The journal of allergy and clinical immunology. Global · 2025
Inflammatory and fibrotic biomarkers in patients with atopic dermatitis treated with cendakimab.
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Li Jie, Gilvary Coryandar, Gao Lu, Dellon Evan S, Charriez Christina M, de Oliveira Claudia H M C, Linaberry Misti J, Harris Sarah, Silverberg Jonathan I
Аннотация
BACKGROUND: Cendakimab is a recombinant, humanized, high-affinity, neutralizing monoclonal antibody that targets IL-13, a cytokine implicated in the pathogenesis of atopic dermatitis (AD).
OBJECTIVE: We evaluated the pharmacodynamic effects of IL-13 inhibition by cendakimab on key serum inflammatory and fibrotic biomarkers in patients with AD.
METHODS: 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.
RESULTS: 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.
CONCLUSION: Cendakimab decreased levels of key inflammatory and fibrotic biomarkers over 16 weeks of treatment in patients with moderate-to-severe AD.
OBJECTIVE: We evaluated the pharmacodynamic effects of IL-13 inhibition by cendakimab on key serum inflammatory and fibrotic biomarkers in patients with AD.
METHODS: 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.
RESULTS: 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.
CONCLUSION: Cendakimab decreased levels of key inflammatory and fibrotic biomarkers over 16 weeks of treatment in patients with moderate-to-severe AD.