Thioridazine (0.01-100 μM; 48 h) reduces the cell viability of NCI-N87 and AGS cells in a concentration-dependent manner [2]. Thioridazine (15 μM; 24 h) reduces cell viability of the cervical (HeLa, Caski and C33A) and endometrial (HEC-1-A and KLE) cancer cells [4]. Thioridazine (1-15 μM; 24-48 h) induces gastric cancer cell death via the mitochondrial apoptosis pathway and mitochondrial pathway [2]. Thioridazine (15 μM; 24 h) modulates the regulation of cell cycle progression by interfering with the PI3K/Akt pathway and induces G 1 cell cycle arrest in cervical and endometrial cancer cells [4]. Thioridazine inhibits the growth of antibiotic-sensitive and multidrug-resistant strains of A. baumannii [3]. Cell Viability Assay [1] Cell Line: NCI-N87 and AGS cells. Concentration: 0.01, 0.1, 0.5, 1, 5, 10, 20, 50, 100 μM. Incubation Time: 48 hours. Result: Exhibited cytotoxicity in gastric cancer cells. Western Blot Analysis [1] Cell Line: NCI-N87 and AGS cells Concentration: 1, 5, 10, 15 μM. Incubation Time: 24, 48 hours. Result: Downregulated the precursors of caspase-9, caspase-8 and caspase-3.

Thioridazine (25 mg/kg; i.p. every 3 days for 3 weeks) extends the survival of tumor-bearing mice and reduces the number of pluripotent embryonal carcinoma (EC) cells within tumors [5]. Thioridazine (1.0-5.0 mg/kg; s.c.) reduces oral behavior and selectively blocks repetitive head bobbing [1]. Animal Model: Nude and Rag2KO mice were injected with iPS cells or NT2D1 cells [5] Dosage: 25 mg/kg. Administration: I.p. every 3 days for 3 weeks. Result: Reduced the number of OCT4-expressing cells within malignant teratocarcinomas and extended the survival of tumor-bearing mice. With no effect on fertility.