Bellicum Raises $20M to Progress Cell Transplant and Cancer Vaccine Products
Phase II trials of T-cell infusion product and prostate cancer vaccine planned for 2012.!--h2>
Bellicum Pharmaceuticals raised $20 million in a Series B financing round with new and existing investors, to support progression of its lead CaspaCIDe™ and DeCIDe™ programs through Phase II clinical development. The DeCIDe platform forms the basis of Bellicum’s drug-activated vaccines technology. Lead candidate BPX-101 is an autologous DeCIDe vaccine in clinical development for treating patients with metastatic castration-resistant prostate cancer.
DeCIDe dendritic cell vaccines contain a CID signaling domain for the membrane protein CD40, which controls dendritic cell activation. The vaccine is activated by turning on CD40 signaling once the DeCIDe dendritic cells have reached the lymph node. This activation is achieved through administration of a lipid permeable, synthetic organic compound, AP1903, 24 hours after vaccination. Bellicum says the approach leads to potent and durable antigen-specific T-cell immune response. BPX-101 is comprised of matured, prostate cancer antigen-expressing dendritic cells derived from patient’s monocytes, which are modified to enable activation by AP1903.
The CaspaCIDe platform has been designed as a cell therapy safety technology that acts as a remote self-destruct switch for transplant therapies in the event of toxicity. Harvested cells to be used for transplantation are engineered to express the CaspCIDe gene, which includes the CID signaling domain for caspase 9, an initiator caspase that triggers apoptosis when activated and leads to rapid elimination of cells expressing the CaspaCIDe protein.
In cases of toxicity developing following cell transplantation, administration of AP1903 effectively triggers the suicide gene, leading to rapid self-elimination by the transplanted cells. Lead CaspaCIDe DLI product is a donor T-cell infusion product administered following a hematopoietic stem cell transplant, which can be activated to instruct donor cells to self-destruct in the event of graft-versus host disease.