SKU: A061  / 
    CAS Number: 75747-14-7



    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.

    Mechanism of Action 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.
    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).
    Molecular Formula C31H43N3O8

    Hawkins LM, Jayanthan AA, Narendran A (2005)  Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) on pediatric acute lymphoblastic leukemia (ALL) with respect to Bcr-Abl status and imatinib mesylate sensitivity. Pediatr Res. 57(3):430-437

    Massimini M et al (2017)  17-AAG and apoptosis, autophagy, and mitophagy in canine osteosarcoma cell lines. Vet. Pathol. 54(3):405-412

    Radujkovic A et al (2005)  Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG. Leukemia. 19(7):1198-1206