Trichostatin A

A potent and reversible inhibitor of histone deacetylase. Blocks cell cycle progression at the G1 phase in HeLa cells and induces a 12-fold increase in intracellular levels of gelsolin. Induces reversion of oncogenic ras-tranformed NIH 3T3 cells to a normal morphology. Inhibits IL-2 gene expression (IC₅₀ = 73 nM) in Jurkat cells and shows immunosuppressive activity in a mouse model. IC₅₀ = 6 nM for HDAC1; 38 nM for HDAC4, and 8.6 nM for HDAC6A.

A potent and reversible, cell-permeable inhibitor of histone deacetylase. Blocks cell cycle progression at the G₁ phase in HeLa cells and induces a 12-fold increase in intracellular levels of gelsolin. Induces reversion of oncogenic ras-transformed NIH/3T3 cells to a normal morphology. Inhibits IL-2 gene expression (IC₅₀ = 73 nM) in Jurkat cells and shows immunosuppressive activity in a mouse model. Down-regulates p57^kip2 in Hep 3Bcells. IC₅₀ = 6 nM for HDAC1; 38 nM for HDAC4, and 8.6 nM for HDAC6A. 10 mM (500 µg/165 µl) solution of Trichostatin A, Streptomyces sp. (Cat. No. 647926) in DMSO is also available.

Cell permeable: yes

Primary Target
histone deactylase

Product does not compete with ATP.

Reversible: yes

Target IC₅₀: 73 nM inhibiting IL-2 gene expressionin Jurkat cells

Toxicity: Harmful (C)

Following reconstitution in DMSO, aliquot and freeze (-20°C). Following reconstitution in ethanol, refrigerate (4°C). DMSO stock solutions are stable for up to 6 months at -20°C. Ethanol stock solutions are stable for up to 3 months at 4°C.

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Taunton, J., et al. 1996. Science 272, 408.
Futamura, M., et al. 1995. Oncogene 10, 1119.
Hoshikawa, Y., et al. 1994. Exp. Cell Res. 214, 189.

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