Inebilizumab as a Potential Therapy for Autoimmune Encephalitis: Gregory Day, MD, MSc, MSCI, FAAN

Video

The neurologist at Mayo Clinic in Jacksonville Florida talked about the significance of the ExTINGUISH trial, regarding care for patients with autoimmune encephalitis. [WATCH TIME: 4 minutes]

WATCH TIME: 4 minutes

“We've known about antiNMDA receptor encephalitis for the last 15 years now and continuing to see more and more cases. But up until the launch of this trial, we haven't had any clinical trials that have really been focused narrowly and specifically on patients with this disease.”

Recently, there have been substantial variability in approved treatments for N-methyl-D-aspartate receptor (NMDAR) encephalitis.1 One potential therapy for patients with NMDAR encephalitis is inebilizumab (Uplizna, Horizon), a humanized anti-CD19 monoclonal antibody previously approved for neuromyelitis optica spectrum disorder.

The phase 2 ExTINGUISH trial (NCT04372615), will assess safety and efficacy in 300 mg doses of inebilizumab (as a therapy for moderate-to-severe NMDAR encephalitis.1 One-hundred and twenty patients are to be enrolled from 22 sites (United States, n = 20; Europe, n = 2), and patients will receive standard “first-line” immunotherapies prior to being randomized. If patients fail to responding to the initial treatment after 6 weeks, cyclophosphamide IV rescue therapy will then be given to them.

Lead investigator of the trial, Gregory Day, MD, MSc, MSCI, FAAN, sat down in a recent interview with NeurologyLive®to talk more about trial, as well as the current state of care for autoimmune encephalitis. Day, a neurologist at Mayo Clinic in Jacksonville Florida, also talked about the current available treatments for patients with the disease along with inebilizumab’s potential as a therapy.

REFERENCES
1. Day G, Titulaer M, Wong KH, et al. The ExTINGUISH Trial: A Phase-2B Randomized Placebo-Controlled Trial of Inebilizumab in Anti-NMDA Receptor Encephalitis (P5-1.004). Neurology. Published May 2022, 98 (18 Supplement) 1651.
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