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Trichostatin A

Catalog No. T6270   CAS 58880-19-6
Synonyms: TSA

Trichostatin A (TSA) is a natural derivative of diene isohydroxamic acids. Trichostatin A is a histone deacetylase inhibitor (IC50=1.8 nM) that is reversible and specific. Trichostatin A leads to the hyperacetylation of core histones, which regulates chromatin structure.

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Trichostatin A Chemical Structure
Trichostatin A, CAS 58880-19-6
Pack Size Availability Price/USD Quantity
1 mg In stock $ 86.00
2 mg In stock $ 112.00
5 mg In stock $ 197.00
10 mg In stock $ 373.00
25 mg In stock $ 522.00
50 mg In stock $ 755.00
1 mL * 10 mM (in DMSO) In stock $ 183.00
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Purity: 98.3%
Purity: 98.05%
Purity: 97.35%
Purity: 97%
Purity: 96.32%
Purity: 96.03%
Purity: 96.01%
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Biological Description
Chemical Properties
Storage & Solubility Information
Description Trichostatin A (TSA) is a natural derivative of diene isohydroxamic acids. Trichostatin A is a histone deacetylase inhibitor (IC50=1.8 nM) that is reversible and specific. Trichostatin A leads to the hyperacetylation of core histones, which regulates 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)
Synonyms TSA
Molecular Weight 302.37
Formula C17H22N2O3
CAS No. 58880-19-6

Storage

store at low temperature,store under nitrogen

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 15.1 mg/mL (50 mM)

Ethanol: 3 mg/mL (10 mM)

TargetMolReferences and Literature

1. Vigushin DM, et al. Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer in vivo. Clin Cancer Res. 2001 Apr;7(4):971-6. 2. Ma J, et al. Trichostatin A, a histone deacetylase inhibitor, suppresses proliferation and promotes apoptosis of esophageal squamous cell lines. Mol Med Rep. 2015 Jun;11(6):4525-31. 3. Chan ST, et al. Quercetin enhances the antitumor activity of trichostatin A through upregulation of p53 protein expression in vitro and in vivo. PLoS One. 2013;8(1):e54255. 4. Huang W, et al. J Biol Chem, 2005, 280(11), 120047-120054. 5. Avila AM, et al. J Clin Invest, 2007, 117(3), 659-671. 6. Li X, Pan L, Wang B, et al. The Histone Deacetylases HosA and HdaA Affect the Phenotype and Transcriptomic and Metabolic Profiles of Aspergillus niger[J]. Toxins. 2019, 11(9): 520. 7. Meng Y, Qian X, Zhao L, et al. Trichostatin A downregulates bromodomain and extra-terminal proteins to suppress osimertinib resistant non-small cell lung carcinoma[J]. Cancer Cell International. 2021, 21(1): 1-12. 8. Xu K, Sun G, Li M, et al. Glibenclamide Targets Sulfonylurea Receptor 1 to Inhibit p70S6K Activity and Upregulate KLF4 Expression to Suppress Non-Small Cell Lung Carcinoma[J]. Molecular cancer therapeutics. 2019, 18(11): 2085-2096. 9. Su Q, Li T, He P F, et al. Trichostatin A ameliorates Alzheimer’s disease-related pathology and cognitive deficits by increasing albumin expression and Aβ clearance in APP/PS1 mice[J]. Alzheimer's Research & Therapy. 2021, 13(1): 1-15.

TargetMolCitations

1. Wang C, Huang M, Lin Y, et al.ENO2-derived phosphoenolpyruvate functions as an endogenous inhibitor of HDAC1 and confers resistance to antiangiogenic therapy.Nature Metabolism.2023: 1-22. 2. Liang X L, Ouyang L, Yu N N, et al.Histone deacetylase inhibitor pracinostat suppresses colorectal cancer by inducing CDK5-Drp1 signaling-mediated peripheral mitofission.Journal of Pharmaceutical Analysis.2023 3. Guo Q, Jing Y, Gao Y, et al.The PIF1/PIF3‐MED25‐HDA19 transcriptional repression complex regulates phytochrome signaling in Arabidopsis.New Phytologist.2023 4. Su Q, Li T, He P F, et al. Trichostatin A ameliorates Alzheimer’s disease-related pathology and cognitive deficits by increasing albumin expression and Aβ clearance in APP/PS1 mice. Alzheimer's Research & Therapy. 2021 Jan 4;13(1):7. doi: 10.1186/s13195-020-00746-8. 5. Yuting Meng,Xixi Qian,Li Zhao,Nan Li,Shengjie Wu,Baoan Chen,Tong Sun,Xuerong Wang Trichostatin A downregulates bromodomain and extra-terminal proteins to suppress osimertinib resistant non-small cell lung carcinoma. Cancer Cell International. 2021, 21(1): 1-12. 6. Zhang L, Shi J, Du D, et al. Ketogenesis acts as an endogenous protective programme to restrain inflammatory macrophage activation during acute pancreatitis. eBioMedicine. 2022, 78: 103959. 7. Li X, Pan L, Wang B, et al. The Histone Deacetylases HosA and HdaA Affect the Phenotype and Transcriptomic and Metabolic Profiles of Aspergillus niger. Toxins. 2019, 11(9): 520. 8. Xu K, Sun G, Li M, et al. Glibenclamide Targets Sulfonylurea Receptor 1 to Inhibit p70S6K Activity and Upregulate KLF4 Expression to Suppress Non-Small Cell Lung Carcinoma. Molecular cancer therapeutics. 2019, 18(11): 2085-2096. 9. Du T, Hu X, Hou Z, et al.Re-expression of epigenetically silenced PTPRR by histone acetylation sensitizes RAS-mutant lung adenocarcinoma to SHP2 inhibition.Cellular and Molecular Life Sciences.2024, 81(1): 1-14.

Related compound libraries

This product is contained In the following compound libraries:
Drug Repurposing Compound Library Microbial Natural Product Library Anti-Cancer Drug Library Anti-Cancer Clinical Compound Library Inhibitor Library Anti-Cancer Active Compound Library Natural Product Library for HTS Chromatin Modification Compound Library Natural Product Library RO5 Drug-like Natural Product Library

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Keywords

Trichostatin A 58880-19-6 Chromatin/Epigenetic DNA Damage/DNA Repair HDAC Histone deacetylases inhibit Inhibitor TSA inhibitor

 

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