Molecular Weight(MW): 721.86
Tubacin is a highly potent and selective, reversible, cell-permeable HDAC6 inhibitor with an IC50 of 4 nM in a cell-free assay, approximately 350-fold selectivity over HDAC1.
Cited by 8 Publications
3 Customer Reviews
Verification of Hdac6 deletion in knockout MEFs. Expression of HDAC6 and acetylation of tubulin were analyzed by immunoblotting.
Nat Biotechnol, 2015, 33(4): 415-23 . Tubacin purchased from Selleck.
Inhibition of HDAC6 by tubacin induced the acetylation and membrane translocation of wild-type PTEN, but not K163R mutant. U-87 MG or NCl-H1650 cells were transfected with EGFP-PTEN or EGFP-PTEN-K163R for 24 h and then treated with tubacin for 24 h. *P<0.01.
Oncogene, 2016, 35(18):2333-44. Tubacin purchased from Selleck.
A, immunoblotting analysis of E-cadherin, ZO-1, Vimentin, N-cadherin, acetyl-α-tubulin, and α-tubulin in MCF-10A cells. Cells were treated with SB431542 (5 μM), Tubacin (5 μM), Paclitaxol (PTX) (5 nM), Nocodazol (NDL) (5 nM), TSA (50 ng/liter), or Nicotiamide (Nico) (10 mM), followed by co-incubation with TGF-β (2 ng/ml).
J Biol Chem, 2016, 291(10):5396-405. Tubacin purchased from Selleck.
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Choose Selective HDAC Inhibitors
|Description||Tubacin is a highly potent and selective, reversible, cell-permeable HDAC6 inhibitor with an IC50 of 4 nM in a cell-free assay, approximately 350-fold selectivity over HDAC1.|
|Features||The first known selective inhibitor of α-tubulin deacetylation.|
Tubacin, without directly stabilizing microtubules, induces an increase in α-tubulin acetylation with EC50 of 2.5 μM in A549 cells. Tubacin inhibits HDAC6-mediated α-tubulin deacetylation, and inhibits the migration of both wild-type and HDAC6-overexpressing cells.  Tubacin, in combination with paclitaxel, synergistically enhances tubulin acetylation.  Tubacin significantly inhibits both drug-sensitive and drug–resistant MM cell growth with IC50 of 5–20 μM, and induces cell apoptosis by activation of caspases. 
|In vivo||In chick embryos, inhibition of HDAC6 activity by Tubacin reduces the formation of new blood vessels in matrigel/nylon mesh. In angioreactors implanted in mice, Tubacin also impairs the formation of new blood vessels. |
Enzyme Inhibition Assay:Enzyme inhibition assays are performed using the Reaction Biology HDAC Spectrum platform. The HDAC1, 2, 4, 5, 6, 7, 8, 9, 10, and 11 assays used 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. Compounds are 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.
-  Butler KV, et al. J Am Chem Soc. 2010, 132(31), 10842-0846.
-  Haggarty SJ, et al. Proc Natl Acad Sci U S A. 2003, 100(8), 4389-4394.
-  Marcus AI, et al. Cancer Res. 2005, 65(9), 3883-3893.
|In vitro||DMSO||100 mg/mL (138.53 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+5% 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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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).
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