New study shows treatment with brodalumab demonstrates clinical response in subjects with PsA
Published on June 13, 2013 at 12:49 AM
Data suggest blocking IL-17 a beneficial new strategy
A new study presented today at EULAR 2013, the Annual Congress of the European League Against Rheumatism, shows that treatment with brodalumab demonstrates significant clinical response and an acceptable safety profile in subjects with psoriatic arthritis (PsA).
PsA is a chronic inflammatory arthritis associated with psoriasis which significantly impacts health-related quality of life in patients, and increases risk of co-morbid cardiovascular and gastrointestinal diseases. Psoriasis occurs in 2-3% of the population, with PsA occurring in up to 30% of those of cases.
IL-17 induces production of anti-microbial peptides and pro-inflammatory cytokines that in turn may help sustain immune responses in the skin. With similar pathways impacting skin and joint diseases, data suggest that cytokine-targeting strategies aimed at blocking signalling through the IL-17 receptor may be a beneficial new strategy in the treatment of PsA.
Lead author of the study Dr Mease, Swedish Medical Center and University of Washington, Seattle, US commented "PsA is a progressive disease associated with a number of co-morbidities, disability and disfigurement. There is a need for therapies to better manage patient outcomes, and prevent long-term bone loss and permanent joint damage, especially in those patients for whom anti-TNF therapy is not effective or tolerated." Dr Mease continued, "these significant patient responses support continued evaluation of brodalumab for the treatment of PsA and clearly show that cytokine-targeting strategies aimed at blocking signalling through the IL-17 receptor may represent an important new treatment strategy."
The study involving 168 patients with at least a 6 month history of PsA demonstrated that 37% and 39% of subjects in the 140- and 280-mg brodalumab groups respectively, achieved the primary endpoint of ACR20 response rates at week 12 compared with 18% of subjects in the placebo group (p <0.05).
A further analysis determined the ACR20 response rates in biologic-na-ve subjects were 36% in the 140 mg group, 37% in the 280 mg group, and 20% in the placebo group; comparable with the respective rates of 37%, 42%, and 16%, in subjects with prior biologic exposure. There were consistent improvements in secondary endpoints including ACR50, DAS 28 and components of the ACR including CRP.