Chugai’s Enspryng (Satralizumab) Approved by European Commission as First At-home Subcutaneous Treatment for Neuromyelitis Optica Spectrum Disorder (NMOSD)
- Enspryng is a new treatment approved for both adults and adolescents with AQP4-IgG seropositive NMOSD in the EU. It is the first treatment approved in the EU for adolescents from 12 years of age with NMOSD.
- Enspryng is the first approved medicine applying Chugai’s proprietary recycling antibody technology. It can be self-administered* subcutaneously at home every four weeks**
- Enspryng significantly reduced risk of relapse in people with AQP4-IgG seropositive NMOSD in two global phase III studies.
The medicine has been approved in 54 countries including
Japan, the United Statesand the EU.
“We are very pleased that Enspryng is now approved in the EU as the first subcutaneous treatment for people with AQP4-IgG seropositive NMOSD, with the option to be treated at home,” said Chugai’s President and CEO, Dr.
The efficacy and safety of Enspryng has been evaluated in large clinical trials representative of the real-world population of people with NMOSD, including those who have only experienced a single NMOSD attack and adolescents. The approval by the
Enspryng is designed to prevent NMOSD relapses by inhibiting IL-6 signal signaling, which is a key driver in NMOSD. Enspryng is currently approved in 54 countries including
The impact on the consolidated financials for the fiscal year ending
*Self-administration is not covered in
**Subcutaneous administration at 2-week intervals up to the fourth week of treatment and at 4-week intervals thereafter
New Data of Chugai’s Enspryng (Satralizumab) on Risk and Severity of Relapse in Neuromyelitis Optica Spectrum Disorder (NMOSD) (
Results from Phase III SAkuraSky Study for Chugai’s Satralizumab in Neuromyelitis Optica Spectrum Disorder Published in
The New England Journal of Medicine Online( November 29, 2019)
Positive Results from the Second Phase III SAkuraStar Study for Chugai’s Satralizumab in Neuromyelitis Optica Spectrum Disorder (NMOSD) Published in The Lancet Neurology (
April 24, 2020)
About neuromyelitis optica spectrum disorder (NMOSD)1
NMOSD is an autoimmune disease of the central nervous system characterized by inflammatory lesions in the optic nerves and spinal cord, and causes a continual and 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 2-5. The inflammatory cytokine IL-6 is now emerging as an important factor in NMOSD pathogenesis 6-10.
Trademarks used or mentioned in this release are protected by law.
1. Neuromyelitis optica spectrum disorder (NMOSD) Online. https://nmosd-online.jp/ Accessed
2. 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.
4. 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.
5. 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.
6. Chihara N, Aranami T, Sato W et al. Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica.
7. Kimura A, Kishimoto T. IL-6: regulator of Treg/Th17 balance. Eur J Immunol 2010;40:1830-5.
8. Lin J, Li X, Xia J. Th17 cells in neuromyelitis optica spectrum disorder: a review. Int J Neurosci2016;126:1051-60.
9. 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.
10. Obermeier B, Daneman R, Ransohoff RM. Development, maintenance and disruption of the blood-brain barrier. Nat Med 2013;19:1584-96.
For US media
For European media
For Taiwanese media