Nusinersen versus Sham Control in Infantile-Onset Spinal Muscular Atrophy
Open accessAbstract
BACKGROUND: Spinal muscular atrophy is an autosomal recessive neuromuscular disorder that is caused by an insufficient level of survival motor neuron (SMN) protein. Nusinersen is an antisense oligonucleotide drug that modifies pre-messenger RNA splicing of the SMN2 gene and thus promotes increased production of full-length SMN protein. METHODS: We conducted a randomized, double-blind, sham-controlled, phase 3 efficacy and safety trial of nusinersen in infants with spinal muscular atrophy. The primary end points were a motor-milestone response (defined according to results on the Hammersmith Infant Neurological Examination) and event-free survival (time to death or the use of permanent assisted ventilation). Secondary end points included overall survival and subgroup analyses of event-free survival according to disease duration at screening. Only the first primary end point was tested in a prespecified interim analysis. To control the overall type I error rate at 0.05, a hierarchical testing strategy was used for the second primary end point and the secondary end points in the final analysis. RESULTS: In the interim analysis, a significantly higher percentage of infants in the nusinersen group than in the control group had a motor-milestone response (21 of 51 infants [41%] vs. 0 of 27 [0%], P<0.001), and this result prompted early termination of the trial. In the final analysis, a significantly higher percentage of infants in the nusinersen group than in the control group had a motor-milestone response (37 of 73 infants [51%] vs. 0 of 37 [0%]), and the likelihood of event-free survival was higher in the nusinersen group than in the control group (hazard ratio for death or the use of permanent assisted ventilation, 0.53; P=0.005). The likelihood of overall survival was higher in the nusinersen group than in the control group (hazard ratio for death, 0.37; P=0.004), and infants with a shorter disease duration at screening were more likely than those with a longer disease duration to benefit from nusinersen. The incidence and severity of adverse events were similar in the two groups. CONCLUSIONS: Among infants with spinal muscular atrophy, those who received nusinersen were more likely to be alive and have improvements in motor function than those in the control group. Early treatment may be necessary to maximize the benefit of the drug. (Funded by Biogen and Ionis Pharmaceuticals; ENDEAR ClinicalTrials.gov number, NCT02193074 .).
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ASO injection is a current standard of care for spinal muscular atrophy and is in five ongoing Phase I trials in ALS, Parkinson's, and Alzheimer's diseases and in Phase III trials for inherited ALS and Huntington's disease.
“ASO injection is a current standard of care for the fatal childhood disease spinal muscular atrophy15 and is in five ongoing Phase I trials in ALS, Parkinson’s, and Alzheimer’s diseases and in Phase III trials for inherited ALS from a mutation in superoxide dismutase16,17 and for Huntington’s disease18.”
From Therapeutically viable generation of neurons with antisense oligonucleotide suppression of PTB (2021) · cites this paper as [15]
The Background identifies nusinersen as an antisense oligonucleotide, and Trial Design and Treatment describes its intrathecal injection in infants with spinal muscular atrophy. The Conclusions report improved survival and motor function, but the paper does not establish that ASO injection is a current standard of care. The claims about trials in other diseases are attached to other citations, not this one. (LLM, conf=0.84)
Experimental — accuracy not yet measuredGene therapy has already been efficacious in other neurodegenerative diseases, most notably spinal muscular atrophy.
“Gene therapy has already been efficacious in other neurodegenerative diseases, most notably spinal muscular atrophy200,201.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [200]
The Results report improved motor-milestone response and survival with nusinersen in infants with spinal muscular atrophy. But the paper describes nusinersen as an antisense oligonucleotide drug, not gene therapy, and its trial does not establish efficacy for gene therapy. Section labels are available in our copy, but page numbers are not. (LLM, conf=0.90)
Experimental — accuracy not yet measuredAntisense oligonucleotides (ASOs) have proved effective in treating diseases such as spinal muscular atrophy (SMA) in human patients.
“Antisense oligonucleotides (ASOs) have proved effective in treating diseases such as spinal muscular atrophy (SMA) in human patients (49, 50); accordingly, the development of ASOs targeting RECK could be one possible intervention to mitigate pathologies associated with amyloidogenic APP processing (2, 51).”
From GDE2-RECK controls ADAM10 α-secretase–mediated cleavage of amyloid precursor protein (2021) · cites this paper as [49]
Several ASO therapies targeting genes in the spinal cord provide clinical benefit after intrathecal administration; Spinraza and Tofersen have extended survival for patients with spinal muscular atrophy and amyotrophic lateral sclerosis, respectively.
“Notably, several ASO therapies targeting genes in the spinal cord provide clinical benefit after intrathecal administration; Spinraza and Tofersen have extended survival for patients with spinal muscular atrophy and amyotrophic lateral sclerosis, respectively [43,51].”
From Elucidating brain transport pathways and cell type-dependent gene silencing of a durable lipid–siRNA conjugate administered into cerebrospinal fluid (2025) · cites this paper as [51]
Several ASO therapies targeting genes in the spinal cord provide clinical benefit after intrathecal administration, with Spinraza and Tofersen extending survival in SMA and ALS patients.
“Notably, several ASO therapies targeting genes in the spinal cord provide clinical benefit after intrathecal administration; Spinraza and Tofersen have extended survival for patients with Spinal Muscular Atrophy and Amyotrophic Lateral Sclerosis, respectively.5,6”
From Lipid-siRNA conjugate accesses a perivascular transport mechanism and achieves widespread and durable knockdown in the central nervous system (2024) · cites this paper as [5]
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- Authors
- Finkel, R. S., Mercuri, E., Darras, B. T., Connolly, A. M., Kuntz, N. L., Kirschner, J., Chiriboga, C. A., Saito, K., Servais, L., Tizzano, E., Topaloglu, H., Tulinius, M., Montes, J., Glanzman, A. M., Bishop, K., Zhong, Z. J., Gheuens, S., Bennett, C. F., Schneider, E., Farwell, W., & De Vivo, D. C.
- Affiliations
- Boston Children's Hospital (US)
- Università Cattolica del Sacro Cuore (IT)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2017-11-02
- Volume
- 377
- Issue
- 18
- Pages
- 1723-1732
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2765483614
- Cited by
- 2,337
- References
- 2
- Citations by year
- 2026: 224 · 2025: 250 · 2024: 299 · 2023: 248 · 2022: 284 · 2021: 313 · 2020: 296 · 2019: 229 · 2018: 180 · 2017: 9 · 2013: 1
- FWCI
- 112.17
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- UNSWorks (UNSW Sydney) (submittedVersion, cc-by-nc-nd)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Universitätsbibliographie, Universität Duisburg-Essen (submittedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- CINECA IRIS Institutial Research Information System (University of Genoa) (submittedVersion)
- Hacettepe University Institutional Repository (hacettepe.edu.tr) (submittedVersion, other-oa)
- Open Repository and Bibliography (University of Liège) (submittedVersion)
- Funders
- Medical Research Council (MR/N020588/1)
- Topics
- Health Sciences › Medicine › Genetics › Neurogenetic and Muscular Disorders Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Physiology › Lysosomal Storage Disorders Research
- Keywords
- spinal muscular atrophy, nusinersen, antisense therapy, SMN2 pre-mRNA splicing, survival motor neuron protein, event-free survival, overall survival, disease duration, early treatment, Hammersmith Infant Neurological Examination, adverse events, neuromuscular disorders
- MeSH terms
- Double-Blind Method, Female, Humans, Infant, Injections, Spinal, Male, Motor Skills, Oligonucleotides, Respiration, Artificial, RNA, Messenger, Spinal Muscular Atrophies of Childhood, Survival Analysis, Oligonucleotides, Antisense, Age of Onset, Disease-Free Survival, Survival of Motor Neuron 2 Protein
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