Nipocalimab meets primary endpoint in Sjögren’s syndrome

Presented byProf. Jacques-Eric Gottenberg, Strasbourg University Hospital, FranceConferenceEULAR 2024TrialPhase 2, DAHLIAS Doihttps://doi.org/10.55788/97a65477 In the DAHLIAS phase 2 trial, patients with Sjögren's disease treated with nipocalimab demonstrated a significant reduction in Clinical EULAR Sjögren's Syndrome Disease Activity Index (clinESSDAI) compared with placebo. These results support the further development of the drug."Sjögren's disease is a chronic systemic autoimmune disease characterised by lymphocytic infiltrates of exocrine glandular tissues and secretion of autoantibodies," Prof. Jacques-Eric Gottenberg (Strasbourg University Hospital, France) stated 1. He underlined the high unmet need for treatment options for Sjögren's disease since no specific drug has been approved so far.Nipocalimab is an anti-neonatal Fc receptor (FcRn) monoclonal antibody that diminishes the circulating IgG and IgG autoantibody levels. Its efficacy and safety were evaluated in the multicentre, randomised-controlled, phase 2 DAHLIAS trial (NCT04968912). The 163 adult participants were treated every 2 weeks with placebo or nipocalimab at 5 or 15 mg/kg plus standard-of-care through 22 weeks. All participants were seropositive for anti-Ro60 and/or anti-Ro52 IgG antibodies. They suffered from moderate-to-severe active primary Sjögren's disease, represented by a clinESSDAI of ≥6. They had a median age of 48 years and over 90% were women. The primary endpoint of change in clinESSDAI was assessed at week 24, while safety follow-up continued to week 30.At week 24, a significant difference in clinESSDAI was detected on the higher dose of nipocalimab with a change from baseline in a least square mean of -6.40 versus -3.73 on placebo (P=0.002; see Figure). The 15 mg/kg regimen of nipocalimab also led to amelioration in a variety of secondary endpoints including Physician Global Assessment (PGA) of disease severity (P<0.001), change in ESSDAI score (P=0.012), Composite of Relevant Endpoints for Sjögren's Syndrome (CRESS; P=0.001), and disease activity level (DAL; P=0.046). Overall, significant differences were not determined for the lower dose of the study drug. Nipocalimab increased the unstimulated whole salivary flow rate by 32% compared with 16% in the placebo group.Figure: Primary endpoint: Change from baseline in clinESSDAI at week 24 1CI, confidence interval; clinESSDAI, clinical EULAR Sjögren's Syndrome Disease Activity Index; LS, least square; NS, not significant; SE, standard error; Q2W, every 2 weeks.At least 1 adverse event was reported in 79.6% of the 15 mg/kg group and 62.5% on placebo. Serious adverse events occurred in 7.4% and 5.4%, respectively. There were no deaths and no opportunistic infections."These findings support the further clinical evaluation of nipocalimab, a new FcRn blocker, in Sjögren's disease and other autoantibody-associated rheumatic diseases," Prof. Gottenberg concluded. Gottenberg J, et al. Efficacy and safety of nipocalimab, an anti-FcRn monoclonal antibody, in primary Sjogren's disease: results from a phase 2, multicentre, randomised, placebo-controlled, double-blind study (DAHLIAS). LBA0010, EULAR 2024 Congress, 12–15 June, Vienna, Austria.Copyright ©2024 Medicom Medical Publishers Fc receptor Nipocalimab DAHLIAS Sjögren's syndrome Posted on 29 July 202429 July 2024 Previous Article « Advanced therapies show promising results in PsA real-world study Next Article Letter from the Editor » Related Articles September 4, 2019 Tapering of prednisone in RA patients who achieved low disease activity or remission with tocilizumab September 4, 2019 Preliminary efficacy and safety data of RG6125 in RA patients with an inadequate response to TNF inhibitors August 17, 2022 Rheumatoid arthritis-associated ILD Register to view our latest news directly from the conference and receive news notifications in your field. Register Now Search for: site created by: © 2024 Medicom Medical Publishers. All rights reserved. Terms and Conditions | Privacy Policy HEAD OFFICE Laarderhoogtweg 25 1101 EB Amsterdam The Netherlands T: +31 85 4012 560 E: publishers@medicom-publishers.com