BML-210

BML-210 is a potent HDAC inhibitor. BML-210 can inhibit the HDAC4-VP16-driven reporter signal with an apparent IC₅₀ of ∼5 µM. BML-210 has a specific disruptive effect on the HDAC4:MEF2 interaction. BML-210 causes an increase in the G0/G1 phase. BML-210 induces apoptosis and displays antitumour activities in orthotopic mammary tumours in mice^[1][2][3]. In Vitro:BML-210 (10, 20 μM; 24, 48 hours) inhibits cell proliferation and growth inhibition of NB4 cells^[2].
BML-210 (10, 20 μM; 24, 48 hours) causes a decrease in the proportion of NB4 cells in the S phase and an increase in the G0/G1 phase^[2].
BML-210 (10, 20 μM; 24, 48 hours) causes cytotoxic effects on NB4 cells at 20 μM. BML-210 at a dose of 10 μM induces apoptotic cell death^[2].
BML-210 (10, 20 μM; 24, 48 hours) inhibits HDAC Expression and Activity in NB4 Cells^[2].
BML-210 (1.0 μM; for 48 h) causes higher expression levels differential expressed genes (DEGs) in mouse EO771 cells^[3].
BML-210 does not reduce the expression of HDAC4-VP16^[1].
In Vivo:BML-210 (20 mg/kg; IP; three times per week for two weeks) notably suppresses the tumour growth and weight. BML-210 has no effect on tumour growth and weight in the immune-deficient nude (Nu/J) mice^[3].