Viromer® YELLOW

mRNA / DNA transfection

Viromer® YELLOW is sold out and will not be continued.

For test samples please refer to Viromer® PLASMID, mRNA or RED.

Sufficient for the average number of * transfections in a 24-well format.


Viromer® YELLOW is sold out and will not be continued. For test samples please refer to Viromer® PLASMID, Viromer® mRNA or Viromer® RED.



Viromer® YELLOW is designed for the DNA transfection into very challenging cells. This reagent differs from the versatile Viromer® RED in its structural chemistry but follows the same workflow: an Active Endosome Escape to deliver properly nucleic acids of interest into cells with no off-target effects. It allows the mRNA or DNA transfection (plasmids) of cells known as “non-transfectable” so far or only accessible by electroporation. Among others, very high efficacy was reported for human primary chondrocytes, rat primary cardiomyocytes, FAO hepatocytes, as for CHO and HeLa standard cell lines. Viromer® YELLOW is a ready-to-use product for DNA transfection coming with an easy and straightforward protocol, and it is compatible with any culture medium and antibiotics.

Convincing results in plasmid transfection in hard-to-transfect cells




  • protein expression / overexpression
  • RNA interference with plasmids encoding for shRNA
  • reporter gene assays
  • cancer research
  • stem cell research
  • cell signaling

Features and Benefits

  • High transfection efficiency due to an active escape of Viromer® complexes from the endosome.
  • Great safety because Viromer complexes are non-charged, gentle on cells and compatible with serum and antibiotics.
  • Easy and fast transfection with consistent results ascribed to straightforward protocol including initial optimization.


  • Buffer YELLOW, pH 6.0 is supplied with the kit
  • for research use only
  • store dry at 2-8°C

Publications for mRNA / DNA transfection with Viromer® YELLOW

Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner.

Bianco et. al., Nat Commun., 2019

RIPK1 and Caspase-8 Ensure Chromosome Stability Independently of Their Role in Cell Death and Inflammation.

Liccardi et. al., Mol Cell., 2019

uPARAP/Endo180 receptor is a gatekeeper of VEGFR-2/VEGFR-3 heterodimerisation during pathological lymphangiogenesis.

Durré et. al., Nat Commun., 2018

NKX2-5 regulates human cardiomyogenesis via a HEY2 dependent transcriptional network.

transfections in supplemental data

Anderson et. al., Nat Commun., 2018

Dexamethasone-induced upregulation of CaV3.2 T-type Ca2+ channels in rat cardiac myocytes.

Falcón et. al., J Steroid Biochem Mol Biol., 2017

FGF23 activates injury-primed renal fibroblasts via FGFR4-dependent signalling and enhancement of TGF-β autoinduction

Smith, Int J Biochem Cell Biol., 2017


O’Reilly – 2017

The endothelial transcription factor ERG mediates Angiopoietin-1-dependent control of Notch signalling and vascular stability.

Shah et. al., Nat Commun., 2017

FGF23 is synthesised locally by renal tubules and activates injuryprimed fibroblasts.

transfections in supplemental data

Smith et. al., Sci Rep., 2017

Point mutations in murine Nkx2-5 phenocopy human congenital heart disease and induce pathogenic Wnt signaling.

Furtado et. al., JCI Insight., 2017

EPHB4 kinase-inactivating mutations cause autosomal dominant lymphatic-related hydrops fetalis.

Martin-Almedina et. al., J Clin Invest. 2016

HIV-Infected Dendritic Cells Present Endogenous MHC Class II-Restricted Antigens to HIV-Specific CD4+ T Cells.

Coulon et. al., J Immunol., 2016

p53 coordinates base excision repair to prevent genomic instability

Poletto, Nucleic Acids Res, 2016

Hypoxia Differentially Modulates the Genomic Stability of Clinical-Grade ADSCs and BM-MSCs in Long-Term Culture.

Bigot, Stem Cells, 2015

Vernakalant activates human cardiac K(2P)17.1 background K(+) channels.

Seyler et. al., Biochem Bophys Res Commun., 2014