Trichostatin A NEW
| Price | $86 | $112 | $197 |
| Package | 1mg | 2mg | 5mg |
| Supply Ability: | 10g |
| Update Time: | 2026-04-21 |
Product Details
| Product Name: Trichostatin A | CAS No.: 58880-19-6 |
| Purity: 98.59% | Supply Ability: 10g |
| Release date: 2026/04/21 |
Product Introduction
Bioactivity
| Name | Trichostatin A |
| 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. |
| 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) |
| 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. |
| 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] |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | DMSO : 50 mg/mL (165.36 mM), Sonication is recommended. Ethanol : 3 mg/mL (9.92 mM), Sonication is recommended. |
| Keywords | Trichostatin A | Inhibitor | inhibit | Histone deacetylases | HDAC |
| Inhibitors Related | Panobinostat | Theophylline monohydrate | Valproic acid sodium salt | Methoxyacetic acid | Sodium 4-phenylbutyrate | Acefylline | Manganese chloride (tetrahydrate) | Curcumin | Valproic Acid | Sodium butanoate | 4-Phenylbutyric acid | Theophylline |
| Related Compound Libraries | Anti-Tumor Natural Product Library | Rare Natural Product Library | Anti-Cancer Clinical Compound Library | Drug Repurposing Compound Library | Natural Product Library | Inhibitor Library | Microbial Natural Product Library | Natural Product Library for HTS | Anti-Aging Compound Library | Bioactive Compounds Library Max | Anti-Cancer Drug Library | Anti-Cancer Active Compound Library |
Company Profile Introduction
Target Molecule Corp. (TargetMol) is a global high-tech enterprise, headquartered in Boston, MA, specializing in chemical and biological research product and service to meet the research needs of global customers.
TargetMol has evolved into one of the biggest global compound library and small molecule suppliers and a customer based on 40+ countries. TargetMol offers over 80 types of compound libraries and a wide range of high-quality research chemicals including inhibitors, activator, natural compounds, peptides, inhibitory antibodies, and novel life-science kits, for laboratory and scientific use. Besides, virtual screening service is also available for customers who would like to conduct the computer-aided drug discovery.
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