Tubastatin-A-Hydrochloride Inhibitor CAS No. 1310693-92-5

Product Name	Tubastatin-A-Hydrochloride
CAS No.	1310693-92-5
Molecular Weight	371.9
Formula	C₂₀H₂₂ClN₃O₂
Chemical Name	N-hydroxy-4-((2-methyl-1,2,3,4-tetrahydropyrido[4,3-b]indol-5-yl)methyl)benzamide hydrochloride
Smiles	C(=O)(c1ccc(cc1)Cn1c2c(c3ccccc13)CN(CC2)C)NO Cl
Chemical Structure

Biological activities

Tubastatin A is a selective histone deacetylase 6 (HDAC6) inhibitor with an IC50 of 15 nM. Besides, tubastatin A inhibits HDAC1 with an IC50 of 16.4 µM, with 1000-fold less selectivity compares with HDAC6. Tubastatin A also shows moderate potency against HDAC8 with an IC50 of 814 nM and low potency against all other isozymes with IC50 more than 30 µM. Tubastatin A confers dose-dependent protection in primary cortical neuron cultures against glutathione depletion-induced oxidative stress. Moreover, tubastatin A induces a-tubulin hyperacetylation at 2.5 µM. Slight induction of histone hyperacetylation is seen for tubastatin A at 10 µM, which may reflect inhibition of the limited histone deacetylase activity of HDAC6 or slight inhibition of class I HDACs at higher concentrations. Tubastatin A displays dose-dependent protection against HCA-induced neuronal cell death starting at 5 µM with near complete protection at 10 µM. Tubastatin A is the first neuroprotective hydroxamic acid-based HDAC inhibitor that does not cause neuronal death when tested alone in the homocysteic acid (HCA) model. ^[1] Tubastatin A treatment results in a significant increase of acetylated α-tubulin amounts in peripheral nerves. Tubastatin A treatment significantly increases the motor performance of HSPB1S135F-expressing mice. ^[2]

Protocols

A 15 mM stock solution of tubastatin A is prepared in DMSO. ^[3]

References

[1] Butler KV, et al. Rational design and simple chemistry yield a superior, neuroprotective HDAC6 inhibitor, tubastatin A. J Am Chem Soc. 2010, 132(31): 10842-10846. [2] d'Ydewalle C, et al. HDAC6 inhibitors reverse axonal loss in a mouse model of mutant HSPB1-induced Charcot-Marie-Tooth disease. Nat Med. 2011, 17(8): 968-974. [3] Wang L, et al. Depletion of HDAC6 enhances cisplatin-induced DNA damage and apoptosis in non-small cell lung cancer cells. PLoS One. 2012, 7(9): e44265.

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