2014年8月4日星期一

Tubastatin A hydrochloride|cas 1310693-92-5| DC Chem|Supplier|Price|Buy  

Tubastatin A hydrochloride|cas 1310693-92-5| DC Chem|Supplier|Price|Buy
DC Cicalhems Supply: Tubastatin A hydrochloride|cas 1310693-92-5,Purity: >98% ,Cat No. DC7330, In stock.

Contact: website: www.dcchemicals.com,
sales@dcchemicals.com,order@dcchemicals.com,info@dcchemicals.com,
Tel: +86-21-61454686;Fax:+86-21-61642799;

Tubastatin A hydrochloride|cas 1310693-92-5 ,Synonym: Tubastatin A HCl; TSA HCl  ,Chemical name: N-hydroxy-4-((2-methyl-1,2,3,4-tetrahydropyrido[4,3-b]indol-5-yl)methyl)benzamidehydrochloride ,Molecular Formula: C20H21N3O2.HCl ,MW:371.86

Tubastatin A hydrochloride, cas 1310693-92-5,Purity: >98%, Best Price and quality from DC Chemicals. Tubastatin A Hcl is a potent and selective HDAC6 inhibitor with IC50 of 15 nM; 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. [1] At 100 ng/mL Tubastatin A increases Foxp3+ T-regulatory cells (Tregs) suppression of T cell proliferation in vitro. [2] 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.[3] 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. [4] 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. [2]

没有评论:

发表评论