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Biological Activity for Macbecin I
Macbecin I is an ansamycin antibiotic compound that inhibits Hsp90 activity (IC50 = 2 μM) by binding to the ATP-binding site. Exhibits antitumor and cytocidal activities (IC50 ~ 0.4 μM) by causing degradation of key oncogenic client proteins such as ErbB2 and cRaf1. Displays higher affinity and potency than geldanamycin (Cat. No. 1368).
Technical Data for Macbecin I
|Storage||Desiccate 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.
Solubility Data for Macbecin I
|Solubility||Soluble in DMSO|
References for Macbecin I
References are publications that support the biological activity of the product.
Ono et al (1982) Antitumor and cytocidal activities of a newly isolated benzenoid ansamycin, macbecin I. Gann. 73 938 PMID: 6186564
Uehara et al (2003) Natural product origins of Hsp90 inhibitors. Curr.Cancer Drug Targets 3 325 PMID: 14529384
Martin et al (2008) Molecular characterization of macbecin as an Hsp90 inhibitor. J.Med.Chem. 51 2853 PMID: 18357975
If you know of a relevant reference for Macbecin I, please let us know.
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Keywords: Macbecin I, Macbecin I supplier, Hsp90, inhibitors, inhibits, Heat, Shock, Protein, 90, MacbecinI, antibiotics, Antibiotics, 3061, Tocris Bioscience
1 Citation for Macbecin I
Citations are publications that use Tocris products. Selected citations for Macbecin I include:
Alford and Brandman (2018) Quantification of Hsp90 availability reveals differential coupling to the heat shock response. J Cell Biol 217 3809 PMID: 30131327
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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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.