CEP1347-VHL-02

CEP1347-VHL-02 (1 μM; 48 h) induces G2/M cell cycle arrest and significantly promotes apoptosis in MDA-MB-468 cells, whereas no such effects are observed in MCF-7 cells^[1].
CEP1347-VHL-02 (0.1-5 μM; 24 h) induces concentration-dependent degradation of overexpressed and endogenous MLK3 in A375, HCC1806, MCF-7 and MDA-MB-468 cells, with DC₅₀ values of 50 nM and 300 nM, and Dmax values of 77% and 63% in MCF-7 and MDA-MB-468 cells, respectively^[1].
Treatment with CEP1347-VHL-02 (0.5-1 μM; 2-48 h) initiates MLK3 degradation in HCC1806_MLK3 cells at 2 h, with nearly complete degradation achieved at 24 h; the reaction half-lives (t_1/2) in MCF-7 and MDA-MB-468 cells are 2.5 h and 4 h, respectively^[1].
CEP1347-VHL-02 (0.1-5 μM; 2-24 h) exhibits no degrading effect on MLK1, MLK2 and MLK4, and proteomics confirms that MLK3 is the only kinase significantly degraded, indicating its high selectivity for MLK3^[1].
The MLK3-degrading effect of CEP1347-VHL-02 (0.25-1 μM; 7 h) is completely blocked by the proteasome inhibitor Carfilzomib (HY-10455) (1 μM), confirming that it functions via the ubiquitin-proteasome system^[1].
CEP1347-VHL-02 (1 μM; 24 h) has no effect on MLK3 mRNA levels, confirming that its degradation effect occurs at the protein level rather than the transcriptional level^[1].
CEP1347-VHL-02 (1 μM; 24 h) significantly inhibits JNK phosphorylation in MCF-7 and MDA-MB-468 cells, but has no effect on ERK pathway activity^[1].
CEP1347-VHL-02 (1 μM; 15 days) significantly reduces the clonogenic capacity of MDA-MB-468 cells, but has no such effect on MCF-7 cells^[1].
CEP1347-VHL-02 (1 μM; 24 h) reduces the migratory potential of MDA-MB-468 TNBC cells and inhibits their sphere formation in 3D culture, but exerts no such effects on MCF-7 ER+ breast cancer cells^[1].

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