Mode of Action 

Enbrel^® is a soluble TNFR fusion protein¹

• Much of the disease pathology in RA, AS and PsO is mediated by proinflammatory molecules that are linked in a network controlled by TNF¹ 
   
• The mechanism of action of Enbrel^® involves the competitive inhibition of TNF binding to the cell surface TNFRs, which thereby inhibits the biological activity of TNF¹
   
• Enbrel^® may also modulate biologic responses controlled by additional downstream molecules (e.g. cytokines, adhesion molecules or proteinases) that are induced or regulated by TNF¹

• Enbrel^® has a specific structure (which binds with human tumour necrosis factor receptor) and mechanism of action^2-4
   
• Enbrel^® mimics the activity of naturally occurring soluble TNFRs by acting as a competitive inhibitor of TNF⁷ and preventing TNF-mediated cellular responses²

Enbrel^® is the only fully human soluble TNFR²

Enbrel^® works like a naturally occurring soluble TNFR and inhibits TNF.²

*Mean half-life of approximately 4.3 days (70–100 hours)

^†PASI 75 improvements were seen as early as 2 weeks with etanercept 25 mg BIW and 50 mg BIW⁵.

Disclaimer: The approved dose for Psoriasis is etanercept 25 mg BIW or 50 mg OW and 50 mg BIW can be used upto 12 weeks followed by 25 mg BIW/ 50 mg OW.

AS, ankylosing spondylitis; Fc, fragment crystallisable; IgG1, immunoglobulin G1; PASI, Psoriasis Area and Severity Index; PsA, psoriatic arthritis; PsO, psoriasis; QoL, quality of life; RA, rheumatoid arthritis; TNF, tumour necrosis factor; TNF-α, tumour necrosis factor alpha; TNFR, tumour necrosis factor receptor.

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