Alvin Wells, MD, PhD: Last year at the ACR [American College of Rheumatology] Convergence meeting, Dr Philip Mease presented some data on the safety profiles comparing 2 very good biologic medications: ixekizumab and adalimumab. We’ve seen these data posted before, but for the first time Dr Mease gave us some glimpse of the 52-week safety data. This is important because this a chronic disease, and patients will need to be on some therapy long-term.
As a treating rheumatologist, it’s important for me to say, “Hey, are there going to be any new infections? Am I going to see blood clots? Am I going to see anything that’s going to impact my patients and their disease?”
The trial that Dr Mease presented looking at ixekizumab vs adalimumab was a head-to-head superiority trial comparing adalimumab with ixekizumab. In this trial, patients were randomized to receive ixekizumab or adalimumab in the normal way they’re given.
Adalimumab is given at 40 mg every other week. Ixekizumab is given at 40 mg once a month. They were randomized and continued on the other background DMARDs [disease-modifying antirheumatic drugs] at a stable dose—a low dose of prednisone—and were followed over a period of 16 weeks, 24 weeks. In this trial, they looked at 52-week data to see if there were any new safety signals that we did not see in the randomized controlled portion of the trial. The take-home message was that ixekizumab was superior to adalimumab in regard to the clinical impact for a patient with psoriatic arthritis. There were no new safety signals that we did not see in the randomized controlled portion of the trial.
When we see patients with psoriatic arthritis who come into the clinic, many of them have not been on the disease-modifying drugs. So the question comes up, what do you see and what impact do drugs like apremilast have on patients who are DMARD-naïve?
Apremilast is a PDE4 inhibitor. It shuts down an enzyme. By doing that, you see some downstream effects. It blocks a number of different cytokines. But here’s the caveat: It blocks a number of different cytokines, but it doesn’t shut them off completely. I tell people this is like turning off a light switch. It essentially dims the light switch, allowing the body’s normal immune system to control the disease.
Indeed, we saw that patients treated with apremilast have 2 times more efficacy compared with other drugs, such as methotrexate and others. In patients who are DMARD-naïve, apremilast gave a better response. In patients who had failed DMARDs like methotrexate, apremilast—a PDE4 inhibitor—does significantly improve active psoriatic arthritis.
As a rheumatologist, it’s exciting to see all the treatment options on the horizon. At this year’s ACR Convergence meeting, some of the new things that are coming out were highlighted. We know that anti–TNF [tumor necrosis factor] drugs are really great. But now we’re beginning to see the impact that biosimilars are going to make. I’m excited about them. We might have some agents that will be less expensive for our patients, meaning wider use and more access. That’s 1 thing that’s exciting. There is a lot of experience coming from my European colleagues, as presented at the meeting last year.
We talk about inhibiting IL-17A. Remember, in the IL-17 family there are a number of cytokines—IL-17A, IL-17B, IL-17C, IL-17D, IL-17E, and IL-17F. Bimekizumab blocks IL-17A and IL-17F. Based on the data that we saw at the ACR Convergence this year, it looks like the combination of blocking IL-17A and IL-17F is going to give you a better clinical impact. So more improvement in the skin, more improvement in the joints in patients with psoriatic arthritis. We still need to see some of the long-term safety data, but this is very exciting to share.
As I came away from the meeting last year, I came back to my office and was really excited. Upon talking to my 2 physician assistants and my nurses, I shared the data and my excitement of the data with them. For patients who have chronic rheumatic disorders, including psoriatic arthritis, it’s exciting to be able to see these new treatment options, which are very close on the horizon and might have an impact on our patients who have active disease.
Transcript Edited for Clarity