Onasemnogene-abeparvovec administration to premature infants with spinal muscular atrophy

Ann Clin Transl Neurol. 2024 Nov;11(11):3042-3046. doi: 10.1002/acn3.52213. Epub 2024 Sep 28.

Abstract

Twin girls born at 30 weeks' gestation with spinal muscular atrophy (SMA) received onsasemnogene-abeparvovec (OA) at 3.5 weeks of life. They had no treatment-related adverse events, normal acquisition of motor milestones, and normal neurological examination at 19 months. Genotyping revealed 0 copies of SMN1 and a single, hybrid SMN2 gene containing the positive genetic modifier c.835-44A>G. This was associated with full-length SMN2 blood mRNA expression levels similar to a 2 copy SMA infant. The observed favorable outcomes are likely due to the genetic modifier combined with early drug administration enabled by prematurity.

Publication types

  • Case Reports

MeSH terms

  • Biological Products / administration & dosage
  • Biological Products / adverse effects
  • Female
  • Humans
  • Infant
  • Infant, Newborn
  • Infant, Premature*
  • Muscular Atrophy, Spinal* / drug therapy
  • Muscular Atrophy, Spinal* / genetics
  • Recombinant Fusion Proteins
  • Survival of Motor Neuron 1 Protein* / genetics
  • Survival of Motor Neuron 2 Protein* / genetics

Substances

  • Survival of Motor Neuron 1 Protein
  • Survival of Motor Neuron 2 Protein
  • Zolgensma
  • Biological Products
  • SMN1 protein, human
  • SMN2 protein, human
  • Recombinant Fusion Proteins