KDOAM-25 trihydrochloride 

KDOAM-25 trihydrochloride is a potent and highly selective histone lysine demethylases 5 (KDM5) inhibitor with IC₅₀s of 71 nM, 19 nM, 69 nM, 69 nM for KDM5A, KDM5B, KDM5C, KDM5D, respectively. KDOAM-25 trihydrochloride increases global H3K4 methylation at transcriptional start sites and impairs proliferation in multiple myeloma MM1S cells^[1].

IC50: 71 nM (KDM5A), 19 nM (KDM5B), 69 nM (KDM5C), 69 nM (KDM5D)^[1]

KDOAM-25 trihydrochloride inhibits most potently KDM5B with an IC₅₀ of ∼50 μM and the other KDM5 family members at concentrations above 100 μM. KDOAM-25 trihydrochloride shows no cellular activity on any of the other tested JmjC family members^[1].
KDOAM-25 trihydrochloride is able to reduce the viability of MM1S cells with an IC₅₀ of ∼30 μM after a delay of 5-7 days^[1].
KDOAM-25 trihydrochloride treatment results in a G1 cell-cycle arrest with an increased proportion of MM1S in G1 and a decrease of the proportion of cells in G2 without an increase in the proportion of cells in the apoptotic sub-G1 phase^[1].
KDOAM-25 trihydrochloride (50 μM) increases with approximately twice as much H3K4me3 in in multiple myeloma cells^[1].

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

416.77

C₁₅H₂₈Cl₃N₅O₂

NC(C1=CC=NC(CNCC(N(CC)CCN(C)C)=O)=C1)=O.Cl.Cl.Cl

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Tumber A, et al. Potent and Selective KDM5 Inhibitor Stops Cellular Demethylation of H3K4me3 at Transcription Start Sites and Proliferation of MM1S Myeloma Cells. Cell Chem Biol. 2017 Mar 16;24(3):371-380.  [Content Brief]