Trichostatin A (58880-19-6) is a potent and selective histone deacetylase (HDAC) inhibitor (Ki = 3.4 nM). Induces reversion of ras transformed cells to normal morphology. Trichostatin A induces dedifferentiation of primordial germ cells into embryonic germ cells. Cell permeable and active in vivo.
Trichostatin A, ready-made solution has been used:
- as a histone deacetylase inhibitor to study its effect on transcriptome changes by stem cell testing
- to inhibit histone deacetylase (HDAC) class I, II, or III in primary pituitary cell cultures and to investigate insulin control of endogenous human growth hormone gene (hGH)
- to treat cells for the HDAC inhibition experiments
Trichostatin A is a histone deacetylase inhibitor that enhances the cytotoxic efficacy of anticancer drugs that target DNA. Trichostatin A displays antifungal, antiprotozoan and antitumour activity
Trichostatin A is a known inhibitor of fibrosis in vitro and in vivo, and is used as an anticancer agent. Potent differentiation inducer of friend leukemic cells.
ChEBI: Trichostatin A is an antibiotic antifungal agent, a trichostatin and a hydroxamic acid. It has a role as a bacterial metabolite, a geroprotector and an EC 3.5.1.98 (histone deacetylase) inhibitor. It is functionally related to a (R)-trichostatic acid.
Trichostatin A is a compound of primary hydroxamic acid.
Selective and potent inhibitor of histone deacetylase (K i = 3.4 nM). Active in vivo . Potential anti-cancer agent. Induces accelerated dedifferentiation of primordial germ cells (PGCs) into embryonic germ (EG) cells.
Inhibits histone deacetylase at nanomolar concentrations; resultant histone hyperacetylation leads to chromatin relaxation and modulation of gene expression. May be involved in cell cycle progression of several cell types, inducing cell growth arrest at both G and G/M phases; may induce apoptosis. Enhances the efficacy of anticancer agents that target DNA.
Trichostatin A is an antifungal antibiotic derived from Streptomyces that inhibits mammalian histone deacetylases. When used at nanomolar concentrations, trichostatin A causes the accumulation of acetylated histones in a quite specific and reversible manner. Trichostatin A has also been shown to inhibit both G1- and G2-phases of the mammalian cell cycle and has been tested for use as a potential anticancer agent.
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[2] M FUTAMURA. Trichostatin A inhibits both ras-induced neurite outgrowth of PC12 cells and morphological transformation of NIH3T3 cells.[J]. Oncogene, 1995, 10 6: 1119-1123.
[3] GABRIELA DURCOVA-HILLS. Reprogramming primordial germ cells into pluripotent stem cells.[J]. PLoS ONE, 2008, 3 10: e3531. DOI:
10.1371/journal.pone.0003531
