Treatment of HT-1080 cells with Deforolimus induces a dose-dependent inhibition of phosphorylation of both S6 and 4E-BP1, with IC50 of 0.2 nM and 5.6 nM, respectively, and leads to a decrease in cell size, an increase in the proportion of cells in the G1 phase of the cell cycle, and inhibition of glucose uptake.
Ridaforolimus (MK-8669) is a potent and selective inhibitor of mTOR, effectively inhibiting ribosomal protein S6 phosphorylation with an IC50 of 0.2 nM in HT-1080 cells[1].
体内研究
Furthermore, Ridaforolimus has been shown to effectively inhibit tumor growth in mice bearing various types of cancer xenografts, including prostate (PC-3), colon (HCT-116), breast (MCF7), pancreas (PANC-1), and lung (A549). The compound reduces tumor growth significantly at doses as low as 0.3 mg/kg, with the most substantial inhibition observed at doses of 3 and 10 mg/kg, demonstrating its dose-dependent antitumor efficacy[1].
体外研究
In HT-1080 fibrosarcoma cells, Ridaforolimus induces a dose-dependent inhibition of phosphorylation for both S6 and 4E-BP1 proteins. The IC50 values for inhibiting these proteins are 0.2 nM and 5.6 nM, respectively, while the EC50s are 0.2 nM for S6 and 1.0 nM for 4E-BP1. The EC50 for inhibiting cell proliferation is closely matched at 0.5 nM, underscoring the efficacy of Ridaforolimus in inhibiting mTOR activity and its downstream effects on cell growth and division in a dose-dependent manner[1].
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