贾纳斯激酶
托法替尼
医学
酪氨酸激酶
酪氨酸激酶2
免疫系统
银屑病
激酶
鲁索利替尼
细胞因子
免疫学
信号转导
癌症研究
药理学
受体
生物
细胞生物学
内科学
类风湿性关节炎
血小板源性生长因子受体
骨髓纤维化
骨髓
生长因子
作者
Peter C Taylor,Ernest Choy,Xenofon Baraliakos,Zoltán Szekanecz,Ricardo Machado Xavier,John D. Isaacs,Sander Strengholt,Julie Parmentier,Ralph Lippe,Yoshiya Tanaka
出处
期刊:Rheumatology
[Oxford University Press]
日期:2023-08-25
卷期号:63 (2): 298-308
被引量:5
标识
DOI:10.1093/rheumatology/kead448
摘要
Abstract Janus kinases (JAKs) are a family of cytosolic tyrosine kinases that regulate cytokine signal transduction, including cytokines involved in a range of inflammatory diseases, such as RA, psoriasis, atopic dermatitis and IBD. Several small-molecule JAK inhibitors (JAKis) are now approved for the treatment of various immune-mediated inflammatory diseases. There are, however, key differences between these agents that could potentially translate into unique clinical profiles. Each JAKi has a unique chemical structure, resulting in a distinctive mode of binding within the catalytic cleft of the target JAK, and giving rise to distinct pharmacological characteristics. In addition, the available agents have differing selectivity for JAK isoforms, as well as off-target effects against non-JAKs. Other differences include effects on haematological parameters, DNA damage repair, reproductive toxicity and metabolism/elimination. Here we review the pharmacological profiles of the JAKis abrocitinib, baricitinib, filgotinib, peficitinib, tofacitinib and upadacitinib.
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