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Spinal Muscular Atrophy (SMA)

Autosomal recessive motor neuron disease caused by SMN1 gene deletion. One of the most successfully treated neurological diseases — three approved therapies (nusinersen, risdiplam, onasemnogene abeparvovec) have transformed outcomes, especially in early-treated patients.

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612
Papers (5yr)
14
Active trials
4
Tracked biomarkers
4
Related diseases
Research signals

SMA has become a model for neurological drug development. NfL's dramatic response to nusinersen has informed biomarker strategies across ALS, FTD, and other motor neuron diseases. Gene therapy combination approaches and next-generation ASOs are in active Phase II trials. View full research signals →

Tracked biomarkers
Neurofilament Light Chain (NfL)Strong evidence

Primary pharmacodynamic biomarker in SMA trials. Dramatic reduction after nusinersen treatment — one of the clearest drug-biomarker responses in neurodegeneration.

SMN protein (blood)Strong evidence

Direct target of all approved SMA therapies. Measured as pharmacodynamic marker for nusinersen, risdiplam, and onasemnogene abeparvovec (OA). Increase confirms mechanism of action.

Phosphorylated NfH (pNfH)Moderate evidence

Heavy chain neurofilament. Marker of axonal degeneration in lower motor neurons. Complements NfL as a disease activity marker in older SMA patients.

CK (Creatine Kinase)Emerging

Marker of muscle degeneration secondary to motor neuron loss. Useful as a progression marker in ambulatory SMA patients where NfL may plateau.

Active clinical trials
NCT IDDrug / InterventionPhaseStatusSponsor
NCT02386553Nusinersen (ASO — SMN2 splicing)Phase IIIActiveBiogen
NCT03032172Risdiplam (oral SMN2 modifier)Phase IIIActiveRoche
NCT03461289OA-101 (AAV9 gene therapy)Phase IIRecruitingNovartis

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Related diseases — shared mechanisms

Phase 1 primary cohort + monitored diseases

Research and educational use only. Information does not constitute medical advice, diagnosis, or treatment recommendations. Verify with primary literature. AI disclaimer →