Search

Laura C Arneson,1,* Kristen J Carroll,1,* Eric M Ruderman2 1Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; 2Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA*These authors contributed equally to this workCorrespondence: Eric M RudermanDepartment of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine, 675 N. St. Clair, Suite 14-100, Chicago, IL, 60611, USATel +1 312-503-3188Fax +1 312-695-0114Email e-ruderman@northwestern.eduAbstract: Bruton’s tyrosine kinase (BTK) inhibitors are an emerging class of drugs that inhibit B cell receptor activation, FC-γ receptor signaling, and osteoclast proliferation. Following on approval for treatment of hematologic malignancies, BTK inhibitors are now under investigation to treat a number of different autoimmune diseases, including rheumatoid arthritis (RA). While the results of BTK inhibitors in RA animal models have been promising, the ensuing human clinical trial outcomes have been rather equivocal. This review will outline the mechanisms of BTK inhibition and its potential impact on immune mediated disease, the types of BTK inhibitors being studied for RA, the findings from both preclinical and clinical trials of BTK inhibitors in RA, and directions for future research.Keywords: evobrutinib, spebrutinib, acalabrutinib, fenebrutinib, rheumatoid arthritis, Bruton’s tyrosine kinase