Viromer®: A novel polymer based transfection reagent mimicking the viral infection process by an active endosome escape mechanism.


After binding RNA or DNA molecules, Viromer complexes enter the cell via endocytosis. Due to an active escape from the endosome a highly efficient delivery of molecules into the cytoplasma occurs. Once reached the cyctoplasma, Viromer complexes disaggregate – releasing RNA or DNA.

The innovative Viromer complexes are non-charged, preventing the aggregation with proteins which are included in fetal calf serum or other cell culture media supplements. This leads to the great advantage, that Viromer is very gentle on cells, compatible with serum, antibiotics and differentiation factors. In addition to this convenience, a magnificent benefit of working with Viromer is the possibility to transfect suspension cells by getting a high efficiency in siRNA or mRNA transfection as zero charged Viromer complexes do not aggregate with the negative charged cellsurface.

Transfection active escape Viromers

In Influenza

the pH-sensitive fusion peptide inserts into the endosomal membrane.

Mechanism relies on protonation of GLU, balanced by hydrophobic ALA.


mimic the influenza mechanism, but use a polymer instead of a fusion peptide.

Fatty acids (red) resemble influenza’s GLU, alkyl (grey) are similar to ALA.

As a result, both influenza and Viromer promote an active endosome escape leading to cytosolic delivery.

1:00h – early endosome

Viromers are taken up at the cell surface.

3:00h – late endosome

Viromers accumulate near the nucleus, ongoing acidification.

4:30h – arrival in the cytosol

Discharge of siRNA from endosomes and starting diffusion.

Model: HeLa, Viromer® GREEN, labelled siRNA

Data courtesy of Chromotek

Read more about the active endosome escape and the exciting technology behind  Viromer® in the following GEN article:

High-Tech Polymers Leveraging Viral Biophysics Can Enhance the Transfection of Nucleic Acids

Panzner, GEN, 2014