Collaborators in the Gray lab at Stanford developed INY-06-061, a potent and selective heterobifunctional degrader of ERK5 to be used as a tool for validating phenotypes associated with ERK5 ablation. Results from a standard PRISM assay using the PR800 cell set verified a lack of dependency on ERK5 expression for cell growth (as no cell lines were sensitive to INY-06-061 treatment).
Acute pharmacological degradation of ERK5 does not inhibit cellular immune response or proliferation