LY-2584702 shows substantial efficacy as a single agent in U87MG glioblastoma and HCT116 colon carcinoma xenograft models at dosages of 2.5 mg/kg twice daily (BID) and 12.5 mg/kg BID. It significantly reduces tumor growth at TMED50 (threshold minimum effective dose 50%) of 2.3 mg/kg and TMED90 (90% threshold dose) of 10 mg/kg in the HCT116 colon carcinoma xenograft model^[1].

To investigate the function of S6K in vivo, EOMA cells with shAkt3 suppression are introduced into nu/nu mice and subsequently treated with LY-2584702 or Rapamycin for 14 days. Post-treatment tumor analysis reveals LY-2584702 nearly matches Rapamycin in inhibiting S6 phosphorylation. Akt3 depletion escalates tumor proliferation compared to pLKO. Solely administering LY-2584702 shows negligible impact on pLKO tumor expansion. Yet, LY-2584702 markedly diminishes the enlargement of tumors harboring shAkt3^[2].

In the S6K1 enzyme assay, LY-2584702 (LY2584702) demonstrates an IC50 of 2 nM. The IC50 for pS6 inhibition in cells is 100 nM. At higher concentrations, LY-2584702 exhibits activity against S6K-related kinases MSK2 and RSK (enzyme assay IC50=58-176 nM). It dose-dependently reduces S6K activity in EOMA cells, as indicated by decreased phosphorylation of the downstream target S6^[2].

LY-2584702 (LY2584702) significantly reduces A549 cell proliferation after 24 hours at a concentration of 0.1 μM (P<0.05), with the decrease becoming more pronounced with extended treatment duration and/or higher drug doses (all P<0.05). Comparable effects are seen in SK-MES-1 cells, though a clear reduction requires LY-2584702 at 0.6 μM (P<0.05), a significantly higher dose than for A549^[3].