Tanespimycin (17-AAG)是一种有效的HSP90抑制剂，无细胞试验中IC50为5 nM，作用于来自肿瘤细胞的HSP90比作用于来自正常细胞HSP90结合亲和力高100倍。

>98 %

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

坦螺旋霉素；替拉替尼；17-烯丙基胺格尔德霉素；Tanespimycin; NSC 330507; CP 127374; 17AAG; 17 AAG; KOS 953

紫色到略带紫色的红色固体

DMSO : 58.6 mg/mL (100 mM)

HSP90

17-AAG, an analog of geldanamycin, exhibits greater than 100 times higher binding affinity for Hsp90 derived from HER-2-overexpressing cancer cells (BT474, N87, SKOV3 and SKBR3) or BT474 breast carcinoma cells with IC50 values of 5-6 nM. 17-AAG causes the degradation of HER2, HER3, Akt, and both mutant and wild-type androgen receptor (AR), leading to the RB-dependent G1 growth arrest of prostate cancer cells such as LNCaP, LAPC-4, DU-145, and PC-3 with IC50 values of 25-45 nM. In addition to inducing apoptosis of Ba/F3 cells transformed with wild-type BCR-ABL with an IC50 of 5.2 μM, 17-AAG has the ability to induce apoptosis of cells transformed with imatinib mesylate-resistant T315I and E255K BCR-ABL mutants with IC50 values of 2.3 μM and 1.0 μM, respectively, by inducing the degradation of both wild-type BCR-ABL protein and mutants.

17-AAG displays significantly higher binding affinity for Hsp90 from 3T3-src, B16 or CT26 xenografts in nude mice with IC50 values of 8-35 nM as compared with that from the normal tissues with IC50 values of 200-600 nM. Administration of 17-AAG (~50 mg/kg) causes significant decline in AR, HER2, HER3, and Akt expression in a dose-dependent manner with >50% decline at dose of 50 mg/kg, resulting in the dose-dependent inhibition of androgen-dependent (CWR22) and -independent (CWR22R and CWRSA6) prostate cancer xenografts growth by 67%, 80% and 68% at dose of 50 mg/kg, respectively.

[1] Kamal A, et al. Nature, 2003, 425(6956), 407-410.
[2] Solit DB, et al. Clin Cancer Res, 2002, 8(5), 986-993.
[3] Gorre ME, et al. Blood, 2002, 100(8), 3041-3044.