Trichostatin A

SKU: orb1300918

Description

Trichostatin A is a potent and reversible histone deacetylase (HDAC) inhibitor that induces histone hyperacetylation, altering chromatin structure. It is widely used in epigenetic research for studying gene expression, cell cycle, and differentiation in both cellular and animal models.

Research Area

Epigenetics & Chromatin, Molecular Biology

Key Properties

• CAS Number: 58880-19-6
• MW: 302.37
• Purity: 98.59% (May vary between batches)
• Formula: C₁₇H₂₂N₂O₃
• SMILES: C[C@H](\C=C(/C)\C=C\C(=O)NO)C(=O)c1ccc(cc1)N(C)C
• Target: HDAC
• Solubility: DMSO:50 mg/mL (165.36 mM);Ethanol:3 mg/mL (9.92 mM)

Bioactivity

• Target IC50:
  HeLa cells:20 nM|MDA-MB-231 cells:500 nM|MCF-7 cells:500 nM|HDAC:1.8 nM|HDAC1:6.0 ± 2.5 nM|HDAC4:38 ± 4 nM|HDAC6:8.6 ± 1.4 nM|HDAC (Vascular Smooth Muscle cells):0.08 μM
• 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. 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.
• 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). 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. 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.
• 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)

Storage & Handling

• Storage: store at low temperature | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Histone deacetylases, HDAC, Inhibitor, inhibit, Trichostatin A, TSA

Compound Identifiers

PubChem CID

444732