American College of Rheumatology Annual Meeting
American College of Rheumatology Annual Meeting
November 27, 2018
3 min read

Bimekizumab improves outcomes among PsA patients

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Photo of Christopher Ritchlin
Christopher T. Ritchlin

CHICAGO — Bimekizumab, a monoclonal antibody that neutralizes both IL-17A and IL-17F, significantly improved both musculoskeletal and skin outcomes among patients with active psoriatic arthritis, according to phase 2b data presented at the ACR/ARHP 2018 Annual Meeting.

Christopher T. Ritchlin, MD, MPH, of the department of allergy, immunology and rheumatology at the University of Rochester Medical Center, said the findings illustrate the potential of bimekizumab — currently in phase 3 development for PsA — as a therapeutic option for psoriatic disease.

Previously, in preclinical and early clinical trials, the neutralization of both IL-17F and IL-17A was effective against psoriasis, PsA and ankylosing spondylitis, according to Ritchlin.

“The rationale for neutralizing IL-17F and IL-17A [is that] both IL-17A and IL-17F share 50% structural homology and have similar proinflammatory functions,” he said during a presentation. “IL-17A and IL-17F are expressed at sites of inflammation and independently cooperate with other cytokines to mediate inflammation in humans. The clinical hypothesis is that neutralizing IL-17F in addition to IL-17A results in a greater suppression of inflammation than inhibition of IL-17A alone.”

For the phase 2b trial, Ritchlin and colleagues randomly assigned 206 patients with active PsA to one of five treatment groups:

  • 16 mg of subcutaneous bimekizumab (n = 41);
  • 160 mg of subcutaneous bimekizumab (n = 41);
  • 160 mg of subcutaneous bimekizumab after a 320 mg loading dose (n = 41);
  • 320 mg of subcutaneous bimekizumab (n = 41); or
  • placebo (n = 42).

After week 12, all patients receiving placebo or 16 mg of bimekizumab were re-randomized to either 160 mg or 320 mg of bimekizumab. During clinic visits at weeks 16, 24 and 36, patients with less than 10% improvement in swollen and tender joint counts were eligible for rescue therapy. The primary endpoint was ACR50 response at week 12; however, safety and efficacy were monitored up to week 48.

Overall, 91.7% of patients completed treatment. By week 12, there was a significantly higher proportion of patients receiving bimekizumab who had an ACR50 response compared with patients receiving placebo. Specifically, ACR50 response was achieved in 26.8% of patients who received 16 mg, 41.5% who received 160 mg, 46.3% who received 160 mg after a 320-mg loading lose, and 24.4% who received 320 mg throughout the study vs. 7.1% who received placebo.

In addition to ACR50, patients receiving bimekizumab also had higher ACR20, ACR70 and PASI90 response rates, and were more likely to achieve minimal disease activity and resolution of enthesitis.


Patients who were re-randomized from placebo to bimekizumab or a higher dose of bimekizumab experienced a rapid improvement in disease activity after switching regimens. All improvements associated with bimekizumab continued to increase up to week 24 and were sustained through week 48.

In a safety analysis, there was no association between bimekizumab dose and treatment-related adverse events, which were reported in 34.1% of patients who received 16 mg of bimekizumab, 43.9% who received 160 mg, 39% who received 160 mg after a 320-mg loading dose, and 48.8% who received 320 mg vs. 57.1% of patients who received placebo. The most common adverse events were nasopharyngitis and upper respiratory tract infections. No deaths or cases of inflammatory bowel disease, major cardiovascular events or hypersensitivity and anaphylactic reactions were reported.

“The safety profile of bimekizumab was consistent with previous bimekizumab studies of psoriasis, PsA and AS,” Ritchlin said.

He concluded that additional research is needed to compare bimekizumab with other treatment types to validate the clinical benefit of dual IL-17A and IL-17F neutralization.

“I would like to see the efficacy of inhibiting IL-17A and IL-17F in comparison to an anti-TNF, as well as in comparison to [a treatment inhibiting] IL-17A alone,” he said. “We’ll have to see if that happens in the future.” – by Stephanie Viguers


Ritchlin CT, et al. Abstract L17. Presented at: ACR/ARHP Annual Meeting, Oct. 20-24, 2018; Chicago.

Disclosure: Ritchlin reports receiving research grants from AbbVie, Amgen and UCB, as well as consulting fees from AbbVie, Amgen, Lilly, Novartis, Pfizer and UCB.