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ACTRIMS 2022 | cosMOG: anti-FcRn agent rozanolixizumab for relapse prevention in MOGAD

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a neuroinflammatory, demyelinating disorder, characterized by pathogenic autoantibodies against MOG, a molecule found on the outer membrane of myelin sheaths. While no treatments are currently approved for the prevention of inflammatory attacks in MOGAD, several retrospective studies have indicated that antibody depleting agents may be able to reduce attack occurrence. Rozanolixizumab is one such promising agent, which blocks the neonatal Fc receptor (FcRn) to reduce the concentration of circulating IgG antibodies. Michael Levy, MD, PhD, Massachusetts General Hospital and Harvard Medical School, Boston, MA, talks on rozanolixizumab and introduces the recently launched cosMOG study (NCT05063162). The randomized, placebo-controlled, Phase III trial aims to enroll more than 100 patients with relapsing MOGAD to assess the ability of rozanolixizumab to prevent relapses. This interview took place at the ACTRIMS Forum 2022 in West Palm Beach, Florida.

Transcript (edited for clarity)

Rozanolixizumab is the name of the drug. It’s an FcRn drug that blocks the activity of the FcRn molecule, which would normally preserve antibodies in the bloodstream from being recycled. By blocking the antibody recycling pathway, the antibodies get degraded quickly, sort of like if you think about how plasma exchange works in removing antibodies in other antibody-mediated diseases.

It works essentially the same way as plasma exchange, and IVIG also has that same sort of mechanism in diluting autoantibodies, except this is more of degrading the autoantibodies...

Rozanolixizumab is the name of the drug. It’s an FcRn drug that blocks the activity of the FcRn molecule, which would normally preserve antibodies in the bloodstream from being recycled. By blocking the antibody recycling pathway, the antibodies get degraded quickly, sort of like if you think about how plasma exchange works in removing antibodies in other antibody-mediated diseases.

It works essentially the same way as plasma exchange, and IVIG also has that same sort of mechanism in diluting autoantibodies, except this is more of degrading the autoantibodies. So any disease in which IVIG and plasma exchange are helpful, we think this drug would be useful for. It’s being developed for myasthenia gravis and Guillain-Barré, for example, and we think since MOG is responsive to IVIG and plasma exchange, that it would be useful as well.

So the trial is launching. It just launched. We recruited our first patient in Japan. We hope to open 50 sites in 20 countries and recruit over 100 patients to this study. And the primary outcome is to prevent relapses in MOG. The duration will be about three and a half years total, and we’re hoping that by 2025 or so, we’ll have a readout.

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Disclosures

Dr Levy reports the following disclosures:
Consulting for UCB, Sanofi, Genentech, Alexion, and Horizon