Tubastatin A hydrochloride

Research use only, not for human use.

Tubastatin A hydrochloride is a potent and selective HDAC6 inhibitor with IC50 of 15 nM in cell-free assays.

Tubastatin A hydrochloride is a potent and selective HDAC6 inhibitor with IC50 of 15 nM in cell-free assays; displays 57-fold selectivity over HDAC8 and >1,000-fold selective against other HDAC isoforms; induces an increase in acetylated-α-tubulin levels and the restoration of primary cilia expression in the cholangiocarcinoma cell lines at 10 uM, shows significant inhibition of TNF-α and IL-6 in LPS stimulated human THP-1 macrophages with IC50 of 272 nM and 712 nM; reduces the growth of cholangiocarcinoma in vivo.(In Vitro):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 CC12 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.(In Vivo):Daily treatment of Tubastatin A at 0.5 mg/kg inhibits HDAC6 to promote Tregs suppressive activity in mouse models of inflammation and autoimmunity, including multiple forms of experimental colitis and fully major histocompatibility complex (MHC)-incompatible cardiac allograft rejection.

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 CC12 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.

Daily treatment of Tubastatin A at 0.5 mg/kg inhibits HDAC6 to promote Tregs suppressive activity in mouse models of inflammation and autoimmunity, including multiple forms of experimental colitis and fully major histocompatibility complex (MHC)-incompatible cardiac allograft rejection.

Tubastatin A HCl | TSA HCl

Cell Cycle/DNA Damage

HDAC

HDAC1|HDAC2|HDAC3|HDAC6|HDAC8

Cancer

——

1310693-92-5

371.86

C20H22ClN3O2

>98% (HPLC)

DMSO: 10.8 mg/mL

Cl.CN1CCC2=C(C1)C1=CC=CC=C1N2CC1=CC=C(C=C1)C(=O)NO

Benzamide, N-hydroxy-4-[(1,2,3,4-tetrahydro-2-methyl-5H-pyrido[4,3-b]indol-5-yl)methyl]-, hydrochloride (1:1)

(-20℃)

With Ice Pack

≥ 2 years