Dermatology practical & conceptual · 2026
Stapokibart (CM310) in Atopic Dermatitis: A Narrative Review of a Next-Generation IL-4Rα Antagonist.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ferreira Esmeraldito, Wu Tong, Chen Yongfeng
Аннотация
INTRODUCTION: The interleukin (IL)-4/IL-13 signaling pathway is central to the pathogenesis of atopic dermatitis (AD). Stapokibart (CM310) is a novel humanized monoclonal antibody targeting the IL-4 receptor alpha (IL-4Rα) subunit.
OBJECTIVE: To summarize current evidence on the mechanism of action, clinical efficacy, safety, and therapeutic potential of stapokibart for moderate-to-severe AD.
METHODS: A narrative review was conducted based on a targeted search of PubMed/MEDLINE and ClinicalTrials.gov covering literature published from January 2015 to January 2026.
RESULTS: Stapokibart binds IL-4Rα with high affinity (KD = 0.25 nM), inhibiting downstream IL-4 and IL-13 signaling. In a phase 3 trial (N=500), stapokibart 300 mg every two weeks demonstrated significant improvements at Week 16, with 66.9% achieving EASI-75 (vs. 25.8% placebo) and 44.2% achieving IGA 0/1 (vs. 16.1% placebo; P<0.0001). Among responders, 92.5% maintained EASI-75 through Week 52. The treatment was generally well tolerated, with upper respiratory tract infections and injection-site reactions being the most common adverse events. Conjunctivitis occurred at low rates (5.0-5.9%).
CONCLUSIONS: Stapokibart shows robust efficacy and a favorable safety profile in adults with moderate-to-severe AD, including sustained long-term responses and low conjunctivitis rates. While early data are encouraging, all comparisons with existing IL-4/IL-13 inhibitors are indirect, and further global phase 3 studies and real-world evidence are needed to define its role within treatment algorithms.
OBJECTIVE: To summarize current evidence on the mechanism of action, clinical efficacy, safety, and therapeutic potential of stapokibart for moderate-to-severe AD.
METHODS: A narrative review was conducted based on a targeted search of PubMed/MEDLINE and ClinicalTrials.gov covering literature published from January 2015 to January 2026.
RESULTS: Stapokibart binds IL-4Rα with high affinity (KD = 0.25 nM), inhibiting downstream IL-4 and IL-13 signaling. In a phase 3 trial (N=500), stapokibart 300 mg every two weeks demonstrated significant improvements at Week 16, with 66.9% achieving EASI-75 (vs. 25.8% placebo) and 44.2% achieving IGA 0/1 (vs. 16.1% placebo; P<0.0001). Among responders, 92.5% maintained EASI-75 through Week 52. The treatment was generally well tolerated, with upper respiratory tract infections and injection-site reactions being the most common adverse events. Conjunctivitis occurred at low rates (5.0-5.9%).
CONCLUSIONS: Stapokibart shows robust efficacy and a favorable safety profile in adults with moderate-to-severe AD, including sustained long-term responses and low conjunctivitis rates. While early data are encouraging, all comparisons with existing IL-4/IL-13 inhibitors are indirect, and further global phase 3 studies and real-world evidence are needed to define its role within treatment algorithms.