New Analysis of MRI Findings Show UPLIZNA (inebilizumab-cdon) Reduced the Formation of Asymptomatic Optic Nerve Lesions in People With Neuromyelitis Optica Spectrum Disorder (NMOSD) - Seite 2

The MRI findings showed that a high proportion of participants experienced subclinical optic nerve findings without new symptoms at the end of the RCP. These were shorter (median length 6 mm) than in those with an optic nerve attack (15 mm, p<0.001) and were not found to be associated with future attacks. Importantly, while the total subclinical findings in the optic nerve were not reduced during the RCP, the number of clinical optic neuritis attacks was significantly reduced during this time period. Moreover, the formation of these subclinical findings was reduced with repeated UPLIZNA treatment over the course of the OLP.

“The use of MRI in the Phase 3 clinical trial has enabled us to better quantify not only the most visible effects of NMOSD attacks, but also changes in disease patterns at the subclinical level that may compound over time,” said Kristina Patterson, M.D., PhD, medical director, neuroimmunology, Horizon. “These data help deepen our understanding of the real biological impact of this medicine not just on the attacks, but also on asymptomatic activity, further reinforcing the robust clinical profile of UPLIZNA in controlling the effects of this challenging disease and supporting long-term patient care.”

About Neuromyelitis Optica Spectrum Disorder (NMOSD)

NMOSD is a unifying term for neuromyelitis optica (NMO) and related syndromes. NMOSD is a rare, severe, relapsing, neuroinflammatory autoimmune disease that attacks the optic nerve, spinal cord, brain and brainstem.^1-2 Approximately 80% of all patients with NMOSD test positive for anti-AQP4 antibodies.³ AQP4-IgG binds primarily to astrocytes in the central nervous system and triggers an escalating immune response that results in lesion formation and astrocyte death.⁴

Anti-AQP4 autoantibodies are produced by plasmablasts and plasma cells. These B-cell populations are central to NMOSD disease pathogenesis, and a large proportion of these cells express CD19.⁵ Depletion of these CD19+ B cells is thought to remove an important contributor to inflammation, lesion formation and astrocyte damage. Clinically, this damage presents as an NMOSD attack, which can involve the optic nerve, spinal cord, brain and brainstem.^4-6 Loss of vision, paralysis, loss of sensation, bladder and bowel dysfunction, nerve pain and respiratory failure can all be manifestations of the disease.⁷ Each NMOSD attack can lead to further cumulative damage and disability.^8-9 NMOSD occurs more commonly in women and may be more common in individuals of African and Asian descent.^10-11