For Patients & Caregivers

ENSPRYNG modulates the immune response by blocking the IL-6 receptor to treat NMOSD3,7-9

ENSPRYNG is the first and only FDA-approved anti-IL-6 receptor monoclonal antibody for NMOSD3,23,40

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IL-6 and NMOSD
ENSPRYNG MOA

Elevated IL-6 levels may be indicative of NMOSD relapse41

Relationship between serum IL-6 levels and NMOSD relapses*
Due to its role in NMOSD, IL-6 is an important therapeutic target13,23-25

*IL-6 levels were assessed at baseline in patients with neuromyelitis optica (NMO) (n=20) who were in clinical remission and not receiving maintenance treatment. After a 2-year follow-up period, patients were stratified by those without clinical relapse (“NO Relapses”; n=9) and those who had at least 1 relapse (“Relapsed”; n=11). Baseline IL-6 levels were compared between NMO groups and healthy controls (n=20).41

Four functions of IL-6 are implicated in NMOSD progression13,23

1. AQP4-lgG production13,23

IL-6 stimulates the differentiation of B cells to plasmablasts, which secrete AQP4-lgG

2. Th17 cell differentiation13,24,25

IL-6 promotes differentiation into inflammatory Th17 cells, which provide support to AQP4-producing plasmablasts

3. BBB permeability13,23-25

IL-6 increases BBB permeability, allowing penetration of AQP4 antibodies and proinflammatory cells into the central nervous system

4. Astrocyte injury and neuronal loss13,23-25

Once in the brain, AQP4 antibodies bind with AQP4 channels on astrocytes, leading to astrocyte injury via the complement cascade and ultimately leading to demyelination and neuronal loss

1. AQP4-lgG production13,23

IL-6 stimulates the differentiation of B cells to plasmablasts, which secrete AQP4-lgG

2. Th17 cell differentiation13,24,25

IL-6 promotes differentiation into inflammatory Th17 cells, which provide support to AQP4-producing plasmablasts

3. BBB permeability13,23-25

IL-6 increases BBB permeability, allowing penetration of AQP4 antibodies and proinflammatory cells into the central nervous system

4. Astrocyte injury and neuronal loss13,23-25

Once in the brain, AQP4 antibodies bind with AQP4 channels on astrocytes, leading to astrocyte injury via the complement cascade and ultimately leading to demyelination and neuronal loss

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IL-6 in NMOSD Brochure

Review the importance of IL-6 in NMOSD in this quick reference resource

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ENSPRYNG modulates the immune response by blocking the IL-6 receptor to treat NMOSD3,7-9

In doing so, ENSPRYNG does not directly affect the innate immune system in the same way that broader ISTs do

ENSPRYNG blocks IL-6 signaling3

While the precise mechanism by which ENSPRYNG exerts therapeutic effects in NMOSD is unknown, it is presumed to involve inhibition of IL-6-mediated signaling via binding to membrane-bound and soluble IL-6 receptors. 

By inhibiting IL-6 signaling, ENSPRYNG is thought to help decrease3,13,23,42:

  • IL-6-mediated autoimmune T- and B-cell activation
  • Differentiation of B cells into AQP4-IgG-secreting plasmablasts

In turn, this targets inflammation, blood-brain barrier permeability, and astrocyte injury—all key drivers of NMOSD.3,13,23-25

Antibody recycling technology23

ENSPRYNG was designed using antibody recycling technology, which allows it to be recycled back into the bloodstream to bind more antigen, prolonging half-life and enabling sustained suppression of IL-6 signaling.

ENSPRYNG is the first and only treatment for AQP4-IgG(+) NMOSD that blocks IL-6 signaling3,6

ENSPRYNG Mechanism of Action

Watch the video to see how IL-6 plays a role in disease development and treatment

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ENSPRYNG mechanism of action

Targeting IL-6 with ENSPRYNG as a treatment for aquaporin-4 (AQP4) immunoglobulin, or IgG antibody positive NMOSD patients1

Neuromyelitis optica spectrum disorder, or NMOSD, is a chronic, severely debilitating autoimmune disease of the central nervous system that primarily damages the optic nerves and spinal cord2-7

People with NMOSD experience unpredictable, severe, and recurrent relapses from which they may not fully recover2-9

Relapses cause cumulative, irreversible neurological damage, and even a single episode can lead to blindness, paralysis, or death2-9

NMOSD is often associated with a pathogenic serum IgG antibody against the water channel AQP4 protein found in the central nervous system4

AQP4-IgG antibody is highly specific and found in up to 80% of NMOSD patients’ serum. Prior to 2019, there was no FDA-approved treatment for NMOSD4

Recent research has led to a better understanding of the pathogenesis of NMOSD, including the pivotal role IL-6 plays in driving the inflammatory response2,10

The autoimmune cascade is active in the periphery, where IL-6 promotes T-cell-mediated inflammation by promoting the maturation of T cells into Th17 cells. IL-6 stimulates the differentiation of B cells to plasmablasts, promotes their survival, and enhances AQP4-IgG antibody secretion2,10-12

In addition, IL-6 increases blood-brain barrier permeability, allowing penetration of AQP4-IgG antibodies and proinflammatory cells into the central nervous system2,10-12

This leads to even more IL-6 production by astrocytes and further damage2,10-12

Once in the brain, AQP4-IgG antibodies bind with AQP4 channels on astrocytes, triggering activation of the complement cascade leading to astrocyte injury, oligodendrocyte loss, demyelination, and neuronal loss. IL-6 also recruits neutrophils and eosinophils. This causes bystander damage and activates microglia which produce TNF-alpha and IL-1 beta, cytokines toxic to neurons and nearby cells2,10-12

IL-6 is therefore an important therapeutic target in the treatment of NMOSD2,10

ENSPRYNG, or satralizumab, is the first and only FDA-approved humanized anti-IL-6 receptor monoclonal IgG2 antibody using novel recycling technology for adults with aquaporin-4 antibody positive NMOSD.  It is also the only treatment that can be given subcutaneously1,10,13

While the precise mechanism by which ENSPRYNG exerts therapeutic effects in NMOSD is unknown, it is presumed to involve inhibition of IL-6-mediated signaling via binding through soluble and membrane-bound IL-6 receptors1

ENSPRYNG was engineered to produce several distinguishing characteristics1,10,14,15

One is a Fab fragment, which allows for high-affinity binding to both soluble and membrane-bound IL-61,10,14,15

ENSPRYNG has an engineered IgG2 structure, designed to allow for neonatal Fc-receptor recycling1,10,14,16

Unlike some conventional monoclonal antibodies that bind to antigen once before being rapidly degraded by the cell, ENSPRYNG is transported back into the bloodstream to bind more antigen through a process called antigen recycling1,10,14,16

This allows for a longer duration of ENSPRYNG antibody circulation and prolonged plasma half-life. The clinical significance of this is unknown1,10,14-16

To summarize, by inhibiting IL-6 signaling, ENSPRYNG is thought to help decrease IL-6 mediated autoimmune T- and B-cell activation, as well as differentiation of B cells into AQP4-IgG-secreting plasmablasts1,10

In turn, this targets inflammation, blood-brain barrier permeability, and astrocyte injury—all key drivers of NMOSD disease1,2,10

ENSPRYNG Important Safety Information

Indication

ENSPRYNG is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.

Contraindications

ENSPRYNG is contraindicated in patients with a known hypersensitivity to satralizumab or any of the inactive ingredients, an active hepatitis B infection, or active or untreated latent tuberculosis

Warnings and Precautions

Infections

An increased risk of infections, including serious and potentially fatal infections, has been observed in patients treated with IL-6 receptor antagonists, including ENSPRYNG. The most common infections reported in a randomized clinical trial of patients treated with ENSPRYNG who were not on other chronic immunosuppressant therapies, and that occurred more often than in patients receiving placebo, were nasopharyngitis (12%) and cellulitis (10%). The most common infections in patients who were on an additional concurrent immunosuppressant, and that occurred more often than in patients receiving placebo, were nasopharyngitis (31%), upper respiratory infection (19%), and pharyngitis (12%). Delay ENSPRYNG administration in patients with an active infection, including localized infections, until the infection is resolved.

Hepatitis B Virus (HBV) Reactivation

Risk of HBV reactivation has been observed with other immunosuppressant therapies. Patients with chronic HBV infection were excluded from clinical trials. Perform HBV screening in all patients before initiation of treatment with ENSPRYNG.  Do not administer ENSPRYNG to patients with active hepatitis. For patients who are chronic carriers of HBV [HBsAg+] or are negative for HBsAg and positive for HB core antibody [HBcAb+], consult liver disease experts before starting and during treatment with ENSPRYNG.

Tuberculosis

Tuberculosis has occurred in patients treated with other IL-6 receptor antagonists. Patients should be evaluated for tuberculosis risk factors and tested for latent infection prior to initiating ENSPRYNG. Consider anti-tuberculosis therapy prior to initiation of ENSPRYNG in patients with a history of latent or active tuberculosis in whom an adequate course of treatment cannot be confirmed, and for patients with a negative test for latent tuberculosis but having risk factors for tuberculosis infection. Consult infectious disease experts regarding whether initiating anti-tuberculosis therapy is appropriate before starting treatment. Patients should be monitored for the development of signs and symptoms of tuberculosis with ENSPRYNG, even if initial tuberculosis testing is negative.

Vaccinations

Live or live-attenuated vaccines should not be given concurrently with ENSPRYNG because clinical safety has not been established. Administer all immunizations according to immunization guidelines at least 4 weeks prior to initiation of ENSPRYNG for live or live-attenuated vaccines and, whenever possible, at least 2 weeks prior to initiation of ENSPRYNG for non-live vaccines.

Elevated Liver Enzymes

Mild and moderate elevations of liver enzymes have been observed in patients treated with ENSPRYNG at a higher incidence than in patients receiving placebo. ALT and AST levels should be monitored every 4 weeks for the first 3 months of treatment, followed by every 3 months for one year, and thereafter, as clinically indicated.

Decreased Neutrophil Counts

Decreases in neutrophil counts were observed in patients treated with ENSPRYNG at a higher incidence than placebo. Neutrophil counts should be monitored 4 to 8 weeks after initiation of therapy, and thereafter at regular clinically determined intervals.

Hypersensitivity Reactions

Hypersensitivity reactions, including rash, urticaria, and fatal anaphylaxis, have occurred with other IL-6 receptor antagonists.

Use in Specific Populations

Pregnancy

Pregnancy Exposure Registry

There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to ENSPRYNG during pregnancy. Healthcare providers are encouraged to register patients and pregnant women are encouraged to register themselves by calling 1-833-277-9338.

There are no adequate data on the developmental risk associated with the use of ENSPRYNG in pregnant women. In an animal reproduction study, no adverse effects on maternal animals or fetal development were observed in pregnant monkeys and their offspring, with administration of ENSPRYNG at doses up to 50 mg/kg/week. In the U.S. general population, the estimated background risk of major birth defect and miscarriage in clinically recognized pregnancies is 2 – 4% and 15 – 20%, respectively. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

Lactation

No information is available on the presence of ENSPRYNG in human milk, the effects of ENSPRYNG on the breastfed infant, or the effects of ENSPRYNG on milk production. ENSPRYNG was excreted in the milk of lactating monkeys administered ENSPRYNG throughout pregnancy. Human IgG is excreted in human milk and the potential for absorption in the infant is unknown. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for ENSPRYNG and any potential adverse effects on the breastfed infant from ENSPRYNG or from the underlying maternal condition.

Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

Geriatric Use

Clinical studies of ENSPRYNG did not include sufficient numbers of patients aged 65 years and older to determine whether they respond differently from younger patients. However, population pharmacokinetic analyses in patients with NMOSD did not show that age affected the pharmacokinetics of ENSPRYNG. In general, caution should be used when dosing the elderly, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant diseases or other drug therapy.

Most Common Adverse Reactions

The most common adverse reactions (≥15% in either trial) were nasopharyngitis (31%), headache (27%), upper respiratory tract infection (19%), rash (17%), arthralgia (17%), extremity pain (15%), gastritis (15%), fatigue (15%), and nausea (15%).

You may report side effects to the FDA at (800) FDA-1088 or www.fda.gov/medwatch. You may also report side effects to Genentech at (888) 835-2555.

For additional safety information, please see the full Prescribing Information and Medication Guide.

References

  1. ENSPRYNG [prescribing information]. South San Francisco, CA: Genentech, Inc. 2022.
  2. Traboulsee A, Greenberg BM, Bennett JL, et al. Safety and efficacy of satralizumab monotherapy in neuromyelitis optica spectrum disorder: a randomised, double-blind, multicenter, placebo-controlled phase 3 trial. Lancet Neurol. 2020;19(6):402-412. doi:10.1016/S1474-4422(20)30078-8
  3. Kawachi I, Lassmann H. Neurodegeneration in multiple sclerosis and neuromyelitis optica. J Neurol Neurosurg Psychiatry. 2017;88(2):137-145. doi:10.1136/jnnp-2016-313300
  4. Jarius S, Wildemann B, Paul F. Neuromyelitis optica: clinical features, immunopathogenesis and treatment. Clin Exp Immunol. 2014;176(2):149-164. doi:10.1111/cei.12271
  5. Yamamura T, Kleiter I, Fujihara K, et al. Trial of satralizumab in neuromyelitis optica spectrum disorder. N Engl J Med. 2019;381(22):2114-2124. doi:10.1056/NEJMoa1901747
  6. Huda S, Whittam D, Bhojak M, et al. Neuromyelitis optica spectrum disorders. Clin Med (Lond). 2019;19(2):169-176. doi:10.7861/clinmedicine.19-2-169
  7. 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(9):3701-3706. doi:10.1073/pnas.1017385108
  8. Knapp RK, Hardtstock F, Wilke T, et al. Evaluating the economic burden of relapses in neuromyelitis optica spectrum disorder: a real-world analysis using German claims data. Neurol Ther. 2021;11(1):247-263. doi:10.1007/s40120-021-00311-x
  9. Carnero Contentti E, Rojas JI, Cristiano E, et al. Latin American consensus recommendations for management and treatment of neuromyelitis optica spectrum disorders in clinical practice. Mult Scler Relat Disord. 2020;45:102428. doi:10.1016/j.msard.2020.102428
  10. Heo Y-A. Satralizumab: first approval. Drugs. 2020;80(14):1477-1482. https://doi.org/10.1007/s40265-020-01380-2
  11. 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. doi:10.1212/NXI.0000000000000311
  12. Obermeier B, Daneman R, Ransohoff RM. Development, maintenance and disruption of the blood-brain barrier. Nat Med. 2013;19(12):1584-1596. doi:10.1038/nm.3407
  13. Rajan K. Satralizumab wins FDA approval for NMOSD. American Academy of Ophthalmology. Published August 18, 2020. Accessed August 10, 2022. https://www.aao.org/headline/satralizumab-wins-fda-approval-nmosd
  14. Chugai Pharmaceutical Co, LTD. SMART-Ig. Accessed August 10, 2022. https://www.chugai-pharm.co.jp/english/ir/rd/technologies/files/eChugaiProprietaryTechnologies.pdf
  15. Igawa T, Tsunoda H, Kuramochi T, Sampei Z, Ishii S, Hattori K. Engineering the variable region of therapeutic IgG antibodies. MAbs. 2011;3(3):243-252. doi:10.4161/mabs.3.3.15234
  16. Data on file. Genentech, Inc. South San Francisco, CA

AQP4=aquaporin-4; BBB=blood-brain barrier; FDA=Food and Drug Administration; IgG=immunoglobulin G; IL-6=interleukin-6; ISTs=immunosuppressive therapies; NMOSD=neuromyelitis optica spectrum disorder; Th17=T helper 17.

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ENSPRYNG has a well-studied safety profile

Patients had a median of 5 years exposure to ENSPRYNG across clinical trials4

View data
ENSPRYNG clinical trial information

ENSPRYNG is the only NMOSD treatment with FDA approval based on 2 distinct phase 3 trials

See study design

Important Safety Information & Indication

Indication

ENSPRYNG is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.

Contraindications

ENSPRYNG is contraindicated in patients with a known hypersensitivity to satralizumab or any of the inactive ingredients, an active hepatitis B infection, or active or untreated latent tuberculosis.

Warnings and Precautions

Infections
An increased risk of infections, including serious and potentially fatal infections, has been observed in patients treated with IL-6 receptor antagonists, including ENSPRYNG. The most common infections reported in a randomized clinical trial of patients treated with ENSPRYNG who were not on other chronic immunosuppressant therapies, and that occurred more often than in patients receiving placebo, were nasopharyngitis (12%) and cellulitis (10%). The most common infections in patients who were on an additional concurrent immunosuppressant, and that occurred more often than in patients receiving placebo, were nasopharyngitis (31%), upper respiratory infection (19%), and pharyngitis (12%). Delay ENSPRYNG administration in patients with an active infection, including localized infections, until the infection is resolved.

Hepatitis B Virus (HBV) Reactivation
Risk of HBV reactivation has been observed with other immunosuppressant therapies. Patients with chronic HBV infection were excluded from clinical trials. Perform HBV screening in all patients before initiation of treatment with ENSPRYNG. Do not administer ENSPRYNG to patients with active hepatitis. For patients who are chronic carriers of HBV [HBsAg+] or are negative for HBsAg and positive for HB core antibody [HBcAb+], consult liver disease experts before starting and during treatment with ENSPRYNG.

Tuberculosis
Tuberculosis has occurred in patients treated with other IL-6 receptor antagonists. Patients should be evaluated for tuberculosis risk factors and tested for latent infection prior to initiating ENSPRYNG. Consider anti-tuberculosis therapy prior to initiation of ENSPRYNG in patients with a history of latent or active tuberculosis in whom an adequate course of treatment cannot be confirmed, and for patients with a negative test for latent tuberculosis but having risk factors for tuberculosis infection. Consult infectious disease experts regarding whether initiating anti-tuberculosis therapy is appropriate before starting treatment. Patients should be monitored for the development of signs and symptoms of tuberculosis with ENSPRYNG, even if initial tuberculosis testing is negative.

Vaccinations
Live or live-attenuated vaccines should not be given concurrently with ENSPRYNG because clinical safety has not been established. Administer all immunizations according to immunization guidelines at least 4 weeks prior to initiation of ENSPRYNG for live or live-attenuated vaccines and, whenever possible, at least 2 weeks prior to initiation of ENSPRYNG for non-live vaccines.

Elevated Liver Enzymes
Mild and moderate elevations of liver enzymes have been observed in patients treated with ENSPRYNG at a higher incidence than in patients receiving placebo. ALT and AST levels should be monitored every 4 weeks for the first 3 months of treatment, followed by every 3 months for one year, and thereafter, as clinically indicated.

Decreased Neutrophil Counts
Decreases in neutrophil counts were observed in patients treated with ENSPRYNG at a higher incidence than placebo. Neutrophil counts should be monitored 4 to 8 weeks after initiation of therapy, and thereafter at regular clinically determined intervals.

Hypersensitivity Reactions
Hypersensitivity reactions, including rash, urticaria, and fatal anaphylaxis, have occurred with other IL-6 receptor antagonists.

Use in Specific Populations

Pregnancy
Pregnancy Exposure Registry
There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to ENSPRYNG during pregnancy. Healthcare providers are encouraged to register patients and pregnant women are encouraged to register themselves by calling 1-833-277-9338.

There are no adequate data on the developmental risk associated with the use of ENSPRYNG in pregnant women. In an animal reproduction study, no adverse effects on maternal animals or fetal development were observed in pregnant monkeys and their offspring, with administration of ENSPRYNG at doses up to 50 mg/kg/week. In the U.S. general population, the estimated background risk of major birth defect and miscarriage in clinically recognized pregnancies is 2 – 4% and 15 – 20%, respectively. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

Lactation
No information is available on the presence of ENSPRYNG in human milk, the effects of ENSPRYNG on the breastfed infant, or the effects of ENSPRYNG on milk production. ENSPRYNG was excreted in the milk of lactating monkeys administered ENSPRYNG throughout pregnancy. Human IgG is excreted in human milk and the potential for absorption in the infant is unknown. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for ENSPRYNG and any potential adverse effects on the breastfed infant from ENSPRYNG or from the underlying maternal condition.

Pediatric Use
Safety and effectiveness in pediatric patients have not been established.

Geriatric Use
Clinical studies of ENSPRYNG did not include sufficient numbers of patients aged 65 years and older to determine whether they respond differently from younger patients. However, population pharmacokinetic analyses in patients with NMOSD did not show that age affected the pharmacokinetics of ENSPRYNG. In general, caution should be used when dosing the elderly, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant diseases or other drug therapy.

Most Common Adverse Reactions
The most common adverse reactions (≥15% in either trial) were nasopharyngitis (31%), headache (27%), upper respiratory tract infection (19%), rash (17%), arthralgia (17%), extremity pain (15%), gastritis (15%), fatigue (15%), and nausea (15%).

You may report side effects to the FDA at (800) FDA-1088 or www.fda.gov/medwatch. You may also report side effects to Genentech at (888) 835-2555.

For additional safety information, please see the full Prescribing Information and Medication Guide.

    • Wingerchuk DM, Hogancamp WF, O'Brien PC, Weinshenker BG. The clinical course of neuromyelitis optica (Devic's syndrome). Neurology. 1999;53(5):1107-1114. doi:10.1212/wnl.53.5.1107

      Wingerchuk DM, Hogancamp WF, O'Brien PC, Weinshenker BG. The clinical course of neuromyelitis optica (Devic's syndrome). Neurology. 1999;53(5):1107-1114. doi:10.1212/wnl.53.5.1107

    • George M, Gantioque R. Neuromyelitis optica spectrum disorder: an early diagnosis to prevent blindness and paraplegia. J Nurse Pract. 2023;19(7):104654. doi:10.1016/j.nurpra.2023.104654

      George M, Gantioque R. Neuromyelitis optica spectrum disorder: an early diagnosis to prevent blindness and paraplegia. J Nurse Pract. 2023;19(7):104654. doi:10.1016/j.nurpra.2023.104654

    • ENSPRYNG [prescribing information]. South San Francisco, CA: Genetech, Inc. 2022.

      ENSPRYNG [prescribing information]. South San Francisco, CA: Genetech, Inc. 2022.

    • Weinshenker B, Yeaman MR, de Seze J, et al. Long-term safety of satralizumab in adults with aquaporin-4-IgG-seropositive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD). Presented at: the 75th Annual Meeting of the American Academy of Neurology; April 22-27, 2023; Boston, MA.

      Weinshenker B, Yeaman MR, de Seze J, et al. Long-term safety of satralizumab in adults with aquaporin-4-IgG-seropositive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD). Presented at: the 75th Annual Meeting of the American Academy of Neurology; April 22-27, 2023; Boston, MA.

    • Yamamura T, Weinshenker B, Yeaman MR, et al. Long-term safety of satralizumab in neuromyelitis optica spectrum disorder (NMOSD) from SAkuraSky and SAkuraStar. Mult Scler Relat Disord. 2022;66:104025. doi:10.1016/j.msard.2022.104025

      Yamamura T, Weinshenker B, Yeaman MR, et al. Long-term safety of satralizumab in neuromyelitis optica spectrum disorder (NMOSD) from SAkuraSky and SAkuraStar. Mult Scler Relat Disord. 2022;66:104025. doi:10.1016/j.msard.2022.104025

    • FDA approves Genentech’s Enspryng for neuromyelitis optica spectrum disorder. News release. Genentech, Inc. August 14, 2020. Accessed February 10, 2025. https://www.gene.com/media/press-releases/14873/2020-08-14/fdaapproves-genentechs-enspryng-for-neu

      FDA approves Genentech’s Enspryng for neuromyelitis optica spectrum disorder. News release. Genentech, Inc. August 14, 2020. Accessed February 10, 2025. https://www.gene.com/media/press-releases/14873/2020-08-14/fdaapproves-genentechs-enspryng-for-neu

    • Songwisit S, Kosiyakul P, Jitprapaikulsan J, Prayoonwiwat N, Ungprasert P, Siritho S. Efficacy and safety of mycophenolate mofetil therapy in neuromyelitis optica spectrum disorders: a systematic review and meta-analysis. Sci Rep. 2020;10(1):16727. doi:10.1038/s41598-020-73882-8

      Songwisit S, Kosiyakul P, Jitprapaikulsan J, Prayoonwiwat N, Ungprasert P, Siritho S. Efficacy and safety of mycophenolate mofetil therapy in neuromyelitis optica spectrum disorders: a systematic review and meta-analysis. Sci Rep. 2020;10(1):16727. doi:10.1038/s41598-020-73882-8

    • Anderson M, Levy M. Advances in the long-term treatment of neuromyelitis optica spectrum disorder. J Cent Nerv Syst Dis. 2024;16:11795735241231094. doi:10.1177/11795735241231094

      Anderson M, Levy M. Advances in the long-term treatment of neuromyelitis optica spectrum disorder. J Cent Nerv Syst Dis. 2024;16:11795735241231094. doi:10.1177/11795735241231094

    • Sellner J, Sitte HH, Rommer PS. Targeting interleukin-6 to treat neuromyelitis optica spectrum disorders: Implications from immunology, the FcRn pathway and clinical experience. Drug Discov Today. 2021;26(7):1591-1601. doi:10.1016/j.drudis.2021.03.018

      Sellner J, Sitte HH, Rommer PS. Targeting interleukin-6 to treat neuromyelitis optica spectrum disorders: Implications from immunology, the FcRn pathway and clinical experience. Drug Discov Today. 2021;26(7):1591-1601. doi:10.1016/j.drudis.2021.03.018

    • Data on file. Genentech, Inc. South San Francisco, CA.

      Data on file. Genentech, Inc. South San Francisco, CA.

    • Kümpfel T, Giglhuber K, Aktas O, et al. Update on the diagnosis and treatment of neuromyelitis optica spectrum disorders (NMOSD) - revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part II: Attack therapy and long-term management [published correction appears in J Neurol. 2024 Jun;271(6):3702-3707. doi: 10.1007/s00415-024-12288-2.]. J Neurol. 2024;271(1):141-176. doi:10.1007/s00415-023-11910-z

      Kümpfel T, Giglhuber K, Aktas O, et al. Update on the diagnosis and treatment of neuromyelitis optica spectrum disorders (NMOSD) - revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part II: Attack therapy and long-term management [published correction appears in J Neurol. 2024 Jun;271(6):3702-3707. doi: 10.1007/s00415-024-12288-2.]. J Neurol. 2024;271(1):141-176. doi:10.1007/s00415-023-11910-z

    • Jarius S, Wildemann B, Paul F. Neuromyelitis optica: clinical features, immunopathogenesis and treatment. Clin Exp Immunol. 2014;176(2):149-164. doi:10.1111/cei.12271

      Jarius S, Wildemann B, Paul F. Neuromyelitis optica: clinical features, immunopathogenesis and treatment. Clin Exp Immunol. 2014;176(2):149-164. doi:10.1111/cei.12271

    • Traboulsee A, Greenberg BM, Bennett JL, 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(5):402-412. doi:10.1016/S1474-4422(20)30078-8

      Traboulsee A, Greenberg BM, Bennett JL, 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(5):402-412. doi:10.1016/S1474-4422(20)30078-8

    • Yamamura T, Kleiter I, Fujihara K, et al. Trial of Satralizumab in Neuromyelitis Optica Spectrum Disorder. N Engl J Med. 2019;381(22):2114-2124. doi:10.1056/NEJMoa1901747

      Yamamura T, Kleiter I, Fujihara K, et al. Trial of Satralizumab in Neuromyelitis Optica Spectrum Disorder. N Engl J Med. 2019;381(22):2114-2124. doi:10.1056/NEJMoa1901747

    • Huda S, Whittam D, Bhojak M, Chamberlain J, Noonan C, Jacob A. Neuromyelitis optica spectrum disorders. Clin Med (Lond). 2019;19(2):169-176. doi:10.7861/clinmedicine.19-2-169

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