# Mitigation of Radiation Injury via Vascular Regeneration and Remodeling

> **NIH NIH U01** · CEDARS-SINAI MEDICAL CENTER · 2021 · $501,000

## Abstract

The theme of the UCLA-CMCR Program is to discover and
develop novel and unique drugs, or to repurpose existing agents, that mitigate acute, delayed, and
long-term radiation syndromes. We have already identified over 30 mitigators of hematopoietic acute
radiation syndrome (H- ARS), some of which are in quite advanced drug development. Some are
effective in multiple models of acute, delayed and long-term radiation tissue damage, which makes
them of particular interest as every cell in the body is damaged after exposure to moderate doses of
radiation and polypharmacy to mitigate every syndrome would be almost impossible to achieve. We
believe that broad activity results from action through primitive, highly conserved, developmental
signaling pathways that are responsible for the formation of body structures, but that also guide
regeneration in damaged tissues and regulate chronic inflammation. The role of these pathways in
diverse radiation syndromes, acute and delayed, form a major theme in this application. Our Projects
will therefore extend our portfolio of mitigators with an emphasis on developmental signaling pathways
in multiple tissues. Two focus on Acute syndromes and two on late syndromes. We believe that
delayed effects of acute radiation exposure (DEARE) are due to incomplete healing during H-ARS,
resulting in skewing of the immune system that generates persistent oxidative stress, chronic
inflammation, and dysregulated homeostasis in multiple tissues. This is consistent with our finding that
mitigation of H-ARS by drugs that trigger developmental pathway signaling can affect DEARE. Our
Service Cores are geared to drug and animal model optimization. They will improve the efficacy and
delivery of drugs through FDA-approved formulation and chemical synthesis that aims to improve
solubility, pharmacokinetics, mechanisms of action, and uniqueness of matter. The animal models will
have pathophysiologically-defined, dose-response relationships for acute and delayed endpoints of
morbidity and mortality using gnotobiotic and germ-free mouse strains. Comparisons will be made to
the effects of FDA-approved H-ARS mitigators in these diverse radiation syndromes. The
Administrative Core serves to integrate projects, service cores, and pilot projects and provides a
conduit to the CMCRC, governmental bodies, industry, and academia. It provides cohesion for the
UCLA-CMCR and ensures that it meets the common goals established by NIAID, the FDA, and the
CMCRC. It also provides an educational infrastructure for members and its Executive Committee helps
investigators prioritize drugs for development and testing, and with regulatory and intellectual property
issues.

## Key facts

- **NIH application ID:** 10313992
- **Project number:** 7U01AI156922-02
- **Recipient organization:** CEDARS-SINAI MEDICAL CENTER
- **Principal Investigator:** John P Chute
- **Activity code:** U01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $501,000
- **Award type:** 7
- **Project period:** 2020-06-05 → 2025-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10313992

## Citation

> US National Institutes of Health, RePORTER application 10313992, Mitigation of Radiation Injury via Vascular Regeneration and Remodeling (7U01AI156922-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10313992. Licensed CC0.

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