17-AAG又称为Tanespimycin、CP 127374，是一种有效的Hsp90抑制剂（IC50=5 nM）。17-AAG作用于肿瘤细胞Hsp90的亲和力比作用于正常细胞中Hsp90亲和力高100倍，另外，17-AAG还能抑制Akt活化及HER2、ErbB2表达。17-AAG抑制多种癌细胞生长，如神经胶质瘤细胞等，在体内外表现出明显的抗肿瘤活性。另外，17-AAG与大量抗癌药如UCN-01，依托泊苷(etoposide)，顺铂(cisplatin)显示协同作用。

17-AAG是格尔德霉素(geldanamycin)的半合成类似物，具有更低的体内毒性和更强的稳定性，目前已用于乳腺癌等疾病Phase II研究阶段。

【该产品仅用于科研实验，不能用于人体】

参考文献

[1] Schulte et al. The benzoquinone ansamycin 17-allylamino-17-demethoxygeldanamycin binds to HSP90 and shares important biologic activities with geldanamycin. Cancer Chemother Pharmacol. 42(4):273-279(1998).

[2] Kamal A, et al. A high-affinity conformation of Hsp90 confers tumour selectivity on Hsp90 inhibitors. Nature 425: 407-410 (2003).

[3] Basso AD, et al. Ansamycin antibiotics inhibit Akt activation and cyclin D expression in breast cancer cells that overexpress HER2. Oncogene 21: 1159-1166 (2002).

[4] Jia W, et al. Synergistic antileukemic interactions between 17-AAG and UCN-01 involve interruption of RAF/MEK- and AKT-related pathways. Blood. 102(5):1824-32(2003).

[5] Qing Y, et al. Synergism between Etoposide and 17-AAG in Leukemia Cells: Critical Roles for Hsp90, FLT3, Topoisomerase II, Chk1, and Rad51. Clin Cancer Res, 13:1591-1600(2007)

[6] Vasilevskava et al. Quantitative effects on c-Jun N-terminal protein kinase signaling determine synergistic interaction of cisplatin and 17-allylamino-17-demethoxygeldanamycin in colon cancer cell lines. Mol Pharmacol 65(1):235-43(2004).

[7] Zsebik B, et al. Hsp90 inhibitor 17-AAG reduces ErbB2 levels and inhibits proliferation of the trastuzumab resistant breast tumor cell line JIMT-1. Immunology Letters 104(1–2): 146–155(2006).

粉末直接保存于-20ºC，有效期2年。