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

    17-AAG

    $162.63

    17-AAG (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.

    Mechanism of Action17-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 ApplicationsCanine osteosarcoma is highly resistant to chemotherapy thus additional information resistance mechanisms is needed. 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. It was found that17-AAG caused a simultaneous increase in apoptosis, 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).
    Cancer Applications17-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.
    Molecular FormulaC31H43N3O8
    References

    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