化学
敌手
促炎细胞因子
药理学
体内
对抗
免疫系统
免疫学
机制(生物学)
中央控制室4
细胞因子
体外
疾病
离体
作用机理
受体拮抗剂
受体
过敏
作者
Mikhail Zibinsky,Delia Bradford,Dirk G. Brockstedt,Ross Corriden,Jeffrey J. Jackson,Scott Jacobson,Sherry Jiao,Paul D. Kassner,John M. Ketcham,Lisa A. Marshall,Akinori Okano,Omar Robles,Jacob B. Schwarz,Oezcan Talay,Parcharee Tivitmahaisoon,Dianna Lester-Zeiner,Heather Milestone,Damian L. Trujillo,Ashkaan Younai,David J. Wustrow
标识
DOI:10.1021/acs.jmedchem.5c01678
摘要
cells, in particular T helper type 2 (Th2) immune cells, allowing these cells to migrate to the inflamed tissue and exacerbate the disease by the production of proinflammatory cytokines such as IL-4, IL-5, and IL-13. Antagonism of the CCR4 receptor is an attractive way to restrict this migration, which offers potential disease modification. Herein we report the discovery of Zelnecirnon (RPT193), a potent and selective small-molecule CCR4 antagonist. Zelnecirnon can effectively inhibit CCR4-induced chemotaxis, has attractive DMPK and drug-like properties, and can reduce CCR4 receptor surface expression. In an in vivo model of atopic dermatitis, Zelnecirnon demonstrated efficacy similar to those of approved biologics in this indication, thus demonstrating the proof of concept for this mechanism and its potential as an effective oral alternative.
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