BXQ-350 Mechanism of Action

BXQ-350 Lysosome Activities

Studies demonstrate that BXQ-350 kills cancer cells consistent with activity at the lysosome.

Cell death occurs through multiple mechanisms of action including necrosis, apoptosis and autophagy effects.


BXQ-350 enters the cell through endocytosis


Under acidic conditions, Saposin C is fusogenic to phosphatidylserine.

Apoptosis, a mechanism of action to kill cancer cells is initiated, resulting in cancer cell death.

BXQ-350 possesses tumor agnostic properties and represents a paradigm shift in the fight against cancer. Utilizing a small lysosomal protein known as Saposin C with a lipid, BXQ-350 targets both externalized phosphatidylserine and tumor lysosomes to initiate tumor cell death. In tumor cells and the blood vessels that feed tumors, some of the phosphatidylserine (PS) move to the outside of the cell membrane to help avoid inflammation and the immune response. Under acidic conditions, Saposin C is fusogenic to phosphatidylserine initiating two distinct mechanisms of action to kill cancer cells.

  1. Endocytosis of BXQ-350 leading to lysosomal degradation and necrosis
  2. Catalysis of acid spingomyelinase leading to ceramide elevation & apoptosis

Conflict of Interest Statement: Dr. Rixe holds a minor (<3%) equity interest in Bexion Pharmaceuticals, Inc.

As shown in the Mechanism of Action (MOA) video on this page, two MOAs have contributed to tumor cell death including necrosis and apoptosis. In addition, the graphic below highlights recent data obtained both pre-clinically and clinically that tumor cell death might occur from autophagy effects. Autophagic type vacuoles are observed in the pre-clinical work with GBM169 neurospheres and from GBM biopsy samples.

BXQ-350 selectively kills cancer cells through multiple mechanisms