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

BRD9876 is a selective inhibitor of MM1S growth.

KDOAM-25 citrate is a potent and highly selective histone lysine demethylases 5 (KDM5) inhibitor with IC 50 s of 71 nM, 19 nM, 69 nM, 69 nM for KDM5A, KDM5B, KDM5C, KDM5D, respectively. Multiple myeloma MM1S cells treated with KDOAM-25 citrate show increased global H3K4 methylation at transcriptional start sites and impaired proliferation [1].

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 is a potent and highly selective inhibitor of histone lysine demethylase 5 (KDM5), acting on KDM5A (IC50: 71 nM), KDM5B (IC50: 19 nM), KDM5C (IC50: 69 nM), KDM5D (IC50: 69 nM). KDOAM-25 trihydrochloride enhances overall H3K4 methylation at the transcription start site and hinders the proliferation of multiple myeloma MM1S cells.