Actemra

 

ACTEMRA binds specifically to both soluble and membrane-bound interleukin-6 (IL-6) receptors (sIL-6R and mIL-6R). ACTEMRA has been shown to inhibit sIL-6R and mIL-6R-mediated signalling. IL-6 is a pleiotropic pro-inflammatory cytokine produced by a variety of cell types including T- and B-cells, monocytes and fibroblasts. IL-6 is involved in diverse physiological processes such as T-cell activation, induction of immunoglobulin secretion, induction of hepatic acute phase protein synthesis and stimulation of haemopoiesis. IL-6 has been implicated in the pathogenesis of diseases including inflammatory diseases, osteoporosis and neoplasia.

 

In clinical studies with ACTEMRA, rapid decrease in C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and serum amyloid A (SAA) were observed. Consistent with the effect on acute phase reactants, treatment with ACTEMRA was associated with reduction in platelet count within the normal range. Increase in haemoglobin levels were observed, through ACTEMRA decreasing the IL-6-driven effects on hepcidin production to increase iron availability. In ACTEMRA treated patients, decrease in the levels of CRP to within normal ranges were seen as early as Week 2, with decrease maintained while on treatment².

References:  

1. 1.Choy E, et al. N Engl J Med 2001; 344:907-916.
2. 2.RoACTEMRA (tocilizumab) Summary of Product Characteristics. Roche Registration Limited. January 2009.