Active agent is the Lysosomal Protein Saposin C Fusogenic to Phosphatidylserine
The Promise of BXQ-350
Sphingolipid activator protein, SapC
80 amino acids, 9kDA
Fermentation and Purification – rDNA, e. Coli
Sphingolipids – contribute to regulation of cell membrane bilayers
Bioactive sphingolipids (like ceramide) involved in regulation of cancer pathogenesis and therapy
Beyond a stress response PS is immunosuppressive
BXQ-350 Anti-Cancer Properties
BXQ-350 is attracted to externalized PS. Preclinical experiments suggest BXQ-350 does not target normal cells.
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 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
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.
Endocytosis of BXQ-350 leading to lysosomal degradation and necrosis
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.