PROTAC CDK4/6 degrader-2

PROTAC CDK4/6 degrader-2 (compound P11) (1.2-300 nM; 24 h) dose-dependently degrades CDK4 and CDK6 in MCF-7 cells with DC₅₀ values of 10.9 nM and 9.6 nM, respectively; treatment at 50 nM for 24 h results in 75% degradation of CDK4^[1].
PROTAC CDK4/6 degrader-2 (50 nM; 3-24 h) begins to degrade CDK4 at 3 h in MCF-7 cells, with near-complete degradation by 24 h, whereas CDK6 is nearly completely degraded within 3 h^[1].
PROTAC CDK4/6 degrader-2 (50 nM; 24 h; 3-48 h after washout) exhibits reversible and sustained CDK4/6 degradation in MCF-7 cells, with protein levels beginning to recover at 12 h after washout and returning to baseline levels at 24 h^[1].
PROTAC CDK4/6 degrader-2 (50 nM; 24 h; pretreatment with MG132 (HY-13259) or Pomalidomide (HY-10984) at 10 μM for 6 h) induced CDK4/6 degradation is blocked by the proteasome inhibitor MG132 and attenuated by the CRBN ligand Pomalidomide, respectively, supporting that it mediates CDK4/6 degradation through CRBN recruitment and the ubiquitin-proteasome system^[1].
PROTAC CDK4/6 degrader-2 (MCF-7: 10-40 nM; T47D: 50-150 nM; 24 h) dose-dependently induces G1 phase arrest and decreases RB phosphorylation, Cyclin D1, and c-MYC protein levels in MCF-7 and T47D cells^[1].
PROTAC CDK4/6 degrader-2 (72 h) inhibits the growth of MCF-7 and T47D breast cancer cells with GI₅₀ values of 10.09 nM and 72.02 nM, respectively; the GI₅₀ for normal MCF-10A cells is 8.687 μM^[1].
PROTAC CDK4/6 degrader-2 maintains growth inhibitory activity in Palbociclib (HY-50767)-resistant MCF-7 cells with a GI₅₀ of 3.10 μM, whereas the GI₅₀ values of Palbociclib and Dalpiciclib (HY-114338) rise to 16.80 μM and 19.40 μM, respectively^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.