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Proof-of-concept evaluation demonstrates selective receptor inhibition in moderate to severe atopic dermatitis, highlighting therapeutic potential across type 2 inflammatory diseases.
Cendakimab selectively targets interleukin (IL)-13, a type 2 cytokine implicated in atopic dermatitis (AD) pathogenesis, by inhibiting binding to its receptors (IL13R-α1 and IL13R-α2). Proof-of-concept work in AD supports using cendakimab for type 2 inflammatory diseases.
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Blauvelt et al. (2024) studied this question.
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