贾纳斯激酶
托法替尼
鲁索利替尼
医学
特应性皮炎
药效学
药理学
斯达
JAK-STAT信号通路
酪氨酸激酶2
信号转导
免疫学
细胞因子
酪氨酸激酶
车站3
药代动力学
受体
生物
内科学
骨髓纤维化
类风湿性关节炎
骨髓
生物化学
血小板源性生长因子受体
生长因子
作者
Laura Calabrese,Andrea Chiricozzi,Clara De Simone,Barbara Fossati,Alessandra D'Amore,Ketty Peris
标识
DOI:10.1080/17425255.2022.2099835
摘要
Atopic dermatitis (AD) is the most common inflammatory skin disorder. Despite the high disease burden, the therapeutic options are limited and their efficacy in controlling AD might be partially satisfactory.Most of the key mediators in AD pathogenesis act through the JAK/STAT signaling pathway, which represents a valid therapeutic target. The first generation of JAK inhibitors, namely tofacitinib and ruxolitinib, inhibit multiple JAKs, whereas newer JAK inhibitors show more selective inhibitory effects for specific JAKs. The aim of this review was to discuss the role of the JAK/STAT pathway in AD and its inhibition, with a special focus on pharmacodynamic properties.JAK inhibitors have different selectivity for various JAK molecules, which influences their pharmacodynamics, efficacy, and safety profile. Since many key cytokines in AD signal through JAK1, the selective JAK1 inhibition may be effective, avoiding the concomitant inhibition of JAK2- and JAK3-dependent pathways could be associated with additional safety issues. Therefore, selective JAK1 inhibitors may represent promising therapeutic agents for AD, as they might prevent off-target effects of JAK inhibitors, especially related to the hematologic profile.
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