mm1s

BRD9876 是一种 MM1S 生长的选择性抑制剂，可将驱动蛋白 5 锁定在增强微管结合的状态，从而导致 MT 的捆绑和稳定。它特异性靶向微管结合的 Eg5，选择性抑制 CD34 细胞的骨髓瘤，有用于多发性骨髓瘤的研究潜力。

KDOAM-25 citrate 是有效且具有高选择性的组蛋白赖氨酸脱甲基酶 5 (KDM5) 抑制剂，对 KDM5A，KDM5B，KDM5C，KDM5D 的IC50分别为 71 nM，19 nM，69 nM，69 nM。用KDOAM-25 citrate 处理的多发性骨髓瘤 MM1S 细胞显示转录起始位点的整体 H3K4 甲基化增加，增殖受损。

KDOAM-25 trihydrochloride increases global H3K4 methylation at transcriptional start sites and impairs proliferation in multiple myeloma MM1S cells. KDOAM-25 trihydrochloride is a potent and highly selective histone lysine demethylases 5 (KDM5) inhibitor

KDOAM-25, a potent and highly selective inhibitor of histone lysine demethylases 5 (KDM5) with IC50 values of 71 nM for KDM5A, 19 nM for KDM5B, 69 nM for KDM5C, and 69 nM for KDM5D, enhances global H3K4 methylation at transcriptional start sites and reduces proliferation in multiple myeloma MM1S cells.

Potent and selective cereblon degrader (DC50 = 1.5 nM). Induces complete degradation of cereblon in MM1S cells. Comprises a cereblon E3 ligase ligand joined by a linker to a ligand for the E3 ligase VHL. Cell-permeable. Steinebach et al (2019) PROTAC-mediated crosstalk between E3 ligases. Chem.Commun.(Camb) 55 1821 PMID:30672516

KDOAM-25 trihydrochloride 是一种有效的、高度选择性的组蛋白赖氨酸脱甲基酶 5 (KDM5) 抑制剂，能够作用于 KDM5A (IC50: 71 nM)、KDM5B (IC50: 19 nM)、KDM5C (IC50: 69 nM)、KDM5D (IC50: 69 nM)。KDOAM-25 trihydrochloride 能够提高转录起始位点的整体 H3K4 甲基化，可阻碍多发性骨髓瘤 MM1S 细胞的增殖。