WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#: 203055
Description: Tubacin is a highly potent and selective, reversible, cell-permeable HDAC6 inhibitor with an IC50 of 4 nM. The IC50 for other HDACs is 1000-fold higher, making tubacin both more selective and more potent than Tubastatin A, which also inhibits HDAC8. Tubacin inhibits alpha-tubulin deacetylation in mammalian cells. Unlike trichostatin A (TSA), which is a broad spectrum HDAC inhibitor, tubacin is specific for the tubulin deacetylase activity of HDAC6.
MedKoo Cat#: 203055
Chemical Formula: C41H43N3O7S
Exact Mass: 721.28217
Molecular Weight: 721.86
Elemental Analysis: C, 68.22; H, 6.00; N, 5.82; O, 15.51; S, 4.44
Tubacin, purity > 98%, is in stock. Current shipping out time is about 2 weeks after order is received. CoA, QC data and MSDS documents are available in one week after order is received.
IUPAC/Chemical Name: N1-(4-((2R,4R,6S)-4-(((4,5-diphenyloxazol-2-yl)thio)methyl)-6-(4-(hydroxymethyl)phenyl)-1,3-dioxan-2-yl)phenyl)-N8-hydroxyoctanediamide
InChi Key: BHUZLJOUHMBZQY-YXQOSMAKSA-N
InChi Code: InChI=1S/C41H43N3O7S/c45-26-28-17-19-29(20-18-28)35-25-34(27-52-41-43-38(30-11-5-3-6-12-30)39(51-41)31-13-7-4-8-14-31)49-40(50-35)32-21-23-33(24-22-32)42-36(46)15-9-1-2-10-16-37(47)44-48/h3-8,11-14,17-24,34-35,40,45,48H,1-2,9-10,15-16,25-27H2,(H,42,46)(H,44,47)/t34-,35+,40+/m1/s1
SMILES Code: O=C(NC1=CC=C([C@@H]2O[C@H](C3=CC=C(CO)C=C3)C[C@H](CSC4=NC(C5=CC=CC=C5)=C(C6=CC=CC=C6)O4)O2)C=C1)CCCCCCC(NO)=O
The following data is based on the product molecular weight 721.86 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.15 mL||5.76 mL||11.51 mL|
|5 mM||0.23 mL||1.15 mL||2.3 mL|
|10 mM||0.12 mL||0.58 mL||1.15 mL|
|50 mM||0.02 mL||0.12 mL||0.23 mL|
1: Siow D, Wattenberg B. The histone deacetylase-6 inhibitor tubacin directly inhibits de novo sphingolipid biosynthesis as an off-target effect. Biochem Biophys Res Commun. 2014 Jul 4;449(3):268-71. doi: 10.1016/j.bbrc.2014.05.016. Epub 2014 May 14. PubMed PMID: 24835950.
2: Salmi M, Bruneau N, Cillario J, Lozovaya N, Massacrier A, Buhler E, Cloarec R, Tsintsadze T, Watrin F, Tsintsadze V, Zimmer C, Villard C, Lafitte D, Cardoso C, Bao L, Lesca G, Rudolf G, Muscatelli F, Pauly V, Khalilov I, Durbec P, Ben-Ari Y, Burnashev N, Represa A, Szepetowski P. Tubacin prevents neuronal migration defects and epileptic activity caused by rat Srpx2 silencing in utero. Brain. 2013 Aug;136(Pt 8):2457-73. doi: 10.1093/brain/awt161. Epub 2013 Jul 5. PubMed PMID: 23831613.
3: Aldana-Masangkay GI, Rodriguez-Gonzalez A, Lin T, Ikeda AK, Hsieh YT, Kim YM, Lomenick B, Okemoto K, Landaw EM, Wang D, Mazitschek R, Bradner JE, Sakamoto KM. Tubacin suppresses proliferation and induces apoptosis of acute lymphoblastic leukemia cells. Leuk Lymphoma. 2011 Aug;52(8):1544-55. doi: 10.3109/10428194.2011.570821. Epub 2011 Jun 23. PubMed PMID: 21699378; PubMed Central PMCID: PMC4113006.
4: Kawada J, Zou P, Mazitschek R, Bradner JE, Cohen JI. Tubacin kills Epstein-Barr virus (EBV)-Burkitt lymphoma cells by inducing reactive oxygen species and EBV lymphoblastoid cells by inducing apoptosis. J Biol Chem. 2009 Jun 19;284(25):17102-9. doi: 10.1074/jbc.M809090200. Epub 2009 Apr 22. PubMed PMID: 19386607; PubMed Central PMCID: PMC2719348.
Tubacin was originally discovered by scientists at the Broad Institute after performing a cell-based screen of a library of over 7000 small molecules. Tubacin is a highly potent, selective, reversible, cell-permeable HDAC6 inhibitor with an IC50 of 4 nM. The IC50 for other HDACs is 1000-fold higher, making tubacin both more selective and more potent than Tubastatin A.
According to Aldana-Masangkay et al's recent publication ( Leuk Lymphoma. 2011 Aug;52(8):1544-55. ) tubacin showed a higher antiproliferative effect in acute lymphoblastic leukemia (ALL) cells than in normal hematopoietic cells. Treatment with tubacin led to the induction of apoptotic pathways in both pre-B and T cell ALL cells at a 50% inhibitory concentration (IC(50)) of low micromolar concentrations. Acetylation of α-tubulin increases within the first 30 min following treatment of ALL cells with tubacin . It was also observed an accumulation of polyubiquitinated proteins and poly(ADP-ribose) polymerase (PARP) cleavage. Furthermore, the signaling pathways activated by tubacin appear to be distinct from those observed in multiple myeloma. The results suggest that targeting HDAC6 alone or in combination with chemotherapy could provide a novel approach to treat ALL.