby demonstrating systemic effects of DUPIXENT on these markers of type 2 inflammation in AFRS2,4,9,*:

*The mechanism of dupilumab action has not been definitively established.2

LOCAL
INFLAMMATION

Physiological features3,4,7

  • Mucus hypersecretion
  • Epithelial barrier dysfunction

Associated clinical features

  • Impaired olfactory function1,8
  • Tissue remodeling4,10
  • Polyp growth and recurrence3,11
  • Eosinophilic mucin4

SYSTEMIC
INFLAMMATION3,7

  • Elevated IgE levels

AFRS, allergic fungal rhinosinusitis; ILC2, type 2 innate lymphoid cells.

Learn How to Identify
Appropriate AFRS Patients