SC144 inhibits cell growth in a panel of human ovarian cancer cell lines with IC ₅₀ s in a submicromolar range (IC ₅₀ =OVCAR-8, OVCAR-5, OVCAR-3= 0.72, 0.49, 0.95 μM).
The potency of SC144 toward NCI/ADR-RES (Paclitaxel- and Doxorubicin-resistant, IC ₅₀ =0.43 μM) and HEY (Cisplatin-resistant, IC ₅₀ =0.88 μM) suggests an ability to overcome drug resistance in ovarian cancer.
SC144 (2 μM; 24 hours) causes significantly more apoptosis in OVCAR-8 and Caov-3 than normal kidney epithelial and normal endometrial cells.
SC144 (0.5-2 μM; 0-6 hours) substantially increases the phosphorylation of gp130 (S782) in both OVCAR-8 and Caov-3 cells in a time- and dose-dependent manner.
SC144 is cytotoxic to ovarian cancer cells via a mechanism involving the inhibition of gp130 activity, leading to the inactivation of Akt and Stat3 as well as the suppression of Stat3-regulated gene expression. As are result, SC144 treatment eventually causes cell-cycle arrest, anti-angiogenesis, and apoptosis.

SC144 (10 mg/kg; i.p.; daily for 58 days) suppresses tumor growth in human ovariancancer xenografts.
SC144 (100 mg/kg;p.o.; daily for 35 days) treatment shows the average tumor volume in mice 82% smaller than that in the control group.