Chugai News Releases are issued to provide stakeholders with the most up-to-date information related to our company. In some instances, information on products or drug candidates under development may be included, but this is intended for members of the media, shareholders, and investors. The information is not intended for promotional or advertising purposes, or as medical advice, etc.

Oct 02, 2023

  • Pharmaceuticals
  • R&D

Chugai’s Enspryng Launched in Taiwan as First Indication for Neuromyelitis Optica Spectrum Disorder (NMOSD)

TOKYO, October 2, 2023 -- Chugai Pharmaceutical Co., Ltd. (TOKYO: 4519) announced that Chugai Pharma Taiwan Ltd., a wholly-owned subsidiary of Chugai, has launched Enspryng®, a drug created by Chugai on October 1 for “the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult and adolescent over 12 years old patients who are anti-aquaporin-4 (AQP4) antibody positive” as the first indication in Taiwan. Enspryng was designated as an orphan drug Ministry of Health and Welfare (MoHW) on September 14, 2022 and approved orphan drug license by Taiwan Food and Drug Administration (TFDA) on July 28, 2023.

<Reference>
Chugai’s Enspryng Approved in Taiwan as First Approved Medicine for Neuromyelitis Optica Spectrum Disorder (NMOSD) (Press release issued on December 9, 2020)
https://www.chugai-pharm.co.jp/english/news/detail/20201209170000_784.html

About Enspryng
Enspryng, designed by Chugai, a member of Roche group, is a pH-dependent binding humanized anti-IL-6 receptor antibody, which was the first product developed by applying our proprietary recycling antibody® technology. The drug is designed to prevent relapse of neuromyelitis optica spectrum disorder (NMOSD) by inhibiting the cytokine IL-6 which is a key driver in NMOSD. Enspryng has been approved for the treatment of NMOSD in more than 85 countries including Japan, the U.S. the EU.

About neuromyelitis optica spectrum disorder (NMOSD)
NMOSD is an autoimmune disease of the central nervous system characterized by inflammatory lesions in the optic nerves and spinal cord, and causes a significant decrease in quality of life due to permanent neurological disability. Patients with NMOSD frequently experience a relapsing disease course with repeated attacks leading to accumulating neurological damage and disability. Symptoms may include visual impairment, motor disability, pain leading to decreased quality of life. In some cases, attacks of NMOSD result in death. Aquaporin-4 antibodies (AQP4-IgG), pathogenic antibodies, are detected in around 70-80% of NMOSD people. AQP4-IgG is known to target and damage a specific central nervous cell type called astrocytes, resulting in inflammatory demyelinating lesions of the optic nerve(s), spinal cord and brain.1-4 The inflammatory cytokine IL-6 is now emerging as an important factor in NMOSD pathogenesis.5-9 Diagnostic criteria introduced in 2006 for NMO were characterized by inflammation of the optic nerve (optic neuritis) and the spinal cord (myelitis). These were revised in 2007 with the definition of NMOSD, proposed for diseases with either optic neuritis or myelitis. In 2015, the definition of NMOSD further revised to include a broader spectrum of diseases. The diagnostic term NMOSD is now accepted.10

Trademarks used or mentioned in this release are protected by law.

Sources

  1. Jarius S, Ruprecht K, Wildemann B et al. Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients. J Neuroinflammation 2012;9:14.
  2. Lennon VA, Wingerchuk DM, Kryzer TJ et al. A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis. Lancet 2004;364:2106-12.
  3. Marignier R, Bernard-Valnet R, Giraudon P et al. Aquaporin-4 antibody-negative neuromyelitis optica: Distinct assay sensitivity-dependent entity. Neurology 2013;80:2194-200.
  4. Takahashi T, Fujihara K, Nakashima I et al. Anti-aquaporin-4 antibody is involved in the pathogenesis of NMO: a study on antibody titre. Brain 2007;130:1235-43.
  5. Chihara N, Aranami T, Sato W et al. Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica. Proc Natl Acad Sci USA 2011;108:3701-6.
  6. Kimura A, Kishimoto T. IL-6: regulator of Treg/Th17 balance. Eur J Immunol 2010;40:1830-5.
  7. Lin J, Li X, Xia J. Th17 cells in neuromyelitis optica spectrum disorder: a review. Int J Neurosci2016;126:1051-60.
  8. Takeshita Y, Obermeier B, Cotleur AC, et al. Effects of neuromyelitis optica-IgG at the blood-brain barrier in vitro. Neurol Neuroimmunol Neuroinflamm. 2016;4(1):e311.
  9. Obermeier B, Daneman R, Ransohoff RM. Development, maintenance and disruption of the blood-brain barrier. Nat Med 2013;19:1584-96.
  10. Wingerchuk DM, Banwell B, Bennett JL et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology 2015;85:177-89.

Contact:

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  • Chugai Pharmaceutical Co., Ltd.
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  • Hideki Sato
  • Tel: +81-3-3273-0881
  • E-mail: pr@chugai-pharm.co.jp
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