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Purpose: Provide 4-yr safety and efficacy data in SLE patients (pts) treated with belimumab. Methods: 449 SLE pts with SELENA SLEDAI (SS) ≥4 enrolled in a phase 2, 52-week (wk), double-blind trial of belimumab (1, 4 or 10 mg/kg, q28d) vs placebo (plc) plus background SLE therapy. At wk 56, plc pts received belimumab 10 mg/kg; belimumab pts could remain on their current dose or receive 10 mg/kg (investigator’s discretion). At wk 80, all remaining pts (296) received belimumab 10 mg/kg in a continuation trial. The 4-yr dataset was divided into eight 6-mo intervals for reporting adverse event (AE) and flare rates. Interval 1 includes the initial belimumab treatment which for plc pts began at wk 56. Analyses of disease activity included the SS SLE Flare Index (SFI) and a post-hoc SLE Responder Index (SRI): improvement in SS (≥4 pt decrease), no new BILAG A or 2 new B flares, and no Physician’s Global Assessment (PGA) worsening (< 0.3 pt increase) vs baseline. Post-hoc analyses identified a serologically active (ANA titer ≥1:80 and/or anti-dsDNA ≥30 IU/mL) pt subgroup (321) for whom belimumab demonstrated increased response. Results: By 4 yrs, overall belimumab exposure was 1,192 pt yrs. The incidence rates (per 100 pt-yrs) of AEs remained the same or decreased over 4 yrs (Table 1). In serologically active pts, SRI rate was 46% at wk 52 (vs plc 29%, p<0.05) which increased to 55% by wk 76 and was maintained through wk 208 (original belimumab pts); the frequency of new BILAG A or 2 B flares decreased from 30% at 6 mo to 23% at 1 yr (vs plc 33% and 25%, respectively) and declined to 5% at 4 yrs; the frequency of flares by SFI decreased from 72% at 6 mo to 62% at 1 yr (vs plc 76% and 73%, respectively) and declined to 16% at 4 yrs. Flare data included plc-to-belimumab pts after yr 1.
Conclusion: Belimumab added to standard of care therapy was generally well tolerated over 4 yrs. Serologically active pts treated with belimumab showed sustained improvement in disease activity and a decline in BILAG and SFI flares over 4 yrs. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Disclosure: M. Petri, HGS, 5, HGS, 2 ; R. Furie, Human Genome Sciences, Inc., 5 ; J. Merrill, None; D. J. Wallace, None; E. M. Ginzler, Aspreva, 5, Aspreva, 2, Bristol-Myers Squibb, 5, Bristol-Myers Squibb, 2, Human Genome Sciences, Inc., 9, Human Genome Sciences, Inc, 2, La Jolla Pharmaceutical, 5, MedImmune, 5, Merck/Serono, 2, Novo Nordisk, 5, Zymogenetics, 5, UCB, 2 ; W. Stohl, Human Genome Sciences, 2, Human Genome Sciences, 9 ; W. Chatham, HGS, 2, Bristol-Myers Squibb, 2, Genentech and Biogen IDEC Inc., 2, UCB Pharma, 2, Merck-Serono, 2 ; J. McCune, Genentech/Roche, 5, Johnson and Johnson, 5, HGS, 2 ; A. Weinstein, Human Genome Sciences, Inc., 2 ; L. Pineda, HGS, 1, HGS, 3 ; Z. J. Zhong, HGS, 1, HGS, 3 ; J. Klein, HGS, 1, HGS, 3 ; D. Hough, Johnson & Johnson, Bristol-Myers Squibb, Roche, Human Genome Sciences, 1, Human Genome Sciences, 3 ; W. Freimuth, HGS, 1, HGS, 3 .