Our lead molecule, Hu5F9-G4, is a first in class monoclonal antibody targeting CD47, a “don’t eat me” signal commandeered by cancer cells to avoid phagocytosis by macrophages. Hu5F9-G4 takes the brakes off of macrophages in a similar way as checkpoint inhibitors take the brakes off T cells and has broad applications spanning multiple tumor types and treatment modalities. CD47 was originally identified more than a decade ago, by our scientific founders at Stanford University, as a cancer target that is over-expressed on tumor cells (to overcome the presence of intrinsic eat me signals) and is correlated with worse clinical outcomes. In several preclinical studies, Hu5F9-G4 has been shown to facilitate phagocytosis and elimination of cancer cells from multiple human tumor types as a monotherapy. Additionally, when used in combination therapy, it engaged macrophages as effector cells to enhance the efficacy of cancer-specific antibodies like rituximab and cetuximab via Antibody Dependent Cellular Phagocytosis (ADCP). Importantly, Hu5F9-G4 also could prime an effective antitumor T-cell response through cross-presentation of cancer cell antigens by macrophages, thus providing anti-tumor protection that can prevent tumor recurrence. As a first-in-class CD47/SIRPÉ‘ targeting therapy, Hu5F9-G4 has the potential for broad anti-tumor activity as a monotherapy or in multiple combination approaches.

Hu5F9-G4 has Applications in Multiple Tumor Types and Treatment Modalities
MOA image
Hu5F9-G4 integrates the adaptive and innate immune systems creating synergy with existing cancer-specific antibodies through ADCP, and potentially with T-cell checkpoint inhibitors through cross-presentation.