Trichostatin A Inhibitor CAS No. 58880-19-6

Cat. No.	Name	Size	Price
KI0156	Trichostatin A	5 mg	$472
	Trichostatin A	10 mg	$752
	Trichostatin A	50 mg	$3000

Chemical Characteristic

Product Name	Trichostatin A
CAS No.	58880-19-6
Molecular Weight	302.4
Formula	C₁₇H₂₂N₂O₃
Chemical Name	(R,2E,4E)-6-(4-(dimethylamino)benzoyl)-N-hydroxy-4-methylhepta-2,4-dienamide
Smiles	C(=O)(/C=C/C(=C/[C@H](C(=O)c1ccc(cc1)N(C)C)C)/C)NO
Chemical Structure

Biological activities

Trichostatin A is a potent and specific inhibitor of the histone deacetylase (HDAC). Trichostatin A inhibits HDAC1, HDAC4, HDAC6, with IC50s of 6.0, 38, 8.6 nM, respectively. Trichostatin A also induces an arrest of the cell cycle, and higher concentrations of trichostatin A induce the cell cycle arrest in HeLa cells. ^[1] In vitro, the partially purified histone deacetylase from wild-type FM3A cells is effectively inhibited by trichostatin A in a noncompetitive manner with K_{i of 3.4 nM. Trichostatin A causes the accumulation of acetylated histones in mammalian cells. Trichostatin A also causes the induction of Friend cell differentiation and specific inhibition of the cell cycle of normal rat fibroblasts in the Gl and G2 phases at the very low concentrations. Trichostatin A markedly prolongs the in vivo half life of the labile acetyl groups on histones in mouse mammary gland tumor cells, FM3A. The histone deacetylase preparation from the mutant shows decreased sensitivity to trichostatin A with Ki of 31 nM. ^[2] Trichostatin A increases activation of a survival motor neuron 2 (SMN2) promoter reporter by approximately 2-fold with an EC50 of 17 nM in a transgenic motor neuronal cell line. Trichostatin A treatment causes increased expression of myogenin, a marker of terminal muscle cell differentiation. ^[3] Trichostatin A enhances global histone acetylation levels and reduces global DNA methylation. Trichostatin A treatment induces expression of E-CADHERIN in human bladder cancer T24 and breast cancer MDA-MB231 cells. Trichostatin A stimulates acetylation of histones associated with E-CADHERIN. Trichostatin A induces global hypomethylation in the absence of DNA replication. ^[4] In vivo, trichostatin A treatment can inhibits the release of the incorporated [3H] acetyl groups in histones. And nanomolar concentrations of trichostatin A cause a marked accumulation of highly acetylated histones. ^[2] A single dose of trichostatin A increases histone acetylation and SMN gene expression in mice. And, repeated doses of trichostatin A also increase SMN2 gene expression, SMN protein levels, and small nuclear ribonucleoprotein (snRNP) assembly activity in spinal muscular atrophy (SMA) mice. Trichostatin A treatment improves survival of SMA mice when started after disease onset. ^[3]}

Protocols

Trichostatin A is dissolved in DMSO to a concentration of 2 or 4 µg/ µL. ^[3]

References

[1] Furumai R, et al. Potent histone deacetylase inhibitors built from trichostatin A and cyclic tetrapeptide antibiotics including trapoxin. Proc Natl Acad Sci U S A. 2001, 98(1): 87-92. [2] Yoshida M, et al. Potent and specific inhibition of mammalian histone deacetylase both in vivo and in vitro by trichostatin A. Tanpakushitsu Kakusan Koso. 2007, 52(13 Suppl): 1788-1789. [3] Avila AM, et al. Trichostatin A increases SMN expression and survival in a mouse model of spinal muscular atrophy. J Clin Invest. 2007, 117(3): 659-671. [4] Ou JN, et al. Histone deacetylase inhibitor Trichostatin A induces global and gene-specific DNA demethylation in human cancer cell lines. Biochem Pharmacol. 2007, 73(9): 1297-1307.

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