A CURE-LIKE state has been achieved in a new Phase III study exploring the effects of baricitinib in rheumatoid arthritis patients with poor responses to previous therapy with other disease modifying anti-rheumatic drugs (DMARDs), such as tumour necrosis factor inhibitors.
In the pathogenesis of rheumatoid arthritis, when binding to cells, extracellular messenger molecules such as interferons or interleukin-6 signal the activation of the intracellular enzyme Janus kinase (JAK)-1 and 2, thus provoking inflammatory responses. Typical attempts to quell this process involve intravenous or subcutaneous therapy with DMARDS, but in a new collaborative study, the far less invasive oral administration of baricitinib has been shown to inhibit the response of JAK in rheumatoid arthritis patients.
Over 24 weeks, a 527 patient cohort was divided into three subgroups and treated at a 1:1:1 ratio: daily dosage of 4 mg baricitinib, 2 mg baricitinib, or placebo. All of these patients had responded poorly to previous therapeutic strategies.
The results were positive; patients treated with baricitinib demonstrated a significant reduction in joint swelling and pain, along with disease activity, which was measured using a number of validated questionnaires and scoring systems. Compared with the placebo group, those treated with the higher 4 mg baricitinib dosage strategy fared even better than those with the lower 2 mg dosage, resulting in full remission in almost 10%, and a significant improvement in nearly 50% of the patient cohort. What’s more, the adverse response rate was similar to current therapeutic strategies.
Prof Josef Smolen, Department of Rheumatology, University Clinic for Internal Medicine III, Medical University of Vienna, Vienna, Austria, elucidated the significance of these results: “With baricitinib, we will have a drug that works even if the currently employed medications are not sufficiently effective,” offering hope to patients unresponsive to typical DMARD therapies.
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