SV119 is a selective σ-2 receptor (σ₂ receptor) ligand with a Ki of approximately 5-10 nM. It induces apoptosis in various human cancer cell lines by activating caspase-3 and promoting mitochondrial depolarization. SV119 can enhance the effects of chemotherapeutic agents such as Paclitaxel, improving their cytotoxicity against tumor cells. In mouse xenograft models, SV119 significantly inhibits tumor growth both alone and in combination. SV119 is applicable for research on cancers such as breast, prostate, and pancreatic cancer.

SV119 induces caspase-3/7 dependent apoptosis in Panc1, CFPAC, ASPC, and PancO2 cells at concentrations ranging from 0-10 µM. The compound exhibits an EC50 of 23.3 μM for the sigma-2 receptor in MDA-MB-231 cells, achieving maximum cytotoxicity of 100%, and an EC50 of 17.6 μM in MCF-7 cells, also with maximum cytotoxicity of 100%. At 30 µM for 24-48 hours, SV119 reduces the protein level of full-length Bid. When combined with Gemcitabine and Paclitaxel, SV119 at 0-10 µM for 24 hours increases apoptosis in ASPC-1, CFPAC, Panc1, and PancO2 cells. Furthermore, SV119 at 10 mM for 1.5 hours decreases the fluorescence of cancer stem cells (CSC) in MDA-MB-435 cells. In a formulation with SV119-PEG-AuNC/DOX and a coverage density of 50%, SV119 significantly reduces breast cell formation and number, and decreases the stemness of breast CSCs in MDA-MB-435 cells when used in combination with photothermal and chemotherapy treatments.

SV119 (1 mg per mouse, administered intraperitoneally once; every other day/daily for 7 consecutive days) when combined with Gemcitabine or Paclitaxel, enhances apoptosis and inhibits tumor growth in pancreatic tumor models in C57BL/6 mice.