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Inhibition of histone deacetylase (HDAC) enzymes by compounds such as trichostatin A can have wide ranging effects in cancer, cell differentiation, and other aspects of gene expression regulation. BML-210 is a small molecule inhibitor of HDAC with an IC₅₀ value of 30 μM when tested in HeLa cell nuclear extracts using 200 μM acetylated fluorometric substrate (substrate available in Cayman’s HDAC Activity and Inhibitor Screening Assay Kits - Item Nos. 10011563 and 10011564).

N1-(2-Aminophenyl)-N8-phenyloctanediamide is a histone deacetylase (HDAC) inhibitor, an anti-cancer target for breast cancer therapeutic intervention.

ChEBI: A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and 1,2-diaminobenzene.

BML-210 is a synthetic benzamide and is a potential tumor inhibitor. It is used as a therapeutic agent to treat promyelocytic leukemia. In human leukemia cell lines (NB4, HL-60, THP-1, and K562), BML-210 modulates histone deacetylase and promotes apoptosis. BML-210 favors frataxin expression in neurodegenerative disease Friedreich′s ataxia (FRDA). It interacts with myocyte enhancer factor-2 (MEF2) via hydrogen-bonding and prevents histone deacetylase 4 (HDAC4) binding.

HDAC4:MEF2

1) Savickiene, et al. (2006), The novel histone deacetylase inhibitor BML-210 exerts growth inhibitory, proapoptotic and differentiation stimulating effects on the human leukemia cell lines; Eur. J. Pharmacol. 549 9 2) Herman, et al. (2006), Histone deacetylase inhibitors reverse gene silencing in Friedreich’s ataxia; Nat. Chem. Biol. 10 551