Cosentyx Shown to Reduce Fatigue for Up to 3 Years in Active AS Patients

Cosentyx Shown to Reduce Fatigue for Up to 3 Years in Active AS Patients
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Treatment with Cosentyx (secukinumab) reduced fatigue for up to three years in people with active ankylosing spondylitis (AS), particularly those who had never received TNF inhibitors, according to two Phase 3 clinical trials.

Age and disease activity before the treatment were found to predict short-term fatigue reductions, while fatigue severity and functional limitations predicted long-term improvements. 

The study, “Secukinumab Provides Sustained Reduction in Fatigue in Patients with Ankylosing Spondylitis: Long‐term Results of Two Phase III Randomized Controlled Trials,” was published in the journal Arthritis Care and Research.

AS is typically treated with physical therapy and medication, such as TNF inhibitors, to relieve symptoms and improve quality of life. Fatigue is a common AS symptom reported in as many as two-thirds of patients and can profoundly affect their well-being.

Developed by Novartis, Cosentyx is a biological therapy that blocks interleukin-17A, a signaling molecule that promotes inflammation and induces TNF production. Two pivotal Phase 3 clinical trials of Cosentyx, MEASURE 1 (NCT01358175) and MEASURE 2 (NCT01649375), demonstrated a significant reduction in AS signs and symptoms after 16 weeks of treatment at doses of 75 or 150 mg.

The U.S. Food and Drug Administration has approved Cosentyx for treating active AS in adults. The more recent approval of a higher 300 mg dose was based on positive results from the three-year MEASURE 3 study (NCT02008916) in 226 adults with active AS, in which the high dose provided more significant long-term improvements, particularly in patients who had received prior anti-TNF treatment.

An international team assessed the long-term effects of 150 mg of Cosentyx (the recommended dose at the time of the study) to treat fatigue in adults with AS. The researchers analyzed data from the MEASURE 1 trial for up to three years and the MEASURE 2 trial for up to two years. A total of 590 patients participated in either study, all adults with active AS who had either not received or had inadequate response/intolerance to prior anti-TNF therapy. 

In the MEASURE 1 study, 371 participants were randomly assigned to receive Cosentyx or a placebo in three 10 mg/kg intravenous (into-the-vein) loading doses administered at baseline, week two, and week four, followed by 75 or 150 mg subcutaneous (under-the-skin) injections every four weeks through the end of the trial. In the MEASURE 2 study, 219 participants were randomly assigned to receive either Cosentyx or a placebo at similar weekly doses from baseline to week four, then every four weeks until the end of the trial.

In both studies, patients were assessed at baseline, weeks four, eight, 12, 16, 24, year one, year two, and year three in MEASURE 1. Fatigue was measured using the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F) scale, in which higher scores correspond with lower fatigue levels.

A total of 125 patients in MEASURE 1 received 150 mg doses of Cosentyx and, of those, 83 completed the three-year extension study. Of the 72 patients treated with 150 mg Cosentyx in MEASURE 2, 60 completed the two-year study. Across both trials, most participants (nearly 70%) were male, the mean age was nearly 41 years, and almost 70% had never received TNF inhibitors. The mean FACIT-F score at the start of both trials was between 22.6 and 25.6, indicating severe fatigue. 

In both trials, participants showed significant reductions in fatigue as early as four weeks into Cosentyx treatment. Fatigue reductions were sustained by 75.6% of patients for three years in MEASURE 1 and by 81.4% of patients for two years in MEASURE 2. Yet, significant sustained decreases in fatigue were observed in those who had not received TNF inhibitors, but not in patients who were unresponsive to such treatment. 

Demographic and disease characteristics at baseline were not consistent predictors of short- or long-term fatigue response to treatment, defined as less fatigue corresponding with minimal clinically important improvement. Older patients were less likely while patients with higher disease activity at baseline were more likely to show short-term fatigue response at 16 weeks. Fatigue severity and degree of functional limitations at baseline were both predictors of long-term fatigue response at the year two assessment.

Fatigue responses correlated with partial remission (low disease activity) at week 16, year one, and year two, and a major decrease in disease activity at two years. Also, response to Cosentyx was moderately to strongly correlated with multiple measures of clinical response. 

“Previously, secukinumab [Cosentyx] has been shown to rapidly improve signs and symptoms, physical function, [health-related quality of life], and fatigue in patients with AS,” the scientists wrote. “Results presented here build upon these findings, demonstrating significant and sustained improvements in fatigue … in the overall population and particularly in the anti-TNF-naive population for up to 3 years.”

The limitations of the study included the lack of a control group after week 16, missing long-term fatigue response data, and the potential selection bias for patients who joined the extension study, the investigators said.

Aisha Abdullah received a B.S. in biology from the University of Houston and a Ph.D. in neuroscience from Weill Cornell Medical College, where she studied the role of microRNA in embryonic and early postnatal brain development. Since finishing graduate school, she has worked as a science communicator making science accessible to broad audiences.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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Aisha Abdullah received a B.S. in biology from the University of Houston and a Ph.D. in neuroscience from Weill Cornell Medical College, where she studied the role of microRNA in embryonic and early postnatal brain development. Since finishing graduate school, she has worked as a science communicator making science accessible to broad audiences.
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