# Increasing biocompatibility of stents via CD47 surface functionalization: Mechanistic and Preclinical studies

> **NIH NIH R01** · CHILDREN'S HOSP OF PHILADELPHIA · 2020 · $708,407

## Abstract

Abstract/Summary
The pathophysiology associated with endovascular stent usage is well documented and is observed in up to
50% of all patients receiving the medical device. CD47 is a ubiquitously expressed transmembrane protein,
that when bound to its cognate receptor Signal Regulatory Protein alpha (SIRP), inhibits the immune
response. We have shown, both ex vivo and in a rat carotid stent model, that immobilized recombinant CD47,
or a 21 amino acid peptide sequence (pepCD47) thereof, significantly inhibited restenosis and thrombosis. The
overall objective of the proposed research is to investigate the anti-restenotic capacity of a pepCD47
functionalized endovascular stent in rabbit and porcine animal models. Three Specific Aims (SA) will test our
central hypothesis that immobilized pepCD47 represents a pragmatic surface modification strategy that will
control adverse immunological and hemocompatibility responses and thus significantly contribute to
biocompatibility of endovascular stents. In SA 1 we will fabricate and perform efficacy and stability analysis
on CD47 functionalized metal surface to test our working hypothesis that rabbit and pig CD47, immobilized
on the bare metal surfaces, will confer a similar anti-platelet and anti-inflammatory activity as human CD47 and
will be amenable to clinically relevant challenges. SA 2 will determine how immobilized CD47 affects
cellular interactions at the blood/stent interface. Our working hypothesis is that immobilized CD47 confers
a biocompatible microenvironment that inhibits inflammatory cell and platelet interactions and permits re-
endothelialization. SA 3 will demonstrate in vivo efficacy of CD47 functionalized stents in the large
animal models. Our working hypothesis is that CD47 modified stents would confer significantly greater
biocompatibility, compared to commercially available bare metal stents and drug eluting stents (DES), which
will be demonstrated by a significant reduction in ISR of the stented site. The rationale for the proposed
research is that demonstration of pepCD47 mediated inhibition of ISR in a large animal model would provide
necessary preclinical and usage data to advance the application of the CD47-functionalized stents into the
clinical realm. The research is significant because it will demonstrate the broad translational importance of
CD47 in regulating the cellular/molecular response to synthetic surfaces that are used in clinically relevant
biomedical devices. The research proposed herein is innovative because it challenges and redirects current
therapeutic strategies, such as DES, by identifying candidate molecular signaling mechanisms that actively
regulate cellular interactions with solid synthetic surfaces, and then incorporating these concepts into the
design and fabrication of metallic stents.

## Key facts

- **NIH application ID:** 9935058
- **Project number:** 5R01EB023921-04
- **Recipient organization:** CHILDREN'S HOSP OF PHILADELPHIA
- **Principal Investigator:** Ilia Fishbein
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $708,407
- **Award type:** 5
- **Project period:** 2017-09-15 → 2022-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9935058

## Citation

> US National Institutes of Health, RePORTER application 9935058, Increasing biocompatibility of stents via CD47 surface functionalization: Mechanistic and Preclinical studies (5R01EB023921-04). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/9935058. Licensed CC0.

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