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OP0129 Effects of Blisibimod, an Inhibitor of B-Cell Activating Factor, on Markers of Renal Disease in Patients with SLE
  1. R. Furie1,
  2. M. Scheinberg3,
  3. G. Leon2,
  4. E. B. Ramiterre4,
  5. M. Thomas5,
  6. A. D. Chu6,
  7. C. Hislop7,
  8. R. S. Martin6,
  9. M. A. Petri8
  1. 1North Shore–Long Island Jewish Health System, Lake Success New York, United States
  2. 2Rheumatology Gynecology & Reproduction Institute, Lima, Peru
  3. 3Rheumatology Hospital Abreu Sodre Pesquisa Clínica, São Paulo, Brazil
  4. 4Brokenshire Memorial Hospital, Davao City, Philippines
  5. 5Health and Research Centre, Trivandrum, Kerala, India
  6. 6Anthera Pharmaceuticals
  7. 7Anthera Pharmaceuticals, Inc, Hayward
  8. 8Johns Hopkins University School of Medicine, Baltimore Maryland, United States

Abstract

Background Elevations of BAFF are observed in patients with SLE. Here we report renal findings from a Phase 2b clinical trial in patients with SLE treated with the subcutaneous BAFF inhibitor, blisibimod.

Objectives To evaluate the effect of 24-week therapy with blisibimod on markers of renal disease in patients with proteinuria or active inflammation.

Methods 547 patients with serologically-active SLE and SELENA SLEDAI ≥6 were randomized to receive placebo or blisibimod. 13.9% of patients had renal involvement at baseline per SELENA-SLEDAI. Proteinuria and inflammation biomarkers were evaluated throughout the study.

Results In a subgroup of subjects with baseline urinary protein equivalent to 1–6g/24hr (n=49), significantly greater reductions in proteinuria were observed with blisibimod compared to placebo from Weeks 8 through 24 (respective mean reductions of 0.73g/24hr (-35.0%) and 0.24g/24hr (-5.1%) at Week 24, p=0.045). Similarly, significantly greater reductions in proteinuria were observed in a subgroup of subjects with active inflammation ie low C3 and high anti-dsDNA (n=195, figure 1 ). Treatment with blisibimod was also associated with significant improvements in markers of B-cell inflammation: anti–dsDNA antibodies, C3 and C4, and B-cell counts.

Conclusions These data confirm and extend the established role of BAFF in SLE by demonstrating that BAFF inhibition is associated with decreased renal inflammation. The findings support further evaluation of blisibimod in SLE, and other autoimmune kidney diseases such as lupus nephritis, IgA nephropathy and idiopathic membranous glomerulonephritis.

Disclosure of Interest R. Furie Consultant for: Anthera Pharmaceuticals, M. Scheinberg: None Declared, G. Leon: None Declared, E. Ramiterre: None Declared, M. Thomas: None Declared, A. Chu: None Declared, C. Hislop Employee of: Anthera Pharmaceuticals, R. Martin Employee of: Anthera Pharmaceuticals, M. Petri Consultant for: Anthera Pharmaceuticals

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