ABSTRACT
Introduction
Psoriatic Arthritis (PsA) is an inflammatory arthritis that is present in approximately 25% of psoriasis patients. Currently, several targeted therapies are available to manage PsA; however, many patients fail these therapies. Several new therapeutic options, with differing mechanisms of action, are currently being evaluated.
Areas covered
This article reviews available results from phase I to phase III trials of several investigational monoclonal antibodies that the FDA has not yet approved for PsA. The proposed mechanisms of the new therapeutic agents and their relevance to the pathogenesis of PsA will be discussed. The investigational agents’ efficacy and safety will be summarized, and their potential clinical applications for managing PsA will be contemplated.
Expert opinion
Due to recent advances in understanding psoriatic arthritis, therapeutic agents are increasingly focused on inhibiting interleukin-17 and interleukin-23 pathways. Various strategies have been used to inhibit these cytokines, demonstrating favorable efficacy and acceptable safety profile.
Article highlights
Psoriatic arthritis is an inflammatory arthritis associated with psoriasis characterized by articular involvement, extra-musculoskeletal manifestations, and associated co-morbid illnesses.
The natural history of PsA is variable; however, most patients with persistent joint inflammation will likely damage their joints if not treated early.
A domain-based management approach is most often used to guide therapeutic choices of biologic therapies.
Despite six classes of targeted therapies to manage PsA, there continues to be an unmet need in managing PsA as some patients fail to respond and others lose response.
Biological inhibitors targeting IL-17A/IL-17F demonstrate robust efficacy in most articular domains for PsA.
Newer therapies under investigation targeting IL-17A and IL-23 are promising for managing PsA.
Declaration of interest
P Rahman has received consulting fees and has participated in the speaker bureau for Abbott, AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, and Pfizer, and has also received research grants from Janssen and Novartis. V Chandran has received research grants from AbbVie, Amgen and Eli Lilly and has received honoraria for advisory board member roles from AbbVie, Amgen, BMS, Eli Lilly, Janssen, Novartis, Pfizer and UCB. His spouse is an employee of AstraZeneca.
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.