Vera Therapeutics

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Atacicept

  • Novel biologic investigational therapeutic: recombinant fusion protein containing the soluble TACI receptor that binds to the cytokines BLyS and APRIL, members of the tumor necrosis factor family that stimulate B cells and plasma cells to produce autoantibodies associated with IgA nephropathy (IgAN)1 and lupus nephritis (LN)2
  • Well-tolerated safety profile in clinical studies including >1,500 patients across multiple indications3
  • Self-administered once weekly by 1-mL subcutaneous injection
  • Vera holds an exclusive worldwide license for the development and commercialization of atacicept in all indications from Merck KGaA, Darmstadt, Germany, a leading science and technology company

BLyS = B lymphocyte stimulator, also known as B-cell activating factor or BAFF; APRIL = A proliferation-inducing ligand; TACI = transmembrane activator and CAML interactor.

1Macpherson AJ, et al. Mucosal Immunol 2008; 2Dillon SR, et al. Arthritis Res Ther 2010; 3Gordon C, et al. Rheumatol Adv Pract 2019 and data on file.

Lupus Nephritis (LN)

Severe renal manifestation of systemic lupus erythematosus (SLE).
Approximately 25% of LN patients develop end stage renal disease.
Current treatment involves combination immunosuppressants and steroids.
Recently approved therapies, yet unmet need for effective and safe therapies remain.

Target the Source

Click the pathways below to see how Atacicept acts on LN Pathophysiology

Glomerulus Glomerulonephritis Progressive renal injury 4 Autoantibodies and immune complexes deposit in glomeruli Immature B-cells survive and mature 2a B-cells differentiate and class switch 2b Plasma cells proliferate and create autoantibodies 2c Autoantibodies circulate and form immune complexes 2d B-Cell Dysregulation BLyS and APRIL promote the survival, maturation and differentiation of B-cells and plasma cells - that then produce disease-causing antinuclear and anti-DNA autoantibodies 2 Cytokine Abnormalities Patients with Systemic Lupus Erythematosus may have higher levels of BLyS and APRIL, contributing to the pathogenesis of Lupus Nephritis 1 Heterotrimer BLyS BLyS BLyS APRIL APRIL APRIL Heterotrimer BLyS BLyS APRIL Heterotrimer BLyS Heterotrimer
Glomerulus Glomerulonephritis Progressive renal injury 4 Autoantibodies and immune complexes deposit in glomeruli Immature B-cells survive and mature 2a B-cells differentiate and class switch 2b Plasma cells proliferate and create autoantibodies 2c Autoantibodies circulate and form immune complexes 2d B-Cell Dysregulation BLyS and APRIL promote the survival, maturation and differentiation of B-cells and plasma cells - that then produce disease-causing antinuclear and anti-DNA autoantibodies 2 Cytokine Abnormalities Patients with Systemic Lupus Erythematosus may have higher levels of BLyS and APRIL, contributing to the pathogenesis of Lupus Nephritis 1 Heterotrimer BLyS BLyS BLyS APRIL APRIL APRIL Heterotrimer BLyS BLyS APRIL Heterotrimer BLyS Heterotrimer
2a

Atacicept blocks BlyS, a factor important for immature B cell survival and maturation, resulting in reduced numbers of disease-causing B cells.
2b

Atacicept also blocks APRIL, which – in combination with BLyS – is important for mature B cell survival, reducing the number of disease-causing plasma cells.
2c

Reductions in B cells and plasma cells work together to cause a reduction in autoantibodies.
2d

Ultimately fewer antibodies, autoantibodies, and immune complexes reduce disease activity.

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