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.
1) Yoshida et al. (1990), Potent and specific inhibition of mammalian histone deacetylase both in vivo and in vitro by trichostatin A ; J. Biol. Chem., 265 17174
2) Futamura et al. (1995), Trichostatin A inhibits both ras-induced neurite outgrowth of PC12 cells and morphological transformation of NIH3T3 cells; Oncogene, 10 1119
3) Durcova-Hills et al. (2008), Reprogramming Primordial Germ Cells into Pluripotent Stem Cells; PLoS-One, 3 e3531
