CI

At a glance

ClinicalIndex Comparison Record
Phase 2Completed· 7 enrolled
Drug / intervention
AVI-4658 (PMO)drug
Likely dose
Not stated in record
Key inclusion· 7
  • Male aged 10–17 years at study drug administration
  • Clinical diagnosis of DMD with documented out-of-frame deletions or absent dystrophin on muscle biopsy, specifically deletions skippable by exon 51 (45-50; 47-50; 48-50; 49-50; 50; 52; 52-63)
  • <5% revertant fibres on muscle biopsy
  • Unable to ambulate or stand independently
Key exclusion· 16
  • Prior EDB muscle removal or resection
  • Stage 4 EDB muscle preservation on MRI
  • Left ventricular shortening fraction <25% or ejection fraction <35% on echocardiography at Visit 1 or within 3 months
  • Nocturnal hypoventilation (mean oxygen saturation ≤94% on overnight sleep study)

Standardized by ClinicalIndex from the ClinicalTrials.gov record · verify against the source.

Search/NCT00159250
NCT00159250Phase 2Completed

Restoring Dystrophin Expression in Duchenne Muscular Dystrophy: A Phase I/II Clinical Trial Using AVI-4658

Imperial College London·interventional·Posted Sep 12, 2005·Updated Dec 5, 2019

In Brief

A Phase 2 clinical trial evaluating AVI-4658 (PMO) for Duchenne Muscular Dystrophy. Completed, enrolled 7 participants across 1 site.

Detailed Summary

Duchenne muscular dystrophy (DMD), a fatal muscle degenerative disorder, arises from mutations in the dystrophin gene. Antisense therapy with the use of antisense oligonucleotides (AON) has the potential to restore effectively the production of dystrophin, the defective protein, in \>70% of DMD. This could result in increased life expectancy through improved muscle survival and function. Recent scientific research has demonstrated the potential of this technique to skip mutated dystrophin exons, restore the reading frame and generate functional dystrophin protein. Having demonstrated proof-of-principle in human cell culture and animal model studies, we now intend to determine efficacy and safety of this approach to induce dystrophin exon skipping in children with DMD. The specific aim of this phase I/II study is to assess efficacy (dystrophin production) and safety of intramuscular administered morpholino oligomer directed against exon 51 (AVI-4658 PMO). We are performing parallel preclinical studies to develop methods of systemic delivery that will be necessary for future phase II/III clinical studies.

Study Details

Study Typeinterventional
Allocation--
Masking--
Primary Purpose--
CountriesUnited Kingdom

Timeline

Phase 2CompletedFinished
2006200720082009201020112012201320142015201620172018201920202021202220232024202520262027
First PostedSep 12, 2005
Enrollment StartOct 26, 2007
Primary CompletionDec 1, 2008
Study CompletionMar 31, 2009
TodayJul 2, 2026
Enrollment to primary: 1.1 yearsPosted 20.8 years ago

Interventions

AVI-4658 (PMO)drug

morpholino antisense oligonucleotide