Novel fully human anti-CD47 antibodies stimulate phagocytosis and promote elimination of AML cells

Although most patients with acute myeloid leukemia (AML) enter remission after induction chemotherapy, the risk of relapse remains considerable. Therefore, some novel therapeutic strategies are still required. This study found that the overexpression of CD47 on AML cells was at least twofold more than that on normal bone marrow (NBM) cells in 81% (17/21) of the investigated patients; no patients had lower expression level of CD47 compared with healthy donors. The study also demonstrated that blocking the CD47/SIRP alpha (signal regulatory protein alpha) signal with the established novel fully human anti-CD47 monoclonal antibodies increased the phagocytosis of AML cells by macrophages in vitro. Furthermore, in vivo experiments showed that the novel fully human anti-CD47 monoclonal antibodies could significantly prolong the survival time of mice. Overall, the novel fully human anti-CD47 antibodies could block CD47/SIRP alpha interaction, increase macrophage-mediated phagocytosis, and enhance the elimination of AML cells.

Automated summary

The study found that AML patients had significantly higher levels of CD47 expression on cells compared to healthy individuals. Using novel fully human anti-CD47 monoclonal antibodies increased macrophage-mediated phagocytosis of AML cells in vitro and prolonged the survival time of mice in vivo, enhancing the elimination of AML cells.