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Tanespimycin

CAS No. : 75747-14-7

MCE 国际站：Tanespimycin

产品活性：Tanespimycin (17-AAG) 是有效的 HSP90 抑制剂，IC₅₀ 为 5 nM，对肿瘤细胞 HSP90 的亲和性比正常细胞高 100 倍。Tanespimycin 消耗细胞内 STK38/NDR1，并降低 STK38 激酶活性。Tanespimycin 还下调 stk38 基因表达。

研究领域：Cell Cycle/DNA Damage  |  Metabolic Enzyme/Protease  |  Autophagy  |  Anti-infection  |  Apoptosis

作用靶点：HSP  |  Autophagy  |  Mitophagy  |  Bacterial  |  Apoptosis  |  Antibiotic

In Vitro: 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).
Tanespimycin (0.1-1 μM) induces a nearly complete loss of ErbB2 on ErbB2-overexpressing breast cancer cells. 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.

In Vivo: Tanespimycin (25-200 mg/kg, i.p.) causes a dose-dependent decline in AR, HER2, and Akt expression in prostate cancer xenografts. Tanespimycin treatment at doses sufficient to induce AR, HER2, and Akt degradation results in the dose-dependent inhibition of androgen-dependent and -independent prostate cancer xenograft growth without toxicity.
Tanespimycin (60 mg/kg) with Rapamycin (30 mg/kg) inhibits A549 and MDA-MB-231 tumor growth and effects tumor cures in MDA-MB-231 tumor-bearing animals by tail vein injection.

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