A Prospective Pilot Study to Explore Efficacy and Safety of Baricitinib in Active Primary Sjogren's Syndrome Patients

Primary Sjogren's syndrome (pSS) is a systemic autoimmune disease characterized by dysfunction of the exocrine glands, which results in sicca symptoms in affected patients. JAK/STAT signaling pathway is activated and playing as a key pathway in the differentiation and activation of many lymphocytes, so that affect the pathogenesis of many autoimmune diseases including pSS. JAK inhibitors have also been widely used in the treatment of rheumatoid arthritis and other autoimmune diseases. Some studies have confirmed that JAK/STAT pathway is activated in patients with pSS, and JAK inhibitor may be effective for pSS. Filgotinib, the selective JAK1 inhibitor, is one of the "secondary generation" JAK inhibitors developed these years. Lee et al. found that filgotinib suppressed the IFN-induced transcription of differentially expressed genes and BAFF in human primary salivary gland epithelial cells. In addition, filgotinib-treated mice exhibited increased salivary flow rates and marked reductions in the lymphocytic infiltration of SGs, indicating that JAK inhibitors may be a novel therapeutic approach for pSS. A randomized phase 2 study is currently in progress to assess the safety and efficacy of filgotinib in adult subjects with active Sjogren's syndrome. So far, there is no evidence of the safety and efficacy of baricitinib in patients with pSS. Baricitinib, an oral inhibitor of JAK1/JAK2, was the second JAK inhibitor approved for clinical use in RA. It has been approved for the treatment for moderate to severe active RA in adult patients who have responded inadequately to, or are intolerant to, one or more disease-modifying anti-rheumatic drugs (DMARDs). The efficacy and safety of baricitinib in RA have been extensively evaluated in pre-clinical animal models of arthritis, as well as in clinical studies. There are also some reports of baricitinib used in other autoimmune diseases, such as systemic lupus erythematosus, dermatomyositis and PMR/GCA. In a double-blind, mult