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Trichostatin A

Trichostatin A
Trichostatin A (TSA), a natural derivative of diene isohydroxamic acids, is a specific and reversible histone deacetylase inhibitor (IC50=1.8 nM) that induces hyperacetylation of core histones to regulate chromatin structure.
Catalog No. T6270Cas No. 58880-19-6
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Purity:98.3%
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Trichostatin A

Purity: 98.3%
Catalog No. T6270Alias TSACas No. 58880-19-6

Trichostatin A (TSA), a natural derivative of diene isohydroxamic acids, is a specific and reversible histone deacetylase inhibitor (IC50=1.8 nM) that induces hyperacetylation of core histones to regulate chromatin structure.
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Pack SizePriceAvailabilityQuantity
1 mg$86In Stock
2 mg$112In Stock
5 mg$197In Stock
10 mg$373In Stock
25 mg$522In Stock
50 mg$755In Stock
1 mL x 10 mM (in DMSO)$183In Stock
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Product Introduction

Bioactivity
Description
Trichostatin A (TSA), a natural derivative of diene isohydroxamic acids, is a specific and reversible histone deacetylase inhibitor (IC50=1.8 nM) that induces hyperacetylation of core histones to regulate chromatin structure.
Targets&IC50
HDAC:1.8 nM
In vitro
METHODS: Eight breast cancer cells MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51 and SK-BR-3 were treated with Trichostatin A (10-12 -10-5 M) for 96 h. The viability of the cells was determined by SRB. Cell viability was determined by SRB
RESULTS: Trichostatin A inhibited the proliferation of eight breast cancer cell lines with a mean IC50=124.4±120.4 nM (range 26.4-308.1 nM). [1]
METHODS: Esophageal squamous cell carcinoma cells EC9706 and EC1 were treated with Trichostatin A (0.3-1 μM) for 48 h. Apoptosis was detected using Flow Cytometry.
RESULTS: There was no significant increase in the percentage of early apoptosis at 0.3 and 0.5 μM Trichostatin A doses. However, 1.0 μM Trichostatin A treatment significantly induced early apoptosis compared with control. In addition, the percentage of mid- and late-stage apoptosis increased in a concentration-dependent manner. [2]
METHODS: Esophageal squamous cell carcinoma cells EC9706 and EC1 were treated with Trichostatin A (0.3-1 μM) for 60 min, and the expression levels of target proteins were detected using Western Blot.
RESULTS: Trichostatin A decreased the protein levels of PI3K as well as p-Akt and p-ERK1/2 in a dose-dependent manner. acetylation of histone H4 was increased in a concentration-dependent manner. [2]
In vivo
METHODS: To assay antitumor activity in vivo, Trichostatin A (500 μg/kg) was injected subcutaneously into rats with NMU-induced mammary carcinoma tumors once daily for four weeks.
RESULTS: Trichostatin A showed significant antitumor activity in vivo. tumors in Trichostatin A-treated rats had benign phenotypes, fibroadenomas or tubular adenomas, suggesting that the antitumor activity of Trichostatin A may be attributable to induction of differentiation. [1]
METHODS: To assay antitumor activity in vivo, Trichostatin A (0.5-1 mg/kg twice weekly) and Quercetin (10 mg/kg three times weekly) were injected intraperitoneally into nude mice bearing human lung adenocarcinoma tumor A549 for thirteen weeks.
RESULTS: High-dose Trichostatin A significantly inhibited tumor growth, while low-dose Trichostatin A and Quercetin alone had no effect. However, the combination of low-dose Trichostatin A and Quercetin significantly inhibited tumor growth. [3]
Kinase Assay
In vitro HDAC activity: Total cellular extracts are prepared from each breast cancer cell line (MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, or SK-BR-3). A 20 μL crude cell extract (~2.5 ×105 cells), in the presence of varying concentrations of Trichostatin A in 0.1% (v/v) ethanol or 0.1% (v/v) ethanol as vehicle control, are incubated for 60 minutes at 25 °C with 1 μL (~1.5 × 106 cpm) of [3H]acetyl-labeled histone H4 peptide substrate (NH2-terminal residues 2-20) that has been acetylated with [3H]acetic acid, sodium salt (3.7 GBq/mmol) by an in vitro incorporation method. Each 200 μL reaction is quenched with 50 μL of 1 M HCl/0.16 M acetic acid and extracted with 600 μL of ethyl acetate, and released [3H]acetate is quantified by scintillation counting. IC50 values are determined graphically using nonlinear regression to fit inhibition data to the appropriate dose-response curve.
Cell Research
Cells are exposed to various concentrations of Trichostatin A for 96 hours. After treatment, cell proliferation is estimated using the sulforhodamine B colorimetric assay. Cell viability is determined by trypan blue exclusion. (Only for Reference)
AliasTSA
Chemical Properties
Molecular Weight302.37
FormulaC17H22N2O3
Cas No.58880-19-6
Storage & Solubility Information
Storagestore at low temperature,store under nitrogen | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
Solubility Information
DMSO: 50 mg/mL (165.36 mM), Sonication is recommended.
Ethanol: 3 mg/mL (10 mM)
Solution Preparation Table
Ethanol/DMSO
1mg5mg10mg50mg
1 mM3.3072 mL16.5360 mL33.0721 mL165.3603 mL
5 mM0.6614 mL3.3072 mL6.6144 mL33.0721 mL
10 mM0.3307 mL1.6536 mL3.3072 mL16.5360 mL
DMSO
1mg5mg10mg50mg
20 mM0.1654 mL0.8268 mL1.6536 mL8.2680 mL
50 mM0.0661 mL0.3307 mL0.6614 mL3.3072 mL
100 mM0.0331 mL0.1654 mL0.3307 mL1.6536 mL

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