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Selective, Hsp90 competitive inhibitor (Ki = 1.7 nM). Displays no significant activity at a range of ATP-binding kinases or Na+K+ ATPase. Induces degradation of HER-2 in vitro (EC50 = 38 nM in MCF-7 cells). Inhibits growth and promotes cell death in a variety of human tumor cells. Orally bioavailable.
|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 318.76. 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|
|1 mM||3.14 mL||15.69 mL||31.37 mL|
|5 mM||0.63 mL||3.14 mL||6.27 mL|
|10 mM||0.31 mL||1.57 mL||3.14 mL|
|50 mM||0.06 mL||0.31 mL||0.63 mL|
References are publications that support the biological activity of the product.
Lundgren et al (2009) BIIB021, an orally available, fully synthetic small-molecule inhibitor of the heat shock protein Hsp90. Mol.Cancer Ther. 8 921 PMID: 19372565
Yin et al (2010) BIIB021, a novel Hsp90 inhibitor, sensitizes head and neck squamous cell carcinoma to radiotherapy. Int.J.Cancer 126 1216 PMID: 19662650
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Keywords: BIIB 021, BIIB 021 supplier, BIIB021, heat, shock, proteins, 90, hsp90, inhibitors, chaperones, HER-2, antitumor, antitumour, CNF2024, inhibits, orally, bioavailable, potent, selective, CNF, 2024, Hsp90, 4608, Tocris Bioscience
Citations for BIIB 021
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Reviews for BIIB 021
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Human osteosarcoma, U2OS, cells were treated with BIIB 021 (1 microM) for 24 h to follow PARP cleavage using Western blot. BIIB 021 activated PARP cleavage in U2OS cells
Literature in this Area
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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.