Gene Therapy

Inomagen’s gene therapy program has demonstrated preclinical success targeting underlying mechanisms of AFib, and is advancing into IND-enabling studies with an independent CRO.

Inomagen is developing a gene therapy with improved efficacy for AFib patients including undertreated patients with early stage (paroxysmal) to advanced stage (persistent) AFib.

We have:

  • Identified major molecular mechanisms that contribute to AFib in a majority of patients with AFib

  • Identified major trans-genes to selectively target these mechanisms in the atrium

  • Utilized electroporation following gene injection to provide therapeutic gene transfer and expression

  • Decreased AFib in clinically relevant, large animal models of AFib

  • Achieved readiness for IND-enabling studies with an independent CRO

Targeting underlying molecular mechanisms of AFib

Inomagen’s gene therapy has demonstrated preclinical success in large animal models of AFib

Preventing Electrical Remodeling – Inomagen’s Gene Therapy (NOX2 shRNA) prevented the onset of AFib in both a short and long-term rapid atrial pacing (RAP) model

Minimizing Structural Remodeling – Inomagen’s Gene Therapy (NOX2 shRNA) Dramatically Reduced AFib Induced Fibrosis

Future Targets – Inomagen has identified other promising proprietary targets for future development (e.g., NGF shRNA targets autonomic nervous system)

Inomagen has developed a non-viral gene (biologic) therapy which utilizes a proprietary NOX2 shRNA plasmid to silence pathways involved in the development of atrial fibrillation.  The therapy is not replacing or editing genes typical of gene therapies for rare diseases, it is silencing the expression of genes causing AF. This approach is designed to address the limitations associated with existing treatment options, particularly for patients with persistent atrial fibrillation.