Tubastatin A

Catalog No.S8049

Tubastatin A Chemical Structure

Molecular Weight(MW): 335.4

Tubastatin A is a potent and selective HDAC6 inhibitor with IC50 of 15 nM in a cell-free assay. It is selective against all the other isozymes (1000-fold) except HDAC8 (57-fold).

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5 Customer Reviews

  • Control and MEC17 KD macrophages (RAW264.7) were treated with TBSA or DMSO for 12 hours followed by LPS treatment for indicated time. p38 phosphorylation were determined by immuno-blotting.

    Nat Commun 2014 5, 3479. Tubastatin A purchased from Selleck.

    Cells apoptosis was confirmed by H33342/PI double staining and representative images of PI-positive cells (red, top row) with H33342 counterstain (blue, middle row) are shown. TUB:Tubastatin A

    Cancer Lett, 2017, 391:89-99. Tubastatin A purchased from Selleck.

  • HDACs inhibited gefitinib-induced apoptosis in NSCLC cells via a decrease in BAX/Ku70 interaction. H358 cells were treated with 5 umol/L tubastatin A (tubA), 0.5 lmol/L gefitinib or a combination of inhibitors for 96 hr as indicated. Endogenous BAX immunoprecipitations were performed and subjected to immunoblotting with Ku70-specific and BAX-specific antibodies. IgG: irrelevant immunoglobulin, used as negative controls. Input: cell lysate not subjected to immunoprecipitation.

    Int J Cancer 2014 134(11):2560-71. Tubastatin A purchased from Selleck.

    J Biol Chem 2013 288(20), 14400-7. Tubastatin A purchased from Selleck.

  • J Biol Chem 2013 288(20), 14400-7. Tubastatin A purchased from Selleck.

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Biological Activity

Description Tubastatin A is a potent and selective HDAC6 inhibitor with IC50 of 15 nM in a cell-free assay. It is selective against all the other isozymes (1000-fold) except HDAC8 (57-fold).
HDAC6 [1]
(Cell-free assay)
15 nM
In vitro

Tubastatin A is selective at all isozymes except HDAC8 and maintains over 1000-fold selectivity against all isoforms excluding HDAC8, where it has approximately 57-fold selectivity. Tubastatin A preferentially induces α-tubulin hyperacetylation at 2.5 μM. Slight induction of histone hyperacetylation is seen for Tubastatin A at 10 μM. Tubastatin A displays dose-dependent protection against homocysteic acid-induced neuronal cell death starting at 5 μM with near complete protection at 10 μM. [1] Tubastatin A (10 μM) induces an increase in acetylated-α-tubulin levels and the restoration of primary cilia expression in the cholangiocarcinoma cell lines (18-fold); and the restoration of primary cilia correlated with downregulated Hedgehog (Hh) and MAPK signaling pathways, as well as decreased cell proliferation rates (in average by 50%) and invasion (by 40%). [2] Tubastatin A shows significant inhibition of TNF-α and IL-6 in LPS stimulated human THP-1 macrophages with an IC50 of 272 nM and 712 nM. Tubastatin A inhibits nitric oxide (NO) secretion in murine Raw 264.7 macrophages dose depenndently with an IC50 of 4.2 μM. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Sf9 cells M{G2dGZ2dmO2aX;uJIF{e2G7 M4j3ZmlvcGmkaYTpc44hd2ZiaIXtZY4hemWlb33ibY5idnRiSFTBR|Yh\XiycnXzd4VlKGmwIGPmPUBk\WyuczDpcoN2[mG2ZXSg[o9zKDJiaILzJJV{cW6pIGLIT2suSWNiZnz1c5Jw\2WwaXOgd5Vje3S{YYTlMEBKSzVyPUG1JI5ONg>? M4jWPFI{ODB7MkCz
human HeLa cells M1v4emZ2dmO2aX;uJIF{e2G7 NGfMRZM3KGh? MnLFTY5pcWKrdHnvckBw\iCKRFHDOkBqdiCqdX3hckBJ\UyjIHPlcIx{KGG|c3Xzd4VlKGG|IILl[JVkfGmxbjDpckBMPDBiaInw[ZJi[2W2eXzheIlwdiCxZjDhcJBp[S22dXL1cIlvKGmwY4XiZZRm\CCob4KgOkBpenNiYomgbY1ufW6xZnz1c5Jme2OnbnPlJIF{e2G7LDDJR|UxRTJwNTFOwG0v Ml\ENlU1PTR{N{C=
human Jurkat cells MVvDfZRwfG:6aXRCpIF{e2G7 NH\JeWE4OiCq NHPE[FBEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBLfXKtYYSgZ4VtdHNiYYPz[ZN{\WRiYYOg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UV{Bie3OjeTygTWM2OD1|LkO4JO69VS5? M{X3dlI1OzB2M{S4
human LNCAP cells MWTDfZRwfG:6aXRCpIF{e2G7 MmTJO|IhcA>? Mo[zR5l1d3SxeHnjbZR6KGGpYXnud5Qh[W6mcn;n[Y4u\GWyZX7k[Y51KGi3bXHuJGxPS0GSIHPlcIx{KGG|c3Xzd4VlKGG|IHfyc5d1cCCrbnjpZol1cW:wIHHmeIVzKDd{IHjyd{BjgSCPVGOgZZN{[XluIFnDOVA:OTBwOEig{txONg>? M1n1dVI1OzB2M{S4
human KB cells MnHkR5l1d3SxeHnjxsBie3OjeR?= MkW0O|IhcA>? MVXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDLRkBk\WyuczDh[pRmeiB5MjDodpMh[nliTWTTJIF{e2G7LDDJR|UxRTF2LkixJO69VS5? NFLhb3kzPTh7OUOzPC=>
mouse B16 cells M2DRRWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NGKxRndIem:5dHigbY5pcWKrdHnvckBw\iCvb4Xz[UBDOTZiY3XscJMhcW6ldXLheIVlKG[xcjC0PEBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUSwMlUh|ryPLh?= MUWyN|AxQTJyMx?=

... Click to View More Cell Line Experimental Data

In vivo Tubastatin A reduces the growth of cholangiocarcinoma in vivo. Tubastatin A (10 mg/kg) induces a 6-fold lower mean tumor weights in syngeneic rat orthotopic model of cholangiocarcinoma, and reduction of the ratios of tumor weight to liver weight and body weight (5- and 5.6-fold, respectively), as well as a greater frequency of ciliated cholangiocytes compared with controls (29% vs 1.4%). Tubastatin A significantly decreases the amount of PCNA-positive cells in the treated tumors compared with vehicle controls (34% vs 65%). [2] Tubastat A shows significant inhibition of paw volume at 30 mg/kg i.p. in a Freund's complete adjuvant (FCA) induced animal model of inflammation. Tubastat A (30 mg/kg i.p.) significant attenuates clinical scores (~ 70%), and IL-6 expression in paw tissues of collagen induced arthritis DBA1 mouse. [3]


Kinase Assay:[4]
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HDAC enzymatic assays:

Tubastatin A is dissolved and diluted in assay buffer (50 mM HEPES, pH 7.4, 100 mM KCl, 0.001% Tween-20, 0.05% BSA, and 20 μM tris(2-carboxyethyl)phosphine) to 6-fold of the final concentration. HDAC enzymes are diluted to 1.5-fold of the final concentration in assay buffer and pre-incubated with Tubastatin A for 10 minutes before the addition of the substrate. The amount of FTS (HDAC1, HDAC2, HDAC3, and HDAC6) or MAZ-1675 (HDAC4, HDAC5, HDAC7, HDAC8, and HDAC9) used for each enzyme is equal to the Michaelis constant (Km), as determined by a titration curve. FTS or MAZ-1675 is diluted in assay buffer to 6-fold the final concentration with 0.3 μM sequencing grade trypsin. The substrate/trypsin mix is added to the enzyme/compound mix and the plate is shaken for 60 seconds and then placed into a SpectraMax M5 microtiter plate reader. The enzymatic reaction is monitored for release of 7-amino-4-methoxy-coumarin over 30 minutes, after deacetylation of the lysine side chain in the peptide substrate, and the linear rate of the reaction is calculated.
Cell Research:[2]
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  • Cell lines: Human cholangiocarcinoma cell lines HuCCT-1
  • Concentrations: ~10 μM
  • Incubation Time: 21 days
  • Method: Anchorage-independent growth is assessed by growing cells in soft agar. About 25,000 cells suspended in 0.4% agar in culture media are layered over a 1% agar layer in a 6-well plate. Media are added twice a week and pictures are taken after 21 days of incubation. The number and size of colonies are analyzed using the Gel-Pro software.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 67 mg/mL (199.76 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 4% DMSO+30% PEG 300 5mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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.

Chemical Information

Molecular Weight 335.4


CAS No. 1252003-15-8
Storage powder
in solvent
Synonyms N/A

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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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID