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Trichostatin A (TSA), is an antifungal antibiotic. It’s cytostatic and differentiating properties are utilized in mammalian cell culture. It is a potent and specific, nonselective HDAC inhibitor, shown to have anti-inflammatory and neuroprotective properties. It inhibits all class I and class II HDAC’s and induces histone acetylation. TSA interacts reversibly with the HDAC catalytic site preventing binding of the substrate. HDACs - Classes I, II, and IV all require a zinc molecule as an essential cofactor in their active site and are inhibited by Zn2+-binding HDAC inhibitor - Trichostatin A (TSA). 

Studies have shown antiproliferative and HDAC inhibitory activity of TSA in vitro, in human breast cancer cell lines. its antitumor efficacy and toxicity has been studied in vivo in a carcinogen-induced rat mammary cancer model, which provided evidence for potent dose-dependent antitumor activity of TSA against breast cancer in vitro and in vivo. These studies strongly support HDAC as a molecular target for anticancer therapy in breast cancer.

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