A Study to Target the Type I IFN Receptor by Administrating Anifrolumab in RA Patients With a High IFN Signature (TarIFNiRA)

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Background: Rheumatoid arthritis (RA) is the most common chronic inflammatory joint disorder with a prevalence of about 0.5-1% and results in joint inflammation and damage, which causes loss-of-function and disability, and ultimately results in loss of labour participation, loss of independence in d...

Background: Rheumatoid arthritis (RA) is the most common chronic inflammatory joint disorder with a prevalence of about 0.5-1% and results in joint inflammation and damage, which causes loss-of-function and disability, and ultimately results in loss of labour participation, loss of independence in daily life and high societal costs. Conventional synthetic DMARDs (csDMARDs), especially methotrexate, represent the first-line treatment in RA. If, however, the treatment target is not achieved with the first DMARD strategy escalation in the treatment regimen is needed. The current praxis is to add a biological (b) DMARD (e.g. TNF inhibitors, TNFi). With the growing evidence that type I IFNs play an important role in RA, inhibition of the biological activity of type I IFNs with anifrolumab may be a novel efficacious therapy for the treatment of RA and its significant unmet medical need. Objective: To evaluate the efficacy of Anifrolumab compared to placebo on RA disease activity in patients with an increased type I IFN gene signature Methods: This is a Phase 2A (proof-of-concept), multicenter, randomised, double-blind, placebo-controlled pilot study, to evaluate the efficacy and safety of an intravenous treatment regimen of 300 mg Anifrolumab versus placebo. Patients with moderately to severely active RA who did not respond to at least one TNFi but who had not more than three bDMARDs and who also have a high IFN- transcript score will be included. Expected Results: The hypothesis underlying this protocol is that blocking type I IFN signaling through the human type I IFN receptor with Anifrolumab will reduce the severity of disease in RA patients, who have an activated type I IFN response.

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