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Inhibitor of heat shock protein 90 (Hsp90) chaperone activity, and an analog of geldanamycin (Cat. No. 1368). Subsequently inhibits the activity of oncogenic proteins such as p185erbB-2 (IC50 = 31 nM), N-ras, Ki-ras and c-Akt. Antitumor in vivo. Also protects neuroprogenitor cells against stress-induced apoptosis at low concentrations (10 nM) in vitro.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 585.7. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.1 mM||17.07 mL||85.37 mL||170.74 mL|
|0.5 mM||3.41 mL||17.07 mL||34.15 mL|
|1 mM||1.71 mL||8.54 mL||17.07 mL|
|5 mM||0.34 mL||1.71 mL||3.41 mL|
References are publications that support the biological activity of the product.
Hostein et al (2001) Inhibition of signal transduction by the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin results in cytostasis and apoptosis. Cancer Res. 61 4003 PMID: 11358818
Schnur et al (1995) Inhibition of the oncogene product p185erbB-2 in vitro and in vivo by geldanamycin and dihydrogeldanamycin derivatives. J.Med.Chem. 38 3806 PMID: 7562911
Yang et al (2001) Disruption of the EF-2 kinase/Hsp90 protein complex: a possible mechanism to inhibit glioblastoma by geldanamycin. Cancer Res. 61 4010 PMID: 11358819
Wang et al (2011) Protection of murine neural progenitor cells by the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin in the low nanomolar concentration range. J.Neurochem. 117 703 PMID: 21395580
If you know of a relevant reference for 17-AAG, please let us know.
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Keywords: 17-AAG, 17-AAG supplier, Selective, Hsp90, inhibitors, inhibits, Heat, Shock, Protein, 90, NSC330507, antibiotics, stem, cells, protects, neural, progenitors, neuorprogenitors, stress-induced, apoptosis, Geldanamycin, NSC, 330507, 17-(Allylamino)-17-demethoxygeldanamycin, Tanespimycin, Antibiotics, Stem, Cell, Signaling, 1515, Tocris Bioscience
6 Citations for 17-AAG
Citations are publications that use Tocris products. Selected citations for 17-AAG include:
Siebert et al (2019) Heat Shock Protein 90 as a Prognostic Marker and Therapeutic Target for Adrenocortical Carcinoma. Front Endocrinol (Lausanne) 10 487 PMID: 31379752
Truman et al (2015) Quantitative proteomics of the yeast Hsp70/Hsp90 interactomes during DNA damage reveal chaperone-dependent regulation of ribonucleotide reductase. J Proteomics 112 285 PMID: 25452130
Sontake et al (2017) Hsp90 regulation of fibroblast activation in pulmonary fibrosis. JCI Insight 2 e91454 PMID: 28239659
Fang et al (2014) HSP90 regulates DNA repair via the interaction between XRCC1 and DNA polymerase β. Nat Commun 5 5513 PMID: 25423885
Donnelly et al (2014) HSF1 deficiency and impaired HSP90-dependent protein folding are hallmarks of aneuploid human cells. EMBO J 33 2374 PMID: 25205676
Hughes et al (2012) Pertuzumab Increases 17-AAG-Induced Degradation of ErbB2, and This Effect Is Further Increased by Combining Pertuzumab with trastu. Pharmaceuticals (Basel) 5 674 PMID: 24281706
Do you know of a great paper that uses 17-AAG from Tocris? Please let us know.
Reviews for 17-AAG
Average Rating: 5 (Based on 1 Review.)
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I used it to down regulate the expression of HSP90. I checked using an antibody for HSP70 and showed upregulation of HSP70 with 10nM of 17-AAG. Easy to use product with informative data sheet. Stable in solution for months.
This is highly cytotoxic to human microglia at a high concentration (>100nM) from our cell viability data. We also confirmed this using imaging.
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Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.