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In the phase III VOYAGE 1 trial (NCT02207231), guselkumab, a fully human monoclonal antibody that inhibits interleukin (IL)-23, demonstrated superior efficacy vs placebo and adalimumab, a tumor necrosis factor-α (TNF-α) inhibitor, in patients with moderate-to-severe plaque psoriasis.1 Results from a biomarker analysis of a subset of patients in the VOYAGE 1 trial were published in JID Innovations by Blauvelt, et al.1 |
Key learnings: |
While both guselkumab and adalimumab reduced serum levels of key cytokines IL-17A, IL-17F, and IL-22 from baseline at Weeks 4, 24, and 48 (p < 0.001 and p < 0.01, respectively), reductions were greater with guselkumab for IL-17A at Weeks 4 and 48 (p < 0.05), IL-17F at Weeks 4, 24, and 48 (p < 0.05), and IL-22 at Weeks 4 and 48 (p < 0.05), highlighting its superior efficacy in modulating the IL-23/IL-17 pathway in psoriasis. |
Treatment with guselkumab led to a more significant impact on the molecular drivers of psoriasis, as demonstrated by a greater normalization of psoriasis-associated gene expression in lesional skin samples at all assessed time points compared with adalimumab. |
The molecular pharmacodynamic findings from the study results are consistent with the clinical responses observed in the VOYAGE 1 trial. |
The results from this study demonstrate that targeted blockade of the IL-23 pathway with guselkumab may offer improved long-term control of moderate-to-severe plaque psoriasis compared with the broader TNF-α blockade by adalimumab. |
References
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