Mechanism of Action

Benlysta is the first and only approved treatment designed to target BLyS, an underlying cause of both SLE and LN1,2

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

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Observations in patients with SLE:

  • BENLYSTA significantly reduced circulating CD19+, CD20+, naïve, and activated B cells, and the SLE B-cell subset at Week 52
  • Reductions in naïve B cells and the SLE B-cell subset were observed as early as Week 8 and sustained to Week 52
  • Memory cells increased initially and slowly declined toward baseline by Week 52
  • Significant reduction in plasma cell subsets were observed by Week 8 and maintained through Week 523
  • Belimumab depletes the levels of circulating naïve and activated B cells to about 50% in a 6-month period and sustains depletion through Week 523
  • BENLYSTA does not bind to B cells directly, but by binding to BLyS, BENLYSTA inhibits the survival of B cells, including autoreactive B cells, and reduces the differentiation of B cells into immunoglobulin-producing plasma cells.4,5
  • The clinical relevance of these effects on B cells has not been established
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Observations in patients with LN:

Histological studies have indicated:

  • BLyS expression can be significantly elevated in the glomeruli of LN patients2,6
  • Serum BLyS levels and increased production of intra-renal BLyS may promote renal inflammation and flares7-9

In patients with active lupus nephritis, following treatment with BENLYSTA:

  • There was a decrease in serum IgG as early as Week 4, and subsequently there was an increase in serum IgG levels which was associated with decreased proteinuria
  • Reductions in autoantibodies, increases in complement, and reductions in circulating total B cells and B‑cell subsets observed were consistent with those observed in patients with SLE
  • The clinical relevance of these results has not been definitively established

BENLYSTA does not bind to B cells directly, but by binding to BlyS, BENLYSTA inhibits the survival of B cells, including autoreactive B cells, and reduces the differentiation of B cells into immunoglobulin-producing plasma cells.

BLyS = B-lymphocyte stimulator protein

41%

Adult patients with SLE on BENLYSTA experienced a 41% reduction in anti-double stranded DNA levels over 52 weeks.3 The clinical relevance of normalizing this biomarker has not been definitively established.

BENLYSTA targets BLyS to reduce autoantibodies