Phase 3 METEROID Insights: Satralizumab Positions Itself as Potential First Approved Therapy for MOGAD

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) remains a challenging neuroinflammatory condition to manage, with no FDA-approved therapies and a heavy reliance on off-label immunosuppressive treatments. Despite increasing recognition as a distinct disease entity over the past decade, therapeutic development has lagged, leaving clinicians to navigate variable responses, access barriers, and uncertainty in long-term disease control.

At the recently concluded 2026 American Academy of Neurology (AAN) Annual Meeting, investigators presented positive data from the phase 3 METEOROID trial (NCT05271409) testing satralizumab, a previously approved therapy for neuromyelitis optica spectrum disorder (NMOSD), in patients with MOGAD. All told, data showed that treatment with the interleukin-6 receptor inhibitor met its primary end point with a 68% reduction in relapse risk compared with placebo.

The randomized, double-blind, placebo-controlled study enrolled adolescents and adults with MOGAD, showing that 87% of treated patients remained relapse-free at 48 weeks versus 67% on placebo, with treatment effects emerging as early as 8 weeks. Additional findings included reductions in annualized relapse rate, MRI lesion activity, and rescue therapy use, with a safety profile consistent with prior experience in NMOSD.

Michael Levy, MD, PhD, associate professor at Harvard Medical School and Massachusetts General Hospital, presented the data at the meeting and spoke with NeurologyLive® about the origins of the trial, key efficacy and safety findings, and what a potential approval could mean for patients with MOGAD, as well as remaining clinical and research questions in this evolving disease space.

NeurologyLive: Why was satralizumab explored in a population of MOGAD?

Michael Levy, MD, PhD: This drug has an older version called tocilizumab, which is twice a month, approved for rheumatoid arthritis and some vasculitic conditions, and the new version, satralizumab, was approved for neuromyelitis optica spectrum disorder. We’ve been using this drug in many of those diseases for quite some time now.

MOG wasn’t really defined until 2017, when the antibody became available in the United States—2015 in Europe. And as it evolved, I should say, prior to it being defined, it was just called seronegative neuromyelitis optica spectrum disorder. We were using IL-6 therapy in those cases, some of which would work, some of which did not.

When the antibody test became available, we started distinguishing MOG from those other patients. We realized the ones who responded were generally the MOG-seropositive ones. We put together a short series—14 patients, that’s it, 14 cases—some using IV, some using subcutaneous, but all very responsive to tocilizumab.

We submitted that to the folks at Roche. The Roche group looked at it and said, now is the time to jump in, because there are other companies considering it, and once you have one pivotal study, it’s hard to enter a market in the rare disease space. They said, all right, let’s do it. And that’s how it evolved.

Can you give some background on the trial design and walk us through the efficacy findings?

Okay, so the trial is placebo controlled. Patients were randomized 50/50, either into placebo—a monthly shot of saline—or a monthly dose of the medication, and it is weight-based. Smaller people get smaller doses, bigger people get bigger doses, and it’s monthly injections.

All we were tracking for efficacy was the first event, the first true relapse. People have symptoms all the time—we didn’t take every symptom as a true relapse. They had to meet a certain set of criteria. It was adjudicated by a committee, and only if the committee said, yes, this is a true relapse, confirmed by MRI, were they then bumped into an open-label phase.

What I presented today was just the double-blinded period, where we saw 68 patients in the satralizumab arm versus 64 in the placebo arm. Twenty-four of the 64 in the placebo group relapsed over the course of two years, and only nine in the satralizumab arm—nine out of 68—relapsed.

The reduction in risk of relapse is 68%, statistically. So, these were very positive results. The curves diverged very early on. Within about eight weeks, we saw the drug take effect, so it’s rapid onset, and it’s very effective.

What did the safety data show? Any concerns?

We’ve been using satralizumab for NMOSD for about six years. We knew what to expect. We did not see any new safety signals. In fact, all of the safety data essentially mirror the NMOSD trials back in 2020 that were published.

Interestingly, there were a lot of adverse events in the placebo arm, as there often are, and there were no meaningful differences between the satralizumab arm in MOGAD and the placebo arm. There were a few serious adverse events, a few more in the satralizumab arm. None were attributed to satralizumab itself.

There was one death. The patient was mine. He had a malignant melanoma that nobody recognized, and within just a couple of months into the study, he got the diagnosis and passed away. It was very rapid disease progression, which also had nothing to do with the satralizumab.

Safety-wise, no new safety signals. Tolerability-wise, we saw a few injection site reactions. We see that in the NMOSD space—they tend to be fairly mild, they go away. It’s a monthly injection, so it goes away within a few days. Compared to placebo, it was just a few more cases. So overall, no major safety concerns.

What would this therapy bring to the MOGAD landscape if approved?

We use a lot of off-label therapy in MOGAD, but much of it is expensive, and trying to get coverage for these off-label therapies for our MOGAD patients has been a true struggle. This is true across the board, in many different countries. There are some less expensive alternatives, which haven’t been very validated at all.

This would be the first proven therapy—scientifically proven, hopefully FDA approved—that would essentially prevent relapses in our MOGAD population.

Now, there’s a lot of work to do still. We did not include patients with monophasic disease. So if you have your first optic neuritis, you test positive for MOG, you come to my clinic and say, I want satralizumab—technically, we didn’t include those patients yet. We don’t know if those patients are even going to have relapsing disease, and we don’t know if they would respond well to satralizumab. We need to evaluate that population.

What other unanswered questions remain?

Kids under 12 make up about 25% of the MOGAD population. We couldn’t include them in this study because we didn’t have pharmacokinetic data for the FDA at the time. Now we have some from the NMOSD world, and we’re going to be doing a separate study in kids under 11. Obviously, smaller body masses will have a smaller dose, and we’ll be able to evaluate them in a separate study.

What lessons did we learn from this trial for future studies?

First of all, MOGAD is a rare disease. Recruitment was fairly challenging. A lot of MOGAD patients do fairly well after their first event. Only about half will relapse, and then a substantial proportion lose their MOG antibody over time. So, they may have relapsing disease but not test positive anymore. Those patients were excluded initially, and we made revisions halfway through to include them back in.

We’ve learned a lot about how to do trials in MOG. As I said, in the rare disease space, once you have something approved, it’s really challenging to get something new approved, because the FDA won’t let you test it against placebo. You’re going to have to do head-to-head trials, and that means more patients, more time, and a lot more money. So I’m not sure how many more phase 3 trials we’re going to have in MOG.

Are there other therapies that could be explored in MOGAD?

Yes, we have four approved in NMOSD. Two are complement therapies, and we’re not quite sure of the role of complement in MOG. We haven’t adequately tested it, either off-label or in a scientific study, so we don’t know if complement therapy would be effective.

The other approved approach in NMOSD is B-cell therapy. We’ve talked to that company several times. They’ve thought about it and might be a little late now, but it could be an approach. CD19 targeting is different from CD20. CD20 depletion therapy with rituximab is not quite as effective—it’s about 50/50.

But in the inebilizumab trial in NMOSD, they accidentally enrolled seven MOGAD patients, and they did well. So, there’s a little bit of data there. We’re thinking maybe they could be treated with inebilizumab, but the company hasn’t decided yet whether to pursue it.

Transcript was edited for clarity. Click here for more AAN 2026 coverage.

REFERENCES
1. Levy M, et al. Safety and Efficacy of Satralizumab in Patients with Relapsing Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease (MOGAD): Results from the Phase 3 METEOROID Trial. Presented at: 2026 AAN Annual Meeting; April 18-22; Chicago, Illinois.
2. Genentech’s Enspryng (Satralizumab) Reduces Risk of Relapses by 68% Demonstrating Potential to Become First Treatment for MOGAD. News release. Genentech. April 21, 2026. Accessed April 21, 2026. https://www.gene.com/media/press-releases/15108/2026-04-21/genentechs-enspryng-satralizumab-reduces