Inflammatory and fibrotic biomarkers in patients with atopic dermatitis treated with cendakimab

Cendakimab is a recombinant, humanized, high-affinity, neutralizing monoclonal antibody that targets IL-13, a cytokine implicated in the pathogenesis of atopic dermatitis (AD).

We evaluated the pharmacodynamic effects of IL-13 inhibition by cendakimab on key serum inflammatory and fibrotic biomarkers in patients with AD.

In the phase 2 (NCT04800315) multicenter, global, randomized, double-blind, placebo-controlled, parallel-group trial, adults with moderate-to-severe AD received cendakimab 360 mg subcutaneously every 2 weeks, 720 mg subcutaneously every 2 weeks, 720 mg subcutaneously weekly, or placebo for 16 weeks. Blood samples were collected, and a panel of biomarkers was assessed in serum predose on day 1 (baseline), weeks 1 and 2, and then every 2 weeks until week 16. The study analyzed eotaxin-3 with an assay (V-PLEX Plus Human Eotaxin-3 Kit from Meso Scale Diagnostics), periostin using ELISA assay (R&D Systems DuoSet ELISA, DY3548B, and DY008), and other biomarkers, including IL-18, matrix metalloproteinase 12, thymus and activation-regulated chemokine/chemokine C-C motif ligand 17 (CCL17), CCL18, and CCL27 using Olink Target 96 panels. Least squares mean percentage change from baseline was evaluated for each group through week 16.

For all 3 doses of cendakimab, there was a significant decrease from baseline in the levels of most inflammatory and fibrotic biomarkers as early as weeks 1 to 4 after treatment and continued through week 16 of cendakimab treatment. Compared with placebo, cendakimab resulted in significantly greater reductions in these biomarker levels through week 16.

Cendakimab decreased levels of key inflammatory and fibrotic biomarkers over 16 weeks of treatment in patients with moderate-to-severe AD.