Vunakizumab for IL-17A-Mediated Diseases: A Review in Psoriasis and Spondyloarthritis.

IF 4.5 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
Biologics : Targets & Therapy Pub Date : 2026-06-08 eCollection Date: 2026-01-01 DOI:10.2147/BTT.S500475
Hongzhuo Yan, Yu Chen, Yali Song, Min Yan, Kexiang Yan
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引用次数: 0

Abstract

The interleukin-17A (IL-17A) cytokine is a key driver in the pathogenesis of chronic immune-mediated diseases, including psoriasis (PsO), psoriatic arthritis (PsA), and ankylosing spondylitis (AS). As a central proinflammatory mediator, IL-17A signals through the IL-17RA/RC receptor complex to promote tissue-specific inflammation. This narrative review outlines the therapeutic rationale for targeting IL-17A and summarizes the current evidence for vunakizumab, a novel humanized monoclonal antibody against IL-17A. We reviewed the biological basis of IL-17A signaling and its pathogenic role in PsO, PsA, and AS. We then synthesized the pharmacokinetic properties of vunakizumab and the clinical evidence from Phase II and III trials evaluating its efficacy and safety. Post hoc analyses across a broad range of clinically relevant patient subgroups further support the consistency of its therapeutic effects. Clinical trial data demonstrate that vunakizumab offers robust efficacy and a favorable safety profile in the treatment of psoriasis and spondyloarthritis (including PsA and AS). Its properties are comparable to other approved IL-17A inhibitors, establishing it as a promising therapeutic option for these IL-17A-mediated diseases.

Vunakizumab治疗il - 17a介导的疾病:银屑病和脊椎关节炎的研究综述
白细胞介素- 17a (IL-17A)细胞因子是慢性免疫介导疾病发病机制的关键驱动因素,包括银屑病(PsO)、银屑病关节炎(PsA)和强直性脊柱炎(AS)。作为一种中枢促炎介质,IL-17A通过IL-17RA/RC受体复合物发出信号,促进组织特异性炎症。本文概述了靶向IL-17A的治疗原理,并总结了目前针对IL-17A的新型人源化单克隆抗体vunakizumab的证据。本文综述了IL-17A信号通路的生物学基础及其在PsO、PsA和AS中的致病作用。然后,我们综合了vunakizumab的药代动力学特性以及评估其有效性和安全性的II期和III期试验的临床证据。在广泛的临床相关患者亚组中进行的事后分析进一步支持其治疗效果的一致性。临床试验数据表明,vunakizumab在治疗银屑病和脊柱炎(包括PsA和AS)方面具有强大的疗效和良好的安全性。其特性与其他批准的IL-17A抑制剂相当,使其成为这些IL-17A介导的疾病的有希望的治疗选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biologics : Targets & Therapy
Biologics : Targets & Therapy MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
8.30
自引率
0.00%
发文量
22
审稿时长
16 weeks
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