Study: Nemolizumab shows promise as prurigo nodularis treatment
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Key takeaways:
- Nemolizumab targets interleukin (IL)-31 receptor alpha.
- Inhibiting IL-31 may disrupt pathways affecting inflammatory, neural and epithelial regulation, which contribute to prurigo nodularis.
Patients with severe prurigo nodularis treated with nemolizumab vs. placebo experienced changes in signaling pathways and biomarkers that affect inflammatory, neural and epithelial regulation, according to a multicenter cohort study.
This response, which indicates an increase in wound healing and a decrease in inflammation and neural and epidermal dysregulation, suggests nemolizumab could be a possible treatment option in severe prurigo nodularis (PN), according to Junwen Deng, MD, of the department of dermatology at Johns Hopkins University School of Medicine, and colleagues.
“[PN] is a debilitating chronic inflammatory skin disease characterized by chronic pruritus and the presence of multiple localized or generalized pruritic, hyperkeratotic nodules that favor the trunk and extremities,” Deng and colleagues wrote. “While the exact pathogenesis of PN remains unclear, immune and neural dysregulation play significant roles.”
Researchers aimed to identify if nemolizumab, a monoclonal antibody that targets interleukin (IL)-31 receptor alpha, was associated with PN in a study of 38 patients from a previous phase 2 clinical trial. These included patients achieved a 4-point or greater decrease in Peak Pruritus Numerical Rating Scale from baseline to week 12 with nemolizumab treatment in the original trial.
Plasma was taken from these patients, as well as those treated with placebo, and mass spectrometry was used to characterize plasma protein expression changes.
Distinctive protein expression trends were identified in the patients treated with nemolizumab compared with those treated with placebo.
Downregulation in inflammatory signaling and pruritus including IL-6, acute-phase response, signal transducer and activator of transcription 3 and interferon gamma were observed in the nemolizumab group, as was neural dysregulation.
“Proteomic analysis of plasma from patients with PN responsive to nemolizumab identified 193 proteins that were differentially expressed after treatment compared with the placebo group of nonresponders, implicating downregulation of inflammatory pathways, neural processes, tissue remodeling and fibrosis, and epidermal differentiation,” Deng and colleagues wrote.
These results show that IL-31 inhibition may be efficacious in disrupting multiple pathways of inflammatory, neural and epithelial regulation, which contribute to PN, according to the study.
“By targeting [IL-31 receptor alpha], nemolizumab represents a promising potential new approach for the clinical management of PN,” the authors wrote.
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