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 leukimia 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