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    Trichostatin A (TSA)
    Trichostatin A (TSA)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0258
    CAS #: 58880-19-6Purity ≥98%

    Description: Trichostatin A (also called TSA) is a novel, potent and specific inhibitor of histone deacetylase (HDAC) with potential anticancer activity. It inhibits HDAC with an IC50 value of 1.8 nM. It is also an antifungal antibiotic agent with cytostatic and differentiating properties that noncompetivively and reversibly inhibits HDAC, at low nanomolar concentrations, in both cultured mammalian cells and fractionated cell nuclear extracts. According to a study investigating the effect of TSA in human breast cancer cell lines, TSA inhibited proliferation of breast carcinoma cell lines (IC50 124.4 ± 120.4 nM), comparing to all cell lines (IC50 2.4 ± 0.5 nM), and resulted in pronounced histone H4 hyperacetylation.

    References: Clin Cancer Res. 2001 Apr;7(4):971-6; J Clin Invest. 2007 Mar;117(3):659-71; Cancer Res. 2003 Nov 1;63(21):7291-300.

    Related CAS #: 122292-85-7 (S-isomer); 58880-19-6 (R-isomer)

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    Molecular Weight (MW)302.4
    FormulaC17H22N2O3
    CAS No.58880-19-6 (R-isomer) 122292-85-7 (S-isomer)  
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 23 mg/mL (76.1 mM) 
    Water: <1 mg/mL
    Ethanol:  <1 mg/mL
    Solubility (In vivo)1% DMSO+30% polyethylene glycol+1% Tween 80, pH 4: 6 mg/mL
    SynonymsTSA; (+)-Trichostatin A; Trichostatin A; Trichostatin A (R-isomer).


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    In Vitro

    In vitro activity: 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.


    Kinase Assay: 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 Assay:  Cells (MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, and SK-BR-3) 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.

    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.
    Animal modelInbred virgin female (Ludwig/Wistar/Olac) rats bearing tumors induced with NMU
    Formulation & DosageDissolved in DMSO; 5 mg/kg/day; s.c. injection
    References

    Clin Cancer Res. 2001 Apr;7(4):971-6; J Clin Invest. 2007 Mar;117(3):659-71; Cancer Res. 2003 Nov 1;63(21):7291-300.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

     

    Trichostatin A (TSA)

     

    Trichostatin A (TSA)

    Trichostatin A (TSA)

     
    Trichostatin A (TSA)
    TSA increases survival, attenuates weight loss, and enhances motor behavior of SMA mice. J Clin Invest. 2007 Mar;117(3):659-71.
    Trichostatin A (TSA)


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