Anti-CD47 antibodies have stalled. The target has not.
Our new Kidney International paper reports an engineered vesicle displaying a high-affinity SIRPα variant on its surface, designed to engage circulating CD47+ myeloid cells in acute kidney injury before they infiltrate the renal parenchyma.
In two AKI models, a single intravenous dose reduced BUN, creatinine, and NGAL, and reprogrammed macrophages toward a pro-resolving phenotype.
The platform combines multivalent surface display, active cellular internalization, and selective enrichment on disease-relevant immune cells. These are capabilities a monoclonal antibody does not have.
That is the asset today.
The same surface-engineering strategy extends as a delivery platform for next-generation immunology payloads, including ASO and siRNA.
Therapeutic on its own. Delivery vehicle for what comes next.
To read the complete publication, please click here.
https://www.sciencedirect.com/science/article/abs/pii/S0085253825010221
Anti-CD47 antibodies have stalled. The target has not.
Our new Kidney International paper reports an engineered vesicle displaying a high-affinity SIRPα variant on its surface, designed to engage circulating CD47+ myeloid cells in acute kidney injury before they infiltrate the renal parenchyma.
In two AKI models, a single intravenous dose reduced BUN, creatinine, and NGAL, and reprogrammed macrophages toward a pro-resolving phenotype.
The platform combines multivalent surface display, active cellular internalization, and selective enrichment on disease-relevant immune cells. These are capabilities a monoclonal antibody does not have.
That is the asset today.
The same surface-engineering strategy extends as a delivery platform for next-generation immunology payloads, including ASO and siRNA.
Therapeutic on its own. Delivery vehicle for what comes next.
To read the complete publication, please click here.
https://www.sciencedirect.com/science/article/abs/pii/S0085253825010221