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通过假定小分子抑制剂破坏TSLP-TSLP受体相互作用,为亚托皮性疾病提供了一种新且高效的治疗选择

Partho Protim Adhikary¹, Temilolu Idowu¹, Zheng Tan¹

¹Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada.

EMBO molecular medicine

|June 14, 2024

概括

研究人员开发了一种新型的小分子抑制剂,其向的是胸膜 stromal lymphopoietin (TSLP) 受体. 这一突破通过阻断关键的炎症通路,为亚托皮性疾病提供了潜在的新疗法.

科学领域:

免疫学免疫学免疫学
药理学药理学是指药理学的学科.
生物技术是生物技术.

背景情况:

胸膜流体淋巴蛋白 (TSLP) 是亚托皮性疾病中的关键细胞因子.
针对TSLP具有重要的治疗意义.
现有的挑战包括缺乏TSLP受体相互作用的小分子抑制剂.

研究的目的:

开发TSLP受体的新型小分子抑制剂.
评估这些抑制剂在临床前的亚托皮性疾病模型中的疗效.

主要方法:

虚拟选和对接超过 1,000,000 个化合物.
代化学合成以识别化合物.
开发一种使用多器官芯片的人类无氧性疾病药物发现平台.
在体外和体外测试在亚托皮肤和肺部模型.

主要成果:

确定BP79作为一种主要的小分子TSLP受体抑制剂.
在低微分子度下,BP79有效地废除了TSLP触发的细胞因子产生.
局部BP79抑制免疫细胞透和关键炎症媒介 (IL-13,IL-4,TSLP,皮质素) 在亚托皮肤模型中.
BP79上调皮肤屏障蛋白质,并在共同培养的肺模型上表现出下游保护作用.
RNA-Seq分析证实了这些发现,并表明了更广泛的保护作用.

结论:

这项研究报告了第一个强大的,假定的小分子TSLP受体抑制剂.
BP79在亚托皮性疾病中显示出治疗和预防策略的巨大潜力.
开发的多器官芯片平台对亚托皮性疾病药物发现有价值.

关键词:

亚托邦性皮肤炎 (Atopic Dermatitis) 是一种不良的疾病.亚托邦性疾病亚托邦性疾病器官在芯片上的器官小分子抑制剂小分子抑制剂这是TSLP的TSLP.

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