Trichostatin A (TSA)
Molecular Weight(MW): 302.4
Trichostatin A (TSA) is an HDAC inhibitor with IC50 of ~1.8 nM in cell-free assays.
Cited by 24 Publications
6 Customer Reviews
Gck expression in WT primary hepatocytes transduced with FOXO1 and KR-FOXO1 adenoviruses in the presence or absence of trichostatinA (TSA).
Cell, 2017, 171(4):824-835.e18. Trichostatin A (TSA) purchased from Selleck.
Effect of TSA, SAHA and silibinin alone and in combination on left panel: IF staining for p-histone H3 Ser 10 and p-MPM-2 Ser /Thr positive cells and a-tubulin for mitotic spindle and DAPI as nuclear stain in H1299 cells. Right panel: % positive p-histone H3 Ser 10 mitotic cells and expression of p-MPM-2 Ser /Thr protein levels in H1299 cells.
Epigenetics 2012 7(10):1161-72. Trichostatin A (TSA) purchased from Selleck.
HCT116 p53 null cells were treated with different HDACIs (1 μM TSA, 5 μM M344, 1 μM MS-275, 5 mM But, 10 mM VPA) for 24 h, and their expression of GRP78, PERK-eIF2α axis and ATF4, ATF3, CHOP and DR5 proteins.
Biochem Biophys Res Commun 2014 10.1016/j.bbrc.2014.01.184. Trichostatin A (TSA) purchased from Selleck.
(B) The mRNA level of PRRT2 in the presence of different concentrations of DAC and TSA.
Biochem Biophys Res Commun, 2017, 485(2):454-460. Trichostatin A (TSA) purchased from Selleck.
Purity & Quality Control
Choose Selective HDAC Inhibitors
|Description||Trichostatin A (TSA) is an HDAC inhibitor with IC50 of ~1.8 nM in cell-free assays.|
Trichostatin A inhibits the proliferation of eight breast carcinoma cell lines including MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, and SK-BR-3 with mean IC50 of 124.4 nM (range, 26.4-308.1 nM), with more potency against cell lines that express ERα than the ERα-negative cell lines. Trichostatin A inhibits HDAC activity similarly in all the breast cancer cell lines with mean IC50 of 2.4 nM (range, 0.6-2.6 nM), and results in pronounced histone H4 hyperacetylation.  Unlike Trapoxin (TPX) and Chlamydocin which potently inhibit HDAC1 or HDAC4 but not HDAC6, Trichostatin A inhibits these HDACs to a similar extent with IC50 of 6 nM, 38 nM, and 8.6 nM, respectively.  Trichostatin A (100 ng/mL) treatment induces the expression of transforming growth factor β type II receptor (TβRII) in MIA PaCa-2 cells through the recruitment of p300 and PCAF into a Sp1-NF-Y HDAC complex that binds the DNA element of TβRII promoter, which is associated with a concomitant acetylation of Sp1 and an overall decrease in the amount of HDAC associated with the complex. 
|In vivo||Administration of Trichostatin A at 0.5 mg/kg for 4 weeks displays potent antitumor activity in the N-methyl-N-nitrosourea carcinogen-induced rat mammary carcinoma model, without any measurable toxicity at doses up to 5 mg/kg.  Single intraperitoneal doses of 10 mg/kg Trichostatin A in nontransgenic and spinal muscular atrophy (SMA) model mice results in increased levels of acetylated H3 and H4 histones and modest increases in survival motor neuron (SMN) gene expression. Administration of Trichostatin A at 10 mg/kg/day improves survival, attenuates weight loss, and enhances motor behavior in the SMA model mice. |
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.
-  Vigushin DM, et al. Clin Cancer Res, 2001, 7(4), 971-976.
-  Furumai R, et al. Proc Natl Acad Sci U S A, 2001, 98(1), 87-92.
-  Kim MS, et al. Cancer Res, 2003, 63(21), 7291-7300.
|In vitro||DMSO||23 mg/mL (76.05 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03735173||Not yet recruiting||Arthropathy Shoulder|Shoulder Pain|Shoulder Osteoarthritis|Shoulder Arthritis|Shoulder Arthropathy Associated With Other Conditions|Necrosis of Bone|Arthritis|Inflammatory Arthritis||Mayo Clinic||December 1 2018||Not Applicable|
|NCT02959905||Unknown status||Metastatic Melanoma||BGI China|Sun Yat-sen University||December 2016||Phase 1|
|NCT03133819||Enrolling by invitation||Diabetes; Neuropathy Polyneuropathy (Manifestation)||Chang Gung Memorial Hospital||November 2016||Not Applicable|
|NCT02486965||Recruiting||Fibromyalgia||University Hospital Brest||October 2015||Not Applicable|
|NCT01954433||Active not recruiting||Glenohumeral Arthritis and/or Rotator Cuff Tear Arthropathy (TSA)|Rotator Cuff Tear (RCR)|Trapeziometacarpal Osteoarthritis (TMC OA)||Matthias Flury|Winterthur Institute of Health Economics (WIG) Switzerland|Schulthess Klinik||November 2013||--|
|NCT01575106||Completed||Pain||Massachusetts General Hospital||June 2012||Not Applicable|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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Frequently Asked Questions
I would like to obtain the enantiomers of TSA, as separate chemicals: R-TSA and S-TSA. Do you have any ideas?
Our S1045 Trichostatin A (TSA) is R enantiomer.