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    Tubastatin A HCl (AG-CR-13900, TubA)
    Tubastatin A HCl (AG-CR-13900, TubA)

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    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V0281
    CAS #: 1310693-92-5Purity ≥98%

    Description: Tubastatin A HCl, the hydrochloride salt of Tubastatin A (also known as TubA, AG-CR-13900), is a tubacin analog that acts as a potent and specific inhibitor of histone deacetylase 6 (HDAC6) with potential antitumor, neuroprotective and anti-inflammatory activities. It exhibits the highest selectivity (>1,000-fold) for inhibiting HDAC6 over other HDAC isoforms excluding HDAC8 for which the IC50 is 0.9 μM. 

    References: J Am Chem Soc. 2010 Aug 11;132(31):10842-6; Mol Cell Biol. 2011 May;31(10):2066-78; PLoS One. 2011;6(12):e28563.

    Related CAS #1310693-92-5 (HCl); 1252003-15-8 (free base)

    Publications Citing Use of InvivoChem Tubastatin A HClScientific Reports | (2020) 10:6064 |

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    Molecular Weight (MW)371.86
    CAS No.1310693-92-5
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 74 mg/mL (199.0 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)1% DMSO+30% polyethylene glycol+1% Tween 80: 30 mg/mL

    AG-CR-13900, TubA; Tubastatin A hydrochloride; Tubastatin A HCl; TSA HCl

    Chemical Name: N-hydroxy-4-((2-methyl-3,4-dihydro-1H-pyrido[4,3-b]indol-5(2H)-yl)methyl)benzamide hydrochloride


    InChi Code: InChI=1S/C20H21N3O2.ClH/c1-22-11-10-19-17(13-22)16-4-2-3-5-18(16)23(19)12-14-6-8-15(9-7-14)20(24)21-25;/h2-9,25H,10-13H2,1H3,(H,21,24);1H

    SMILES Code: O=C(NO)C1=CC=C(CN2C3=C(CN(C)CC3)C4=C2C=CC=C4)C=C1.[H]Cl 

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    In Vitro

    In vitro activity: Tubastatin A is substantially selective for all 11 HDAC isoforms and maintains over 1000-fold selectivity against all isoforms excluding HDAC8, where it has approximately 57-fold selectivity. In homocysteic acid (HCA) induced neurodegeneration assays, Tubastatin A displays dose-dependent protection against HCA-induced neuronal cell death starting at 5 μM with near complete protection at 10 μM. At 100 ng/mL Tubastatin A increases Foxp3+ T-regulatory cells (Tregs) suppression of T cell proliferation in vitro. Tubastatin A treatment in C2C12 cells would lead to myotube formation impairment when alpha-tubulin is hyperacetylated early in the myogenic process; however, myotube elongation occurs when alpha-tubulin is hyeperacetylated in myotubes. A recent study indicates that Tubastatin A treatment increases cell elasticity as revealed by atomic force microscopy (AFM) tests without exerting drastic changes to the actin microfilament or microtubule networks in mouse ovarian cancer cell lines, MOSE-E and MOSE-L.

    Kinase Assay: Enzyme inhibition assays are performed by the Reaction Biology Corporation, Malvern, PA, using the Reaction Biology HDAC Spectrum platform. ( The HDAC1, 2, 4, 5, 6, 7, 8, 9, 10, and 11 assays use isolated recombinant human protein; HDAC3/NcoR2 complex is used for the HDAC3 assay. Substrate for HDAC1, 2, 3, 6, 10, and 11 assays is a fluorogenic peptide from p53 residues 379-382 (RHKKAc); substrate for HDAC8 is fluorogenic diacyl peptide based on residues 379-382 of p53 (RHKAcKAc). Acetyl-Lys (trifluoroacetyl)-AMC substrate is used for HDAC4, 5, 7, and 9 assays. Tubastatin A is dissolved in DMSO and tested in 10-dose IC50 mode with 3-fold serial dilution starting at 30 μM. Control Compound Trichostatin A (TSA) is tested in a 10-dose IC50 with 3-fold serial dilution starting at 5 μM. IC50 values are extracted by curve-fitting the dose/response slopes.

    Cell Assay: Primary cortical neuron cultures are obtained from the cerebral cortex of fetal Sprague-Dawley rats (embryonic day 17) as described previously. All experiments are initiated 24 hours after plating. Under these conditions, the cells are not susceptible to glutamate-mediated excitotoxicity. For cytotoxicity studies, cells are rinsed with warm PBS and then placed in minimum essential medium (Invitrogen) containing 5.5 g/L glucose, 10% fetal calf serum, 2 mM L-glutamine, and 100 μM cystine. Oxidative stress is induced by the addition of the glutamate analogue homocysteate (HCA; 5 mM) to the media. HCA is diluted from 100-fold concentrated solutions that are adjusted to pH 7.5. In combination with HCA, neurons are treated with Tubastatin A at the indicated concentrations. Viability is assessed after 24 hours by MTT assay (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) method.

    In VivoDaily treatment of Tubastatin A at 0.5mg/kg inhibits HDAC6 to promote Tregs suppressive activity in mouse models of inflammation and autoimmunity, including multiple forms of experimental colitis and fully major histocompatibility complex (MHC)-incompatible cardiac allograft rejection.
    Animal modelCD45RBhi CD4+ CD25- cells (1 × 106) from WT or HDAC6-/- mice Are injected i.p. into B6/Rag1-/-mice.
    Formulation & DosageSolubilized in DMSO; 0.5 mg/kg; i.p. injection

    J Am Chem Soc. 2010 Aug 11;132(31):10842-6; Mol Cell Biol. 2011 May;31(10):2066-78; PLoS One. 2011;6(12):e28563.

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


    Tubastatin A HCl

    Comparison of histone and α-tubulin hyperacetylation for TSA, Tubastatin A, and Tubacin. J Am Chem Soc. 2010 Aug 11;132(31):10842-6

    Tubastatin A HCl

    HCA oxidative stress assay: neurons were treated with Tubastatin A, with or without addition of HCA. J Am Chem Soc. 2010 Aug 11;132(31):10842-6

    Tubastatin A HCl


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