| Bioactivity | Tanespimycin (17-AAG) is a potent HSP90 inhibitor with an IC50 of 5 nM, having a 100-fold higher binding affinity for tumour cell derived HSP90 than normal cell derived HSP90[1][5]. Tanespimycin depletes cellular STK38/NDR1 and reduces STK38 kinase activity. Tanespimycin also downregulates the stk38 gene expression[3]. |
| Invitro | Tanespimycin causes the degradation of HER2, Akt, and both mutant and wild-type AR and the retinoblastoma-dependent G1 growth arrest of prostate cancer cells. Tanespimycin inhibits prostate cancer cell lines with IC50s ranged from 25-45 nM (LNCaP, 25 nM; LAPC-4, 40 nM; DU-145, 45 nM; and PC-3, 25 nM)[1]. Tanespimycin (0.1-1 μM) induces a nearly complete loss of ErbB2 on ErbB2-overexpressing breast cancer cells[2]. Tanespimycin inhibits cell growth and induces G2/M cell cycle arrest and apoptosis in CCA cells together with the down-regulation of Bcl-2, Survivin and Cyclin B1, and the up-regulation of cleaved PARP[3]. |
| Name | Tanespimycin |
| CAS | 75747-14-7 |
| Formula | C31H43N3O8 |
| Molar Mass | 585.69 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | 4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light) |