BSJ-03-123

BSJ-03-123 (50-1000 nM; 30 min-4 h) induces CRBN-dependent, concentration- and time-dependent, paralog-selective degradation of CDK6 (but not CDK4) in cultured cells, with comparable binding affinity for the cellular targets of CDK4 and CDK6^[1].
BSJ-03-123 (100 nM; 2 h) exhibits genome-wide proteome selectivity for CDK6 degradation in MOLT4 cells^[1].
BSJ-03-123 (200-1000 nM; 8-12 days, treatment refreshed every 2 days) selectively inhibits the proliferation of CDK6-dependent AML cell lines (MV4-11, MOLM13, P31/FUJ) without affecting CDK4-dependent cell lines^[1].
BSJ-03-123 (200 nM; 24 h) induces G1-phase cell cycle arrest in MV4-11 and MOLM13 acute myeloid leukemia (AML) cells without increasing apoptosis^[1].
BSJ-03-123 (200 nM; 2 h) aberrantly regulates the phosphorylation levels of 197 peptides in MV4-11 cells. Its regulatory targets are enriched in CDK motifs, and both known and novel CDK6 substrates are identified^[1].
BSJ-03-123 (200 nM; 6 h) induces transcriptional changes in MV4-11 cells, which are highly correlated with those induced by palbociclib, affecting pathways including cell cycle regulation, DNA replication and chromatin organization^[1].
BSJ-03-123 (0.1-5 μM; 4 h) induces CRBN-dependent selective degradation of CDK6 in wild-type Jurkat cells, with no such effect on CDK4, IKZF1 or IKZF3^[2].
BSJ-03-123 (250 nM; 5 h) selectively degrades CDK6 in Molt4 cells without reducing the levels of CDK4, IKZF1 or IKZF3^[2].
BSJ-03-123 (500 nM-2 μM; 10 min) selectively induces the formation of a ternary complex between CDK6 and CRBN in CRBN-deficient HEK293T cells (but fails to induce such a complex between CDK4 and CRBN), while pretreatment with Palbociclib (HY-50767) or lenalidomide (HY-A0003) blocks the formation of this complex^[1].
BSJ-03-123 (200 nM; 8-24 h) reduces the phosphorylation level of Rb at the S780 site in cultured cells in a CRBN-dependent manner, with an effect comparable to that of CDK4/6 inhibitors^[1].
BSJ-03-123 (3 μM; 72 h) regulates CD4+ effector T cell-mediated immune responses in human peripheral blood mononuclear cells (PBMCs), and supports the modulation of Th17/Treg balance associated with the pathogenesis of autoimmune uveitis^[3].
BSJ-03-123 (3 μM; 72 h) regulates IRBP-stimulated CD4⁺ T cell activity, including Th17 cell differentiation, in mouse CDLN cells^[3].

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