# Mechanism of F-18-fluorodeoxyglucarate accrual in myocardial injury

> **NIH HL R01** · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · 2026 · $362,500

## Abstract

PROJECT SUMMARY
Each year millions of individuals suffer from heart ailments such as myocardial infarction (MI), myocarditis,
cardiomyopathies, etc. that lead to heart failure. Most heart failures are due to the loss of conductivity and
contractility secondary to fibrosis that develops as a common response to these cardiac conditions. Early
localization of myocardial fibrosis and its resolution is critical to address functional deficit in the failing heart
as some types of cardiac fibrosis can be reversed by timely treatment before changes become irreversible.
Current diagnostic methods to localize cardiac fibrosis are limited to either myocardial biopsy (invasive, risky,
and prone to sampling error) or contrast-magnetic resonance imaging (low sensitivity and only able to detect
fibrosis at an advanced and irreversible stage). The objective of this project is to investigate a novel radiotracer
18F-fluoroglucaric acid (18F-FGA) for early detection of cardiac fibrosis by positron emission tomography
(PET). PET is a superior imaging technology because of its high resolution, sensitivity, and lack of attenuation.
Using molecular techniques, our lab has recently reported that 18F-FGA interacts with an early fibrosis protein
called fibronectin. Earlier, we developed a novel rapid technique of synthesizing 18F-FGA from commercially
available 18F-fluorodeoxyglucose (18F-FDG), and we reported highly sensitive detection of myocardial
infraction and drug-induced cardiomyopathy in preclinical models. The overarching hypothesis of this
proposal is that the interaction of 18F-FGA with fibronectin and its distribution in myocardial injury can be
exploited to non-invasively detect onset and progress of cardiac fibrosis by PET imaging. We will 1) determine
the dynamics of interaction between 18F-FGA and fibronectin (Aim 1); 2) determine time-course of fibronectin
accrual in myocardial injury and correlate with 18F-FGA/PET findings (Aim 2), and; 3) assess toxicity and
internal dosime

## Key facts

- **NIH application ID:** 11311850
- **Project number:** 5R01HL169530-03
- **Recipient organization:** UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR
- **Principal Investigator:** VIBHUDUTTA  AWASTHI
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** HL
- **Fiscal year:** 2026
- **Award amount:** $362,500
- **Award type:** 5
- **Project period:** 2024-04-01T00:00:00 → 2028-03-31T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11311850

## Citation

> US National Institutes of Health, RePORTER application 11311850, Mechanism of F-18-fluorodeoxyglucarate accrual in myocardial injury (5R01HL169530-03). Retrieved via AI Analytics 2026-07-13 from https://api.ai-analytics.org/grant/nih/11311850. Licensed CC0.

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