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We recently demonstrated that anti-CD47 monoclonal antibodies (mAbs) promote the phagocytosis of solid tumor cells in vitro and inhibit the growth and metastasis of human solid tumors in xenotransplantation models (1). We also observed a significant inhibition of tumor growth in a syngeneic mouse tumor model treated with MIAP410, an anti-mouse CD47 (mCD47) mAb. In contrast, a second blocking anti-mCD47 mAb (MIAP301) produced a moderate, yet insignificant, antitumor effect. The reasons for the lack of MIAP301 activity in this model are unclear, but could simply be due to the statistical power of the study. MIAP410 was previously reported to not block mCD47–mSIRPα interactions (2). In contrast, we have determined that MIAP410 does block mCD47–mSIRPα interactions (Fig. 1). This discrepancy may be attributable to the N-terminal GST-CD47 fusion protein used in the prior blocking assays (2). Polypeptide additions at the N terminus of CD47 prevent the N-terminal glutamine residue of CD47 from forming pyroglutamic acid. As seen in the SIRPα–CD47 complex crystal structure (3), this residue is critical …

Reply to Soto-Pantoja et al. and Zhao et al.: Targeting CD47 on human solid tumors