Dermatology Handbook
For UK audiences

The essential guide to product selection

Etanercept (Enbrel)
Systemic psoriasis treatments Pfizer

Etanercept (Enbrel)

Enbrel (etanercept) is a fully human soluble TNF receptor fusion protein. TNF is a dominant cytokine in the inflammatory process of rheumatoid arthritis. Elevated levels of TNF are also found in the synovium and psoriatic plaques of patients with psoriatic arthritis and in serum and synovial tissue of patients with ankylosing spondylitis. In plaque psoriasis, infiltration by inflammatory cells, including T-cells, leads to increased TNF levels in psoriatic lesions compared with levels in uninvolved skin. Etanercept is a soluble TNF receptor that is a competitive inhibitor of TNF binding to its cell surface receptor, thereby inhibiting biological activity of TNF. This product entry refers to Enbrel, not biosimilars of etanercept

Indications

Treatment of active and progressive psoriatic arthritis in adults when the response to previous disease-modifying antirheumatic drug therapy has been inadequate. Ankylosing spondylitis (AS): treatment of adults with severe active AS who have had an inadequate response to conventional therapy. Non-radiographic axial spondyloarthritis: treatment of adults with severe non-radiographic axial spondyloarthritis with objective signs of inflammation as indicated by elevated C-reactive protein (CRP) and/or magnetic resonance imaging (MRI) evidence, who have had an inadequate response to nonsteroidal anti-inflammatory drugs (NSAIDs). Plaque psoriasis: treatment of adults with moderate to severe plaque psoriasis who failed to respond to, or who have a contraindication to, or are intolerant to other systemic therapy, including ciclosporin, methotrexate or psoralen and ultraviolet-A light (PUVA). Enbrel in combination with methotrexate is indicated Treatment of moderate to severe active rheumatoid arthritis in adults when the response to disease-modifying antirheumatic drugs, including methotrexate (unless contraindicated), has been inadequate. Treatment of polyarthritis (rheumatoid factor positive or negative) and extended oligoarthritis in children and adolescents from the age of 2 years who have had an inadequate response to, or who have proved intolerant of, methotrexate. Treatment of chronic severe plaque psoriasis in children and adolescents from the age of 6 years who are inadequately controlled by, or are intolerant to, other systemic therapies or phototherapies

Price

  • 10mg powder and solvent for solution for injection (paediatric dosing only), £CS
  • 25mg powder and solvent for solution for injection, £CS
  • 50mg solution for injection in pre-filled syringe, £CS
  • 25mg solution for injection in pre-filled syringe, £CS
  • 50mg solution for injection in pre-filled pen, £CS

Systemic psoriasis treatments

All Systemic psoriasis treatments
Adalimumab (Amgevita)
Amgen

Adalimumab (Amgevita)

Biosimilar of adalimumab (Humira).
Adalimumab (Hyrimoz)
Sandoz

Adalimumab (Hyrimoz)

Biosimilar of adalimumab (Humira).
Etanercept (Erelzi)
Sandoz

Etanercept (Erelzi)

Biosimilar of etanercept (Enbrel).
Infliximab (Zessly)
Sandoz

Infliximab (Zessly)

Biosimilar of infliximab (Remicade).
Ixekizumab (Taltz)
Lilly

Ixekizumab (Taltz)

Ixekizumab is an IgG4 monoclonal antibody that binds with high affinity (<3 pM) and specificity to interleukin 17A (both IL-17A and IL-17A/F). Elevated concentrations of IL-17A have been implicated in the pathogenesis of psoriasis by promoting keratinocyte proliferation and activation, as well as in the pathogenesis of psoriatic arthritis by driving inflammation leading to erosive bone damage and pathological new bone formation. Neutralisation of IL-17A by ixekizumab inhibits these actions.
Secukinumab (Cosentyx)
Novartis

Secukinumab (Cosentyx)

Secukinumab is a fully human IgG1/k; monoclonal antibody that selectively binds to and neutralises the proinflammatory cytokine interleukin-17A (IL-17A). Secukinumab works by targeting IL-17A and inhibiting its interaction with the IL-17 receptor, which is expressed on various cell types including keratinocytes. As a result, secukinumab inhibits the release of proinflammatory cytokines, chemokines and mediators of tissue damage and reduces IL-17A-mediated contributions to autoimmune and inflammatory diseases. Clinically relevant levels of secukinumab reach the skin and reduce local inflammatory markers. As a direct consequence treatment, secukinumab reduces erythema, induration and desquamation present in plaque psoriasis lesions.