| 规格或纯度 | 10mM in DMSO |
|---|---|
| 英文名称 | Tubastatin A HCl |
| 生化机理 | Tubastatin A HCl (TSA) is a potent and selective HDAC6 inhibitor with IC50 of 15 nM in a cell-free assay. It is selective (1000-fold more) against all other isozymes except HDAC8 (57-fold more). |
| 储存温度 | -80℃储存 |
| 运输条件 | 超低温冰袋运输 |
| 产品介绍 |
Information Tubastatin A HCl (TSA) is a potent and selectiveHDAC6inhibitor withIC50of 15 nM in a cell-free assay. It is selective (1000-fold more) against all other isozymes except HDAC8 (57-fold more). 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. In?vivo Daily treatment of Tubastatin A at 0.5mg/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. cell?lines：HeLa cells and PtK1 cells Concentrations：0-10 μM Incubation?Time：24 hours Powder?Purity:≥97% Information Tubastatin A HCl (TSA) is a potent and selectiveHDAC6inhibitor withIC50of 15 nM in a cell-free assay. It is selective (1000-fold more) against all other isozymes except HDAC8 (57-fold more). 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. In?vivo Daily treatment of Tubastatin A at 0.5mg/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. cell?lines：HeLa cells and PtK1 cells Concentrations：0-10 μM Incubation?Time：24 hours Powder?Purity:≥97% |
| IC50 | HDAC8, IC50: 854 nM |
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| Canonical SMILES | Cl.CN1CCC2=C(C1)C3=C(C=CC=C3)[N]2CC4=CC=C(C=C4)C(=O)NO |
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| 分子量 | 371.86 |
| 溶解性 | Solubility (25°C) In vitro DMSO: 39 mg/mL (198.93 mM); ? ? |
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