Low Rates of Immunogenicity With Secukinumab Therapy in PsA and AS

antibodies attacking virus
3d illustration of antibodies attacking virus particles in the bloodstream.
Secukinumab therapy has been associated with low rates of immunogenicity among patients with psoriatic arthritis and ankylosing spondylitis.

Secukinumab therapy has been associated with low rates of immunogenicity among patients with psoriatic arthritis (PsA) and ankylosing spondylitis (AS), according to research published in the Journal of Rheumatology.

Researchers used antibody-bridging assays to examine the immunogenicity of secukinumab therapy, indicated by the presence of treatment-emergent antidrug antibodies, in patients with PsA and AS. Seven studies were included in the analysis, 3 of which included patients with PsA (FUTURE 1-3) and 4 of which included patients with AS (MEASURE 1-4). The researchers collected blood samples at baseline and at weeks 16, 24, and 52; week 16 analyses included the AS studies only.

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Treatment-emergent antidrug antibodies were defined as antidrug antibodies that developed post-secukinumab treatment in patients with no detectable antidrug antibodies before treatment. Secukinumab immunogenicity was defined as a positive treatment-emergent antidrug antibody signal in at least 1 post-treatment sample in patients who were previously negative.

In total, 1414 and 1164 patients with PsA and AS, respectively, were included in the immunogenicity evaluation. Over 52 weeks, 5 patients with PsA (1 patient in FUTURE 1, 1 in FUTURE 2, and 3 in FUTURE 3) and 8 patients with AS (2 patients in MEASURE 1, 1 in MEASURE 2, 1 in MEASURE 3, and 4 in MEASURE 4) developed treatment-emergent antidrug antibodies (0.35% and 0.69% of patients, respectively).

Of the patients with PsA who developed treatment-emergent antidrug antibodies, 2 received concomitant methotrexate, and 1 also received corticosteroids. Among those with AS, 1 received concomitant methotrexate, 2 received concomitant sulfasalazine, and 3 received concomitant corticosteroids.

The frequency of treatment-emergent antidrug antibodies did not appear to vary based on an increase in secukinumab dose. At the multiple immunogenicity measurement time points, 96% of patients had secukinumab serum concentrations below 53.8 µg/mL. All but 1 treatment-emergent antidrug antibodies were non-neutralizing; none were associated with immunogenicity-related adverse events.

In all 7 studies, treatment-emergent antidrug antibodies were associated with normal secukinumab pharmacokinetics.

Among patients with AS, concentrations at week 16 were higher than concentrations at later time points owing to the loading regimens during the first month. At weeks 24 and 52, mean concentrations remained stable, with mean and median concentrations approximately 2-fold higher with a 300 mg dose vs a 150 mg dose of secukinumab.

Previous research has identified the presence of antidrug antibodies as “an important contributor to reduced treatment efficacy and the increased risk of [adverse events] in patients receiving biologic therapy.” The low incidence of immunogenicity of secukinumab could “be an important clinical consideration when selecting a therapy for patients with chronic immune mediated inflammatory disease.”

The researchers of the study concluded that “[the] results presented here add to the consistent evidence of low immunogenicity incidence with secukinumab and, therefore, provide useful information for clinicians considering therapeutic options for patients with PsA and AS.”


Multiple authors reported relationships with the pharmaceutical industry. For a complete list of disclosures, please see the full text of the study online.


Deodhar A, Gladman DD, McInness IB, et al. Secukinumab immunogenicity over 52 weeks in patients with psoriatic arthritis and ankylosing spondylitis [published online June 15, 2019]. J Rheumatol. doi: 10.3899/jrheum.190116