Dermatology Handbook
For UK audiences

The essential guide to product selection

DH
Adalimumab (Yuflyma)
Systemic psoriasis treatments Celltrion Healthcare

Adalimumab (Yuflyma)

Adalimumab binds specifically to TNF and neutralises the biological function of TNF by blocking its interaction with the p55 and p75 cell surface TNF receptors.

Indications

Treatment of severe chronic plaque psoriasis in children and adolescents from 4 years of age who have had an inadequate response to or are inappropriate candidates for topical therapy and phototherapies.

Price

  • 80mg solution for injection in pre-filled pen £633.70

  • 40mg solution for injection in pre-filled pen, £633.70
  • 20mg solution for injection in pre-filled syringe, £316.93

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.