Effect of CD47 Blockade on Vascular Inflammation

This correspondence presents a retrospective analysis examining the vascular effects of magrolimab a CD47-blocking macrophage checkpoint inhibitor administered in a phase 1b–2 trial for lymphoma. CD47 overexpression impairs efferocytosis and contributes to vascular inflammation in atherosclerosis. Nine patients with cardiovascular risk factors underwent PET-CT imaging before and after 9 weeks of magrolimab treatment. Carotid artery inflammation, measured via ^18F-FDG uptake, was significantly reduced (SUV: 2.68 ± 0.59 to 2.06 ± 0.52; TBR: 1.56 ± 0.22 to 1.28 ± 0.11). No changes were observed in systemic ^18F-FDG uptake or traditional risk markers (blood pressure, glucose). The study, limited by sample size and lack of controls, suggests magrolimab may modulate arterial inflammation, supporting further investigation in atherosclerosis settings.

This correspondence presents a retrospective analysis examining the vascular effects of magrolimab a CD47-blocking macrophage checkpoint inhibitor administered in a phase 1b–2 trial for lymphoma. CD47 overexpression impairs efferocytosis and contributes to vascular inflammation in atherosclerosis. Nine patients with cardiovascular risk factors underwent PET-CT imaging before and after 9 weeks of magrolimab treatment. Carotid artery inflammation, measured via ^18F-FDG uptake, was significantly reduced (SUV: 2.68 ± 0.59 to 2.06 ± 0.52; TBR: 1.56 ± 0.22 to 1.28 ± 0.11). No changes were observed in systemic ^18F-FDG uptake or traditional risk markers (blood pressure, glucose). The study, limited by sample size and lack of controls, suggests magrolimab may modulate arterial inflammation, supporting further investigation in atherosclerosis settings.