CQ3196 is an oral RIOK2 inhibitor with a Kd value of 14 nM. It effectively suppresses the ATPase activity of RIOK2, showing an IC50 value of 72 nM. CQ3196 also impedes cell proliferation and colony formation in gastric cancer cell lines, inducing apoptosis (apoptosis) in HGC-27 and AGS cells. Furthermore, CQ3196 inhibits downstream signaling pathways of RIOK2, reducing mTOR and AKT phosphorylation, while modulating ribosome function and protein synthesis. It inhibits tumor growth and can be utilized in both in vivo and in vitro studies of gastric cancer.

CQ3196 effectively inhibits the proliferation of various cancer cells, with IC 50 values recorded as 0.46 μM (HGC-27), 0.73 μM (AGS), 2.34 μM (KATO III), 2.09 μM (PC-9), 1.56 μM (A549), 1.42 μM (H3255), 0.75 μM (Mia paca-2), 1.75 μM (Hela), 1.46 μM (Molt 4), 0.90 μM (K562), and 1.52 μM (HEK-293). Within the range of 30-1000 nM over 14 days, CQ3196 fully suppresses colony formation in HGC-27 and AGS cells at concentrations of 300 nM and above. Additionally, CQ3196 induces both early and late apoptosis in a concentration-dependent manner in HGC-27 and AGS cells when administered at 30-1000 nM over 48 hours. The compound significantly decreases the phosphorylation of mTOR and AKT in HGC-27 cells at concentrations between 30-1000 nM. CQ3196 also reduces the expression of the ribosomal small subunit RPS2 following 48-hour exposure at 30-1000 nM. At 1 μM for 24 hours, CQ3196 downregulates ribosomal proteins RPS, RPL, and some ribosome-associated proteins, thereby modulating ribosomal function and protein synthesis.

CQ3196, administered orally at doses of 25 and 50 mg/kg every other day for 12 days, demonstrated a dose-dependent antitumor effect in an HGC-27 gastric cancer xenograft model established in BALB/c nude mice.