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Only DUPIXENT inhibits signaling of IL-4 and IL-13, two of the key drivers of type 2 inflammation1,2

Dual inhibition of IL-4 and IL-13 signaling may help1:

REDUCE TYPE 2 INFLAMMATION
REDUCE ITCH
ACHIEVE SUSTAINED REMISSION
The mechanism of dupilumab action has not been definitively established.

Type 2 cytokines such as IL-4 and IL-13 may contribute to the development of the itch and lesions of bullous pemphigoid3‑10

aIL-4 acts on both type I and type II receptors to mediate type 2 inflammation.2

bType 2 cytokines (such as IL-4, IL-13, and IL-31) may also be produced by other immune cells, such as ILC2.11,12

IL-4 and IL-13 signaling help drive type 2 inflammation by promoting Th2 response, driving Ig class switching, and recruiting inflammatory cells3,7,8

DUPIXENT binds to IL-4 receptor alpha, inhibiting IL-4 and IL-13 induced inflammatory responses1,2

The mechanism of dupilumab action has not been definitively established.
IL-4 SIGNALING (TYPE I RECEPTOR)
IL-4/IL-13 SIGNALING (TYPE II RECEPTOR)

aDimerization is when 2 protein subunits combine to form a larger complex. IL-4 signaling through type I receptor requires dimerization of the IL-4Rα with the gamma chain. IL-4 or IL-13 signaling through type II receptor requires dimerization of IL-4Rα with IL-13Rα1.

Assess when your patients might be ready for DUPIXENT

Identifying patients

BP, bullous pemphigoid.