17-AAG

A potent Hsp90 inhibitor with IC50 of 5 nM in cell-free assays; induces cytosolic accumulation of cytochrome c and cleavage and activities of caspase-9 and caspase-3, triggering apoptosis of HL-60/Bcr-Abl and K562 cells; causes the degradation of HER2, HER3, Akt, and both mutant and wild-type androgen receptor; inhibits prostate cancer xenografts growth in mice.Skin Cancer Phase 2 Discontinued (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.

75747-14-7

Tanespimycin | NSC 330507 | CP 127374 | 17AAG | 17 AAG

>98% (HPLC)

DMSO: ≥ 55 mg/mL

NC (O[C@@H] (/C (C) =C/[C@H] (C) [C@@H] (O) [C@@H] (OC) C[C@H] (C) CC1=C2NCC=C) [C@@H] (OC) /C=C/C=C (C) /C (NC (C1=O) =CC2=O) =O) =O

C31H43N3O8

585.6884

Storage temperature: -20°C. Stability: ≥ 2 years

For research use only.