作者
Phil B. Alper,Claudia Betschart,Cédric André,Thomas Boulay,Cheng Dai,Jonathan A. Deane,Michael Faller,Roland Feifel,Ralf Glatthar,Dong Han,R. Hemmig,Tao Jiang,Thomas Knoepfel,Jillian Maginnis,Daniel Mutnick,Pei Wei,Giulia Ruzzante,Peter M. Syka,Guobao Zhang,Yi Zhang,F. Zink,Géraldine Zipfel,Stuart Hawtin,Tobias Junt,Pierre‐Yves Michellys
摘要
Toll-like receptor (TLR) 7 and TLR8 are endosomal sensors of the innate immune system that are activated by GU-rich single stranded RNA (ssRNA). Multiple genetic and functional lines of evidence link chronic activation of TLR7/8 to the pathogenesis of systemic autoimmune diseases (sAID) such as Sjögren's syndrome (SjS) and systemic lupus erythematosus (SLE). This makes targeting TLR7/8-induced inflammation with small-molecule inhibitors an attractive approach for the treatment of patients suffering from systemic autoimmune diseases. Here, we describe how structure-based optimization of compound 2 resulted in the discovery of 34 (MHV370, (S)-N-(4-((5-(1,6-dimethyl-1H-pyrazolo[3,4-b]pyridin-4-yl)-3-methyl-4,5,6,7-tetrahydro-1H-pyrazolo[4,3-c]pyridin-1-yl)methyl)bicyclo[2.2.2]octan-1-yl)morpholine-3-carboxamide). Its in vivo activity allows for further profiling toward clinical trials in patients with autoimmune disorders, and a Phase 2 proof of concept study of MHV370 has been initiated, testing its safety and efficacy in patients with Sjögren's syndrome and mixed connective tissue disease.