# Using Cardiac Targeting Peptide to deliver miRNA for molecular reversal of heart failure

> **NIH NIH R41** · VIVASC THERAPEUTICS INC. · 2022 · $284,668

## Abstract

PROJECT SUMMARY/ABSTRACT
Heart failure (HF) is a common disease with well-documented morbidity and mortality that affects
approximately 23 million people globally, including 6 million in the US. Current HF medications such as
Angiotensin Converting Enzyme (ACE) Inhibitors or Angiotensin Receptor Blockers (ARBs) treat the symptoms
of HF versus the root cause of the disease, which includes stressed myocardium that leads to hypertrophic
cardiomyocytes and endothelial inflammation.
CaMKIIδ is a signaling molecule that regulates cellular pathways involved in excitation‑contraction coupling
and relaxation events in the heart and transcriptional activation of genes related to cardiac hypertrophy,
inflammation, and arrhythmias. If left uncorrected, CaMKIIδ‑regulated changes culminate in a dysfunctional
myocardium and HF. The goal of this STTR Phase I project is to address this root cause of HF by delivering
miRNA to cardiomyocytes to down-regulate the over-expression and/or activation of CaMKIIδ because this
may allow damaged cardiomyocytes to regain normal function.
To achieve this goal, a specific miRNA will be selected that effectively inhibits the expression of CaMKIIδ in
vivo. This miRNA will then be conjugated to the proprietary cell penetrating peptide, Cardiac Targeting Peptide
(CTP), developed by Vivasc Therapeutics. This will create a CTP-miRNA conjugate that will deliver this
nucleotide specifically and directly to cardiomyocytes. CTP is a novel, synthetic peptide that has transduced (i)
normal mouse hearts in vivo (peak uptake at 15 minutes after injection), (ii) explanted human heart tissue, and
(iii) human derived iPSC beating cardiomyocytes. CTP has demonstrated robust transduction of normal
cardiomyocytes while sparing myofibroblasts, endothelial cells, and fibroblasts present in scar tissue. To date,
CTP conjugates have transduced cardiomyocytes carrying intact cargoes as diverse as radioisotopes, nucleic
acids, other peptides, and conjugates as large as the biotin-streptavidin complex. The team’s preliminary data
has shown that CTP is fully capable of carrying miRNA in a similar manner.
The hypothesis is that CTP-miRNA will deliver miRNA to cardiomyocytes that are over expressing CaMKIIδ,
thereby allowing damaged cardiomyocytes to regain normal function. The aims are: 1) deliver specific miRNAs
to the hearts of HF mouse models to demonstrate their efficacy in reversing HF physiology and 2) test the in
vivo biodistribution of CTP-miRNA using a dual-labeled CTP-miRNA.
Phase II plans include conducting studies of optimized CTP-miRNA in larger animal models of HF and IND-
enabling studies to support an Investigational New Drug (IND) submission for approval of a Phase 1 clinical
trial. Upon approval, this treatment could potentially be prescribed to HF patients with cardiac hypertrophy,
inflammation, and arrhythmias.

## Key facts

- **NIH application ID:** 10481720
- **Project number:** 1R41HL164212-01
- **Recipient organization:** VIVASC THERAPEUTICS INC.
- **Principal Investigator:** G IAN GALLICANO
- **Activity code:** R41 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $284,668
- **Award type:** 1
- **Project period:** 2022-07-13 → 2024-07-12

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10481720

## Citation

> US National Institutes of Health, RePORTER application 10481720, Using Cardiac Targeting Peptide to deliver miRNA for molecular reversal of heart failure (1R41HL164212-01). Retrieved via AI Analytics 2026-05-28 from https://api.ai-analytics.org/grant/nih/10481720. Licensed CC0.

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