To review the pharmacological characteristics, clinical evidence, and place in therapy of satralizumab for the treatment of neuromyelitis optica spectrum disorders (NMOSDs).
Data Sources
A comprehensive literature search was conducted in PubMed (January 2000 to October 15, 2020). Key search terms included satralizumab and neuromyelitis optica spectrum disorders. Other sources were derived from product labeling and ClinicalTrials.gov.
Study Selection and Data Extraction
All English-language articles identified from the data sources were reviewed and evaluated. Phase I, II, and III clinical trials were included.
Data Synthesis
NMOSD is an autoimmune disease characterized by inflammatory lesions in the optic nerves and spinal cord. Interleukin-6 is involved in the pathogenesis of the disorder. Satralizumab is a humanized monoclonal antibody targeting the interleukin-6 receptor. Phase III trials showed that protocol-defined relapse was 30% for satralizumab and 50% for placebo (P = 0.018) when patients with NMOSD were treated with satralizumab monotherapy; protocol-defined relapse was 20% for satralizumab and 43% for placebo (P = 0.02) when satralizumab was added to immunosuppressant treatment. Satralizumab is generally well tolerated, with common adverse effects including injection-related reaction.
Relevance to Patient Care and Clinical Practice
Satralizumab has the potential to become a valuable treatment option for patients with NMOSD.
Conclusion
Satralizumab appears to be safe and effective as monotherapy or in combination with an immunosuppressant for patients with NMOSD and has the potential to become a valuable treatment option for these patients.
WingerchukDMBanwellBBennettJL, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology. 2015;85:177-189. doi:10.1212/WNL.0000000000001729
4.
FangCWWangHPChenHMLinJWLinWS. Epidemiology and comorbidities of adult multiple sclerosis and neuromyelitis optica in Taiwan, 2001-2015. Mult Scler Relat Disord. 2020;45:102425. doi:10.1016/j.msard.2020.102425
SchmidtFZimmermannHMikolajczakJ, et al. Severe structural and functional visual system damage leads to profound loss of vision-related quality of life in patients with neuromyelitis optica spectrum disorders. Mult Scler Relat Disord. 2017;11:45-50. doi:10.1016/j.msard.2016.11.008
7.
AkaishiTNakashimaIMisuTFujiharaKAokiM. Depressive state and chronic fatigue in multiple sclerosis and neuromyelitis optica. J Neuroimmunol. 2015;283:70-73. doi:10.1016/j.jneuroim.2015.05.007
JeongIHParkBKimSHHyunJWJooJKimHJ. Comparative analysis of treatment outcomes in patients with neuromyelitis optica spectrum disorder using multifaceted endpoints. Mult Scler. 2016;22:329-339. doi:10.1177/1352458515587752
10.
CollonguesNAyme-DietrichEMonassierLde SezeJ. Pharmacotherapy for neuromyelitis optica spectrum disorders: current management and future options. Drugs. 2019; 79:125-142. doi:10.1007/s40265-018-1039-7
11.
IçözSTüzünEKürtüncüM, et al. Enhanced IL-6 production in aquaporin-4 antibody positive neuromyelitis optica patients. Int J Neurosci. 2010;120:71-75. doi:10.3109/00207450903428970
Chugai Pharmaceutical Co, Ltd. Chugai receives orphan drug designation for satralizumab in neuromyelitis optica and neuromyelitis optica spectrum disorder from the Ministry of Health, Labour and Welfare. Published September 13, 2019. Accessed October 20, 2020. https://www.chugai-pharm.co.jp/english/news/detail/20190913140000_646.html
HudaSWhittamDBhojakMChamberlainJNoonanCJacobA. Neuromyelitis optica spectrum disorders. Clin Med (Lond). 2019;19:169-176. doi:10.7861/clinmedicine.19-2-169
16.
Do RegoCACollonguesN. Neuromyelitis optica spectrum disorders: features of aquaporin-4, myelin oligodendrocyte glycoprotein and double-seronegative-mediated subtypes. Rev Neurol (Paris). 2018;174:458-470. doi:10.1016/j.neurol.2018.02.084
17.
Ikeshima-KataokaH. Neuroimmunological implications of AQP4 in astrocytes. Int J Mol Sci. 2016;17:1306. doi:10.3390/ijms17081306
18.
TakeshitaYObermeierBCotleurAC, et al. Effects of neuromyelitis optica-IgG at the blood-brain barrier in vitro. Neurol Neuroimmunol Neuroinflamm. 2016;4:e311. doi:10.1212/NXI.0000000000000311
Cobo-CalvoARuizARichardC, et al. Purified IgG from aquaporin-4 neuromyelitis optica spectrum disorder patients alters blood-brain barrier permeability. PLoS One. 2020;15:e0238301. doi:10.1371/journal.pone.0238301
21.
BradlMReindlMLassmannH. Mechanisms for lesion localization in neuromyelitis optica spectrum disorders. Curr Opin Neurol. 2018;31:325-333. doi:10.1097/WCO.0000000000000551
22.
FujiharaKBennettJLde SezeJ, et al. Interleukin-6 in neuromyelitis optica spectrum disorder pathophysiology. Neurol Neuroimmunol Neuroinflamm. 2020;7:e841. doi:10.1212/NXI.0000000000000841
23.
ArakiM. Blockade of IL-6 signaling in neuromyelitis optica. Neurochem Int. 2019;130:104315. doi:10.1016/j.neuint.2018.10.012
24.
DuLChangHXuW, et al. Effect of NMO-IgG on the interleukin-6 cascade in astrocytes via activation of the JAK/STAT3 signaling pathway. Life Sci. 2020;258:118217. doi:10.1016/j.lfs.2020.118217
25.
Rose-JohnS. IL-6 trans-signaling via the soluble IL-6 receptor: importance for the pro-inflammatory activities of IL-6. Int J Biol Sci. 2012;8:1237-1247. doi:10.7150/ijbs.4989
26.
ChiharaNAranamiTSatoW, et al. Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica. Proc Natl Acad Sci U S A. 2011;108:3701-3706. doi:10.1073/pnas.1017385108
27.
LinJLiXXiaJ. Th17 cells in neuromyelitis optica spectrum disorder: a review. Int J Neurosci. 2016;126:1051-1060. doi:10.3109/00207454.2016.1163550
28.
XueTYangYLuQGaoBChenZWangZ. Efficacy and safety of monoclonal antibody therapy in neuromyelitis optica spectrum disorders: evidence from randomized controlled trials. Mult Scler Relat Disord. 2020;43:102166. doi:10.1016/j.msard.2020.102166
29.
RossoMSaxenaSChitnisT. Targeting IL-6 receptor in the treatment of neuromyelitis optica spectrum: a review of emerging treatment options. Expert Rev Neurother. 2020;20: 509-516. doi:10.1080/14737175.2020.1757434
30.
HeoYA. Satralizumab: first approval. Drugs. 2020;80:1477-1482. doi:10.1007/s40265-020-01380-2
31.
TraboulseeAGreenbergBMBennettJL, et al. Safety and efficacy of satralizumab monotherapy in neuromyelitis optica spectrum disorder: a randomised, double-blind, multicentre, placebo-controlled phase 3 trial. Lancet Neurol. 2020;19:402-412. doi:10.1016/S1474-4422(20)30078-8
32.
YamamuraTKleiterIFujiharaK, et al. Trial of satralizumab in neuromyelitis optica spectrum disorder. N Engl J Med. 2019;381:2114-2124. doi:10.1056/NEJMoa1901747
33.
BruscoliniASacchettiMLa CavaM, et al. Diagnosis and management of neuromyelitis optica spectrum disorders—an update. Autoimmun Rev. 2018;17:195-200. doi:10.1016/j.autrev.2018.01.001
34.
CaiMTZhengYShenCH, et al. Evaluation of brain and spinal cord lesion distribution criteria at disease onset in distinguishing NMOSD from MS and MOG antibody-associated disorder. Mult Scler. 2020;27(6):871-882. doi:10.1177/1352458520939008
35.
UzawaAMoriMAraiK, et al. Cytokine and chemokine profiles in neuromyelitis optica: significance of interleukin-6. Mult Scler. 2010;16:1443-1452. doi:10.1177/1352458510379247
36.
O’ConnellKHamilton-ShieldAWoodhallM, et al. Prevalence and incidence of neuromyelitis optica spectrum disorder, aquaporin-4 antibody-positive NMOSD and MOG antibody-positive disease in Oxfordshire, UK. J Neurol Neurosurg Psychiatry. 2020;91:1126-1128. doi:10.1136/jnnp-2020-323158
37.
TrebstCJariusSBertheleA, et al. Update on the diagnosis and treatment of neuromyelitis optica: recommendations of the Neuromyelitis Optica Study Group (NEMOS). J Neurol. 2014;261:1-16. doi:10.1007/s00415-013-7169-7
38.
BorisowNMoriMKuwabaraSScheelMPaulF. Diagnosis and treatment of NMO spectrum disorder and MOG-encephalomyelitis. Front Neurol. 2018;9:888. doi:10.3389/fneur.2018.00888
39.
UzawaAMoriMSawaiS, et al. Cerebrospinal fluid interleukin-6 and glial fibrillary acidic protein levels are increased during initial neuromyelitis optica attacks. Clin Chim Acta. 2013;421:181-183. doi:10.1016/j.cca.2013.03.020
40.
UchidaTMoriMUzawaA, et al. Increased cerebrospinal fluid metalloproteinase-2 and interleukin-6 are associated with albumin quotient in neuromyelitis optica: their possible role on blood-brain barrier disruption. Mult Scler. 2017;23: 1072-1084. doi:10.1177/1352458516672015
41.
WuYZhongLGengJ. Neuromyelitis optica spectrum disorder: pathogenesis, treatment, and experimental models. Mult Scler Relat Disord. 2019;27:412-418. doi:10.1016/j.msard.2018.12.002
