By binding to soluble BLyS and reducing the autoreactive B cell population, belimumab decreases the production of autoantibodies.1,2

Patients on BENLYSTA experienced a 41% reduction in anti-double stranded DNA over 52 weeks.2

The clinical relevance of normalizing this biomarker has not been definitively established.

  • BLyS is a protein involved in SLE3-5
  • BLyS plays a role in B-cell survival3
  • BENLYSTA binds to and inhibits BLyS
    • Allows more B cells, including autoreactive B cells, to undergo apoptosis4,6
    • Reduces the differentiation of B cells into immunoglobulin-producing plasma cells4
  • BENLYSTA does not directly bind to B cells and does not directly deplete B-cell populations4,6
  • BENLYSTA significantly reduced circulating CD19+, CD20+, naïve, and activated B cells, and the SLE B-cell subset at Week 521
  • Reductions in naïve and the SLE B-cell subset were observed as early as Week 8 and sustained to Week 521
  • Memory cells increased initially and slowly declined toward baseline by Week 521
  • Significant reduction in plasma cell subsets were observed by Week 8 and maintained through Week 522
  • Belimumab depletes the levels of circulating naïve and activated B cells to about 50% in a 6-month period and sustains depletion through Week 522
  • The clinical relevance of these effects on B cells has not been established.

BENLYSTA selectively inhibits soluble BLyS, an important factor in SLE3-5

In many patients with SLE, higher concentration of BLyS promotes increased B-cell survival, including the survival of autoreactive B-cells.3

BENLYSTA is a targeted human monoclonal antibody that binds to soluble BLyS, inhibiting its binding to B-cell receptors.4

By reducing the autoreactive B-cell population, BENLYSTA decreases the production of autoantibodies.


  1. BENLYSTA [package insert]. Research Triangle Park, NC: GlaxoSmithKline, 2017.
  2. Stohl W, Hiepe F, Latinis KM, et al. Belimumab reduces autoantibodies, normalizes low complement levels, and reduces select B cell populations in patients with systemic lupus erythematosus. Arthritis Rheum. 2012;64(7):2‍328-2337.
  3. Cancro MP, D’Cruz DP, Khamashta MA. The role of B lymphocyte stimulator (BLyS) in systemic lupus erythematosus. J Clin Invest. 2009;119(5):1066-1073.
  4. Baker KP, Edwards BM, Main SH, et al. Generation and characterization of LymphoStat-B, a human antibody that antagonizes the bioactivities of B lymphocyte stimulator. Arthritis Rheum. 2003;48(11):3‍253-3265.
  5. Petri M, Stohl W, Chatham W, et al. Association of plasma B lymphocyte stimulator levels and disease activity in systemic lupus erythematosus. Arthritis Rheum. 2008;58(8):2‍453-2459.
  6. Do RKG, Hatada E, Lee H, et al. Attenuation of apoptosis underlies B-lymphocyte stimulator enhancement of humoral immune response. J Exp Med. 2000;192(7):953-964.

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