JB300

JB300 binds to AURORA-A in intact HEK293T cells with an EC₅₀ of 373.0 nM^[1].
JB300 binds to AURORA-A in digitonin-permeabilized HEK293T cells with an EC₅₀ of 193.0 nM, exhibiting excellent cell permeability^[1].
JB300 degrades AURORA-A in MV4-11^AURORA-HiBiT cells, with a DC₅₀ of 30 nM, and the maximum degradation rate reaches 78% after 6 hours of incubation^[1].
Incubation of MV4-11 cells with JB300 (0.002-10 μM; 6 h) selectively degrades endogenous AURORA-A but not AURORA-B in a dose-dependent manner, with a hook effect observed at 10 μM^[1].
JB300 (0.625 μM; 6 h)-induced AURORA-A degradation in MV4-11 cells is completely blocked by MG132 (HY-13259) (10 μM); co-incubation with MK-5108 (HY-13252) (1 μM) or Thalidomide (HY-14658) (1, 10, 20 μM) also completely blocks AURORA-A depletion, indicating that this process depends on AURORA-A, Cereblon binding and the proteasome^[1].
In quantitative proteomic analysis of MV4-11 cells, JB300 (0.625 μM; 6 h) induces the most significant reduction in AURORA-A among 5469 detected proteins (log₂FC = -2.3); PTK2B shows only a weak but significant decrease (log₂FC = -0.7), while no significant changes occur in other proteins or known Cereblon neosubstrates^[1].
JB300 (0.625 μM; 18 h) reduces BrdU signals in the S phase of MV4-11 cells and induces mild G₂/M cell cycle arrest^[1].
JB300 (0.625 μM; 1-72 h) induces rapid and persistent degradation of AURORA-A in MV4-11^AURORA-HiBiT cells; after a single dose of 0.625 μM, the degradation reaches the maximum level at 9 h and persists up to 72 h^[1].
JB300 (incubated for 72 h) reduces the viability of MV4-11 cells, with an EC₅₀ of 478 nM after 72 h of incubation^[1].

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