Cellular Phosphorylation Testing Service (intracellular kinase activity assay) for EGF-R Kinase Mutant Panel
| wild-type | Δ752-759 |
| G719S | T790M |
| Δ746-750/T790M | T790M/L858R |
| Δ746-750/C797S | T790M/C797S/L858R |
| Δ746-750/T790M/C797S | L858R |
| Δ747-749/A750P | L861Q |
Rat1 fibroblasts express the cellular domain of EGF-R Mutants fused to a designed transmembrane domain. The designed transmembrane domain causes a constitutive EGF-R mutant autophosphorylation.
- same cellular background
- HTS feasible
- standardized assay procedure
Gefitinib (additional validation data) and Lapatinib (primary reference compound) were tested for the inhibition of EGF-R phosphorylation on selected EGF-R mutants Both compounds lack efficient inhibition of EGF-R mutant T790M and T790M/L858R.
- IC50 values are determined by testing 8 compound concentrations in semi-logarithmic steps (each concentration in duplicates).
- Quality assurance is provided by calculation of Z’ factors for Low/High controls on each assay plate and by including a full IC50 curve for a reference inhibitor to monitor adequate dose/response relation in your assay run.
Freiburg, Germany
More information can be found on our website Cellular Phosphorylation Assay Services.
EGF-R Mutants carrying the C797S mutation in comparison to primary reference compound
EGF-R Mutants carrying the C797S mutation in comparison to additional validation data
