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factory 1310693-92-5 1310693-92-5 in stock Buy TubaststinA HCl
factory 1310693-92-5 1310693-92-5 in stock Buy TubaststinA HCl

factory 1310693-92-5 1310693-92-5 in stock Buy TubaststinA HCl

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10 Gram

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factory 1310693-92-5 1310693-92-5 in stock Buy TubaststinA HCl

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factory 1310693-92-5 in stock Buy TubaststinA HCl

Tubastatin A hydrochloride is a potent HDAC6 inhibitor (IC50 = 0.015 μM). Exhibits some selectively for HDAC6 over HDAC8 and 1 (IC50 values are 0.854 and 16.4 μM, respectively). Induces elevated levels of α-tubulin and protects against glutathione-induced oxidative stress in primary neuronal cell culture. Reverses the axonal loss in peripheral neurons in a mouse model of Charcot-Marie-Tooth disease.

Tubastatin A is a potent and selective HDAC6 inhibitor. Tubastatin A was substantially more selective than the known HDAC6 inhibitor Tubacin at all isozymes except HDAC8. Tubastatin A is a potent HDAC6 inhibitor with an IC50 value of 15 nM. Tubastatin A induces α-tubulin hyperacetylation at 2.5 μM in primary cortical neuron cultures. In a model of oxidative stress induced by glutathione depletion, tubastatin A displays dose-dependent neuronal protection of primary cortical neuron cultures at 5-10 μM

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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. 

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