Cellular Phosphorylation Testing Service for MET Kinase Mutant Panel
- constitutive c-MET phosphorylation induced by designed transmembrane domain
- robust phosphorylation
- standardized assay procedure, HTS feasible
- common Rat1 fibroblast cell background
- real cellular MET Kinase Mutant Panel profiling possible
- reference inhibitors demonstrate comparable inhibition to Reaction Biology standard MET phosphorylation assay using MKN45
- 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.
- Recombinant MET Kinase Mutant Panel
- Biochemical MET Kinase Mutant Panel screening
- Cellular Soft Agar Growth with MET Kinase Mutants
Freiburg, Germany
More information can be found on our website Cellular Phosphorylation Assay Services.
Primary reference compound example
BMS777607 was tested for the inhibition of MET phosphorylation on the MET Mutant Panel. BMS777607 a “type II” MET inhibitor. “Type II” inhibitors don’t need tyrosine 1230[1]. The MET Mutations (e.g. D1228N) and wildtype form (wt) are depicted.
[1] Undiner et al. (2010). Anti-Cancer Agents in Medicinal Chemistry 10: 7-27
Additional validation data example
PHA665752 was tested for the inhibition of MET phosphorylation on the MET Mutant Panel. PHA665752 is a “type I” MET inhibitor. “Type I” MET inhibitors have a u-shaped geometry and need tyrosine 1230 (Y1230) for binding [1]. The graphs show the result of a representative experiment and emphasize the need of tyrosine 1230 for PHA665752 inhibition of MET kinase. The MET Mutations (e.g. D1228N) and wildtype form (wt) are depicted.
[1] Undiner et al. (2010). Anti-Cancer Agents in Medicinal Chemistry 10: 7-27