A Review of Brodalumab, an IL-17 Receptor Antagonist, for Moderate-to-Severe Plaque Psoriasis

Yun Tong, MD; Andrew J. Peranteau, MD; Zeena Nawas, MD; Stephen K. Tyring, MD, PhD


Skin Therapy Letter. 2017;22(1) 

In This Article

Abstract and Introduction


Psoriasis is a chronic immune-mediated inflammatory disease with epidermal hyperplasia that affects 2–3% of the population. Interleukin (IL)-17 signaling has a central role in its pathogenesis. Brodalumab is a monoclonal antibody that neutralizes IL-17 receptor type A. Brodalumab is highly effective in the reversal of psoriatic phenotype and gene expression patterns.


An immune-mediated disease, psoriasis affects approximately 120 million people or 2% of the population.[1,2] The most common form of the disease, psoriasis vulgaris, accounts for 80% of all cases.[3] Psoriasis is increasingly recognized as more than a skin disease and may be associated with a constellation of comorbidities including psoriatic arthritis,[4] stroke, heart failure, obesity, hypertension, and diabetes. Severe psoriasis is considered an independent risk factor for cardiovascular mortality[5] and psychiatric disorders including depression, anxiety, and suicidal tendency from physical and mental distress.[6] Even patients with limited psoriatic involvement often report a substantial negative impact on their daily quality of life (QoL).

For people with moderate-to-severe plaque psoriasis (17% of all psoriasis patients[2]), topical medications usually provide unsatisfactory results.[3] Advances in the understanding of cytokines in psoriasis have led to the development of more efficacious therapeutic options including biological agents targeting tumor necrosis factor (TNF)-α, interleukin (IL)-23, and IL-17. Current pathogenic models indicate dysfunctional IL-17 signaling may play a pivotal inflammatory role in the pathophysiology of psoriasis.[3,7]