Alvespimycin (17-DMAG) is a potent inhibitor ofHsp90, binding toHsp90with anEC₅₀of 62 ± 29 nM.

Alvespimycin (17-DMAG) is a potent inhibitor of Hsp90, binding to Hsp90 with an EC₅₀of 62 nM. Alvespimycin (17-DMAG) inhibits the growth of the human cancer cell lines SKBR3 and SKOV3, which overexpress Hsp90 client protein Her2, and causes down-regulation of Her2 as well as induction of Hsp70 consistent with Hsp90 inhibition, for Her2 degradation with EC₅₀of 8 ± 4 nM and 46 ± 24 nM in SKBR3 and SKOV3 cells, respectively; for Hsp70 induction with EC₅₀of 4 ± 2 nM and 14 ± 7 nM in SKBR3 and SKOV3 cells, respectively^[1]. Compared with the vehicle control, Alvespimycin (17-DMAG) dose-dependent apoptosis (P<0.001 averaged across 24- and 48-hour time points) at concentrations of 50 nM to 500 nM, which represent pharmacologically attainable doses. Similar to many other agents, Alvespimycin (17-DMAG) also demonstrates time-dependent apoptosis (P<0.001, averaged across all doses) in chronic lymphocytic leukemia (CLL) cells with extended exposure from 24 to 48 hours. In addition,Alvespimycin (17-DMAG) is much more potent after 24 and 48 hours of treatment than 17-AAG^[2].

The tumors are grown for two months before the start of i.p. injections every four days over one month with 0, 50, 100 and 200 mg/kg dipalmitoyl-radicicol or 0, 5, 10 and 20 mg/kg Alvespimycin (17-DMAG). Despite sample heterogeneity, the HSP90 inhibitor-treated animals have significantly lower tumour volumes than the vehicle control-treated animals. HSP90 inhibitors have been shown to cause liver toxicity in an animal model of gastrointestinal cancer. Nevertheless, the reduction in tumor size using dipalmitoyl-radicicol is statistically significant at 100 mg/kg, while Alvespimycin (17-DMAG) at either 10 or 20 mg/kg elicits a significant reduction in tumor size^[3].

616.75

C₃₂H₄₈N₄O₈

467214-20-6

阿螺旋霉素

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