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17-AAG (KOS953)

Potent inhibitor of chaperone protein Hsp90

17-AAG (KOS953)

Catalog No. A4054
Size Price Stock Qty
Evaluation Sample $28.00  All Inclusive In stock
10mg $60.00 In stock
50mg $175.00 In stock
100mg $315.00 In stock
200mg $515.00 In stock

All inclusive: Shipping and all other fees included

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Sample solution is provided at 25 µL, 10mM.

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Chemical structure

17-AAG (KOS953)

Related Biological Data

17-AAG (KOS953)

Related Biological Data

17-AAG (KOS953)

Biological Activity

Description 17-AAG (Tanespimycin) is a potent inhibitor of HSP90 with IC50 of 5 nM.
Targets HSP90          
IC50 5 nM          

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Chemical Properties

Cas No. 75747-14-7 SDF Download SDF
Synonyms Tanespimycin
Chemical Name [(3R,5S,6R,7S,8E,10S,11S,12Z,14E)-6-hydroxy-5,11-dimethoxy-3,7,9,15-tetramethyl-16,20,22-trioxo-21-(prop-2-enylamino)-17-azabicyclo[16.3.1]docosa-1(21),8,12,14,18-pentaen-10-yl] carbamate
Canonical SMILES CC1CC(C(C(C=C(C(C(C=CC=C(C(=O)NC2=CC(=O)C(=C(C1)C2=O)NCC=C)C)OC)OC(=O)N)C)C)O)OC
Formula C31H43N3O8 M.Wt 585.7
Solubility Soluble in DMSO Storage Store at -20°C
Shipping Condition: Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

1. Mode of cell death induced by the HSP90 inhibitor 17-AAG (tanespimycin) is dependent on the expression of pro-apoptotic BAX. Oncotarget. 2013 Nov;4(11):1963-75.
Abstract
17-AAG induced BAX-dependent apoptosis at pharmacologically relevant concentrations in BAX knockout HCT116 human colon carcinoma cells both in vitro and in tumor xenografts in vivo, where 17-AAG predominantly inhibited cell proliferation rather than promoting cell death.
4. Combined delivery of paclitaxel and tanespimycin via micellar nanocarriers: pharmacokinetics, efficacy and metabolomic analysis. PLoS One. 2013;8(3):e58619. doi: 10.1371/journal.pone.0058619. Epub 2013 Mar 7.
Abstract
A serious disadvantage in the promising Paclitaxel/17-AAG combination cancer therapy is the requirement of large quantities of toxic organic surfactants and solvents to solubilize the drug.
5. Molecular mechanism of 17-allylamino-17-demethoxygeldanamycin (17-AAG)-induced AXL receptor tyrosine kinase degradation. J Biol Chem. 2013 Jun 14;288(24):17481-94. doi: 10.1074/jbc.M112.439422. Epub 2013 Apr 29.
Abstract
17-AAG induced the down-regulation of AXL expression in a time- and dose-dependent manner through promoting AXL polyubiquitinlation and subsequent proteasomal degradation, in which 17-AAG requires AXL intracellular domain regardless of AXL receptor phosphorylation.

Background

17-AAG is an ansamycin antibiotic which acts as an anti-tumor agent.