AH078

AH078 potently binds to CK1δ in permeabilized cells, with an EC₅₀ of 3.2 nM^[3].
AH078 degrades CK1δ in MV4-11 HiBiT-CK1δ cells, with a DC₅₀ of 0.55 μM and a Dmax of 70.1% after 6 h of incubation^[3].
AH078 (3-10 μM; 9 h) induces a dose-dependent slowdown of cell cycle progression in MEC-1 WT cells. At the concentration of 10 μM, it reduces the accumulation of cells at the G₂/M phase boundary and increases the proportion of S-phase cells^[2].
AH078 (3-10 μM; 9 h) induces a dose-dependent slowdown of cell cycle progression in HG-3 WT cells, reduces cell accumulation at the G₂/M phase boundary, and increases the proportion of S-phase cells at a concentration of 10 μM^[2].
AH078 (3-10 μM; 6 d) significantly inhibits microenvironment-induced proliferation of primary human chronic lymphocytic leukemia (CLL) cells in a dose-dependent manner, with the strongest effect observed under the incubation condition of 10 μM for 6 days^[2].
AH078 (0.01-30 μM; 6 h) potently degrades endogenous CK1δ (DC₅₀=200 nM) and CK1ε in HEK293 cells after a 6 h incubation, while only exerting weak degradation effects on CK1α at concentrations ≥10 μM^[3].
AH078 (0.03-1.19 μM; 6 h)-mediated degradation of CK1δ depends on functional Cullin ring ligases, which is confirmed by experimental results showing that the degradation is reversed upon treatment with the neddylation inhibitor MLN4924^[3].

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