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Merck
CN

V900931

Trichostatin A 

From Streptomyces sp., ≥98%, HDAC inhibitor

Synonym(s):

Trichostatin A, TSA, [R-(E,E)]-7-[4-(Dimethylamino)phenyl]-N-hydroxy-4,6-dimethyl-7-oxo-2,4-heptadienamide

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About This Item

Empirical Formula (Hill Notation):
C17H22N2O3
CAS Number:
58880-19-6
Molecular Weight:
302.37
MDL number:
MFCD03848392
UNSPSC Code:
12352200
PubChem Substance ID:
329830233

Key Documents

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Product Name

Trichostatin A , Vetec™, reagent grade, from Streptomyces sp., ≥98%

biological source

Streptomyces sp.

grade

reagent grade

product line

Vetec™

Assay

≥98%

storage temp.

−20°C

SMILES string

C[C@H](\C=C(C)\C=C\C(=O)NO)C(=O)c1ccc(cc1)N(C)C

InChI

1S/C17H22N2O3/c1-12(5-10-16(20)18-22)11-13(2)17(21)14-6-8-15(9-7-14)19(3)4/h5-11,13,22H,1-4H3,(H,18,20)/b10-5+,12-11+/t13-/m1/s1

InChI key

RTKIYFITIVXBLE-QEQCGCAPSA-N

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Biochem/physiol Actions

Trichostatin A (TSA) 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 serves as an epigenetic modifier.
Trichostatin A inhibits histone deacetylase at nanomolar concentrations; resultant histone hyperacetylation leads to chromatin relaxation and modulation of gene expression.

Legal Information

Vetec is a trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

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Certificates of Analysis (COA)

Lot/Batch Number
WXBF7482V
WXBF5307V
WXBF3804V
WXBF0575V
WXBF1295V

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Harriet E Jackson et al.
Skeletal muscle, 5(1), 2-2 (2015-02-12)
The transcription factor Sox6 has been implicated in regulating muscle fiber type-specific gene expression in mammals. In zebrafish, loss of function of the transcription factor Prdm1a results in a slow to fast-twitch fiber type transformation presaged by ectopic expression of
Masato Yuasa et al.
The Journal of clinical investigation, 125(8), 3117-3131 (2015-07-28)
Bone formation during fracture repair inevitably initiates within or around extravascular deposits of a fibrin-rich matrix. In addition to a central role in hemostasis, fibrin is thought to enhance bone repair by supporting inflammatory and mesenchymal progenitor egress into the
Gavin Rumbaugh et al.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 40(10), 2307-2316 (2015-04-04)
Histone deacetylases (HDACs) are promising therapeutic targets for neurological and psychiatric disorders that impact cognitive ability, but the relationship between various HDAC isoforms and cognitive improvement is poorly understood, particularly in mouse models of memory impairment. A goal shared by
Anni Niskakoski et al.
Epigenetics, 9(12), 1577-1587 (2015-01-28)
Diagnosis and treatment of epithelial ovarian cancer is challenging due to the poor understanding of the pathogenesis of the disease. Our aim was to investigate epigenetic mechanisms in ovarian tumorigenesis and, especially, whether tumors with different histological subtypes or hereditary
Hannes Hartman et al.
Digestive diseases and sciences, 60(5), 1284-1289 (2014-12-11)
The onset of acute pancreatitis (AP) is characterized by early protease activation followed by inflammation and organ damage, but the mechanisms are poorly understood. We hypothesized that histone deacetylase (HDAC) inhibition might exert protective effects on AP and investigated the
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