Scientific Basis

Phosphatidylserine (PS) is known to be selectively exposed on the surface of cells undergoing apoptotic or programmed cell death, marking them for engulfment by phagocytes such as macrophages as well as neighboring cells. The rapid phagocytosis of PS-expressing apoptotic cells and apoptotic bodies prevents the release of pro-inflammatory cellular contents of ingested cells and provides for rapid, safe removal of dying or otherwise unwanted cells as part of normal tissue homeostasis. PS also has profound suppressive effects on the immune system. In fact, many viruses, parasites, bacteria and tumor cells utilize externalized PS to evade recognition and attack by the innate and adaptive immune systems in a process known as “apoptotic mimicry.”

Role of PS in Normal Cell Undergoing Apoptosis

 
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IMM-010

We are developing IMM-010 (annexin V), a naturally occurring protein that binds to PS, for the treatment of multiple high value oncology and serious infectious disease indications. We believe that by binding to active PS expressed disproportionately on tumor cells and infective organisms IMM-010 will allow the inherent immunosuppressive (checkpoint) role that PS plays in both normal cellular apoptosis and active evasive immune responses to be eliminated, reduced or diminished. 

IMM-010 has been effective in generating immune responses resulting in slowing tumor size (comparable to approved checkpoint antibodies) and increased survival as well as anti-intracellular pathogen effects in animal models of disease. Additionally, Francis Blankenberg, MD, at the Stanford University School of Medicine, and Jonathan Rayner, PhD, at University of South Alabama are conducting studies on the efficacy of IMM-010. Based on these studies, Immunomodulation is working to drive the execution of its development plan.

Annexin V has been studied extensively as an imaging agent in multiple Phase 2 and Phase 3 clinical trials in the U.S. and Europe. Collaboratively, it has been demonstrated that IMM-010 is effective in generating an immune response which dramatically slowed tumor growth, significantly increased survival and was more effective than either anti-PD-1 or anti-CTLA-4 antibody immune checkpoint therapy. Additional studies have shown the combination of PD-1, CTLA-4, and IMM-010 significantly improves survival compared to antibody or IMM-010 intervention alone.