Baricitinib, a Janus kinase inhibitor, in the treatment of rheumatoid arthritis: a systematic literature review and meta-analysis of randomized controlled trials

Janus kinases (JAKs) play an important role in intracellular signaling for multiple cytokines in the pathogenesis of RA. Baricitinib is an oral, selective JAK 1 and 2 inhibitor which has been shown to be effective in the treatment of RA in several clinical trials. This meta-analysis aims to aggregate currently available data to assess the overall efficacy and safety of baricitinib in RA. We searched PubMed, EMBASE, and Cochrane CENTRAL from inception through 09/24/17 with restriction to English language. We excluded meeting abstracts without full text publication. We used RevMan 5.3 to perform meta-analysis between groups on baricitinib (2 and 4 mg daily) and placebo using random effect model calculating odds ratio (OR) as well as 95% confidence interval (CI). Compared to placebo, 2 mg of baricitinib was more effective in achieving ACR20 [54 vs. 36.6%; OR 2.09; 95% CI 1.60-2.71; p < 0.00001; I (2) 0%], ACR50 [31.6 vs. 10.3%; OR 2.3; 95% CI 1.68-3.15; p < 0.00001; I (2) 0%], and ACR70 responses [18.7 vs. 5.1%; OR 4.05; 95% CI 2.54-6.44; p < 0.00001; I (2) 0%]. Similarly, 4 mg of baricitinib daily was more effective than placebo. Baricitinib 2 mg once daily did not increase any adverse events [65.3 vs. 62.4%; OR 1.03; 95% CI 0.80-1.34; p = 0.8; I (2) 0%], serious adverse events [3.5 vs. 5%; OR 0.68; 95% CI 0.37-1.27; p = 0.22; I (2) 0%], and herpes zoster [1.2 vs. 0.4%; OR 2.34; 95% CI 0.27-20.47; p = 0.44; I (2) 37%] as compared to placebo. Similarly, 4 mg of baricitinib did not increase the risk of serious adverse events but increased herpes zoster infection [OR 3.88; 95% CI 1.36-11.06; p = 0.01; I (2) 0%] when compared to placebo. Baricitinib is effective in treatment of RA, and did not appear to have significant safety concerns during the first 6 months of treatment.