|Baricitinib-induced inhibition of JAKs 1 and 2, down-modulates the intracellular signalling that is induced by multiple proinflammatory cytokines, including IL-6 and IL-23 that are elevated in patients with autoimmune diseases. This action evokes an improvement in clinical measures of autoinflammatory diseases.
Unfortunately, baricitinib causes adverse events (thrombosis and elevated platelet counts) that don't appear to be common to other JAK inhibitors that are in development, for example the JAK1-selective inhibitors upadacitinib and filgotinib, which suggests that inhibition of JAK2 may be the culprit. Note that as immunosuppressants, all currently marketed JAK inhibitor class drugs (ruxolitinib and tofacitinib for human treatment) pose the risk of serious side-effects, such as increased risk of serious infection or malignancy. This risk is exemplified by the boxed warning on the package insert for Pfizer's JAK3-selective inhibitor tofacitinib (Xeljanz®).