- Independent peer-reviewed study shows enhanced cell transduction with adeno-associated virus (AAV) vectors, commonly used in gene therapy, when integrating Altamira’s peptide-based delivery technology
- Increased potency may help to reduce AAV immunogenicity and resistance to AAVs in certain cell types
The study sought to find ways of increasing the endosomal release of AAV-based therapeutics by using peptides derived from melittin, a component of bee venom known for its ability to permeabilize biological membranes. The research group evaluated 76 melittin derivatives, including p5RHH, the peptide underlying Altamira’s OligoPhore™ / SemaPhore™ nanoparticle platform for RNA delivery. The scientists discovered that insertion of p5RHH into the AAV vector (p5RHH-rAAV) not only enhanced cell transduction, but also succeeded in transducing cell lines typically considered resistant to AAVs. Further, an in vivo study in mice showed that the addition of p5RHH to the AAV capsid of several AAV serotypes significantly enhanced liver transduction compared to non-modified AAV vectors, observed up to the last time point four weeks after systemic administration.
“The study results once again highlight the strong capability of our technology to promote the release of nucleic acids from the endosome into the cytoplasm, which has remained a key limiting factor for both non-viral vectors and viral-derived delivery vehicles such as AAVs,” commented Covadonga Pañeda, Ph.D., Altamira Therapeutics’ Chief Operating Officer. “Better transduction efficiency means that lower doses of AAVs may be used, which could lower the risk for deleterious immune responses and increase the safety of AAV-based vectors. In addition, the integration of the p5RHH peptide into different serotypes of AAV vectors may open new possibilities in AAV-based gene therapy in cells and tissues that are not typically amenable to AVV transduction.”
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1 Meng et al. (2024), Melittin analog p5RHH enhances recombinant adeno-associated virus transduction efficiency, J Integr Med, in press.
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2024 GlobeNewswire, Inc., source