17-AAG

- Overview
  - 17-AAG (Tanespimycin; 17-N-Allylamino-17-demethoxygeldanamycin) is a geldanamycin-derived anti-tumor agent currently used in cancer research. It is an inhibitor of heat shock protein 90. The compound epletes cellular STK38/NDR1 and reduces STK38 kinase activity.
    17-AAG is soluble in DMSO but practically insoluble in water.
    
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    Background
    
    17-AAG targets and inactivates Hsp90 (heat shock protein 90), which is expressed in certain types of leukemia and lymphomas as well as solid tumors.
- Properties
  - CAS Number
    
    75747-14-7
    
    Molecular Formula
    
    C31H43N3O8
    
    Molecular Weight
    
    585.69
    
    Appearance
    
    Purple powder
    
    Solubility
    
    Soluble in DMSO. Practically insoluble in water.
    
    Other Properties
    
    Source: Synthetic
    Identification: Positive (HPLC)
    Purity Level: ≥98.0% (HPLC)
    
    Storage
    
    -20 °C
    
    * For research use only
- Applications
  - Application Description
    
    Eukaryotic Cell Culture Applications: 17-AAG has been shown to induce cell-cycle arrest and apoptosis in cultured ALCL cells irrespective of ALK expression. In addition, 17-AAG has shown promising results in the treatment of uveal melanoma through inhibition of HSP-90 in tandem with c-Kit inhibition.
    
    Cancer Applications: Canine osteosarcoma is highly resistant to chemotherapy. An investigation with 17-AAG in canine osteosarcoma cell lines was undertaken to understand the relationship between cell death, autophagy and mitophagy in regulating cancer cell viability and death. Authors tested 2 cell lines (D22, and D17 from primary and metastatic tumors respectively. Authors found that 17-AAG caused a simultaneous increase in apoptosis and autophagy, and mitophagy was observed in the D22 cell lines, but only slight apoptosis in the D17 cell line. This study revealed that a treatments based on pro-apoptotic chemotherapy with autophagy regulators could benefit from in vitro screening, since there are differences in cell responses based on cell type (Massimini et al, 2017).