Overview
Overview
Parent Cell: Akira Cardiac Progenitor Cells differentiated from UCT-WJ-MSCs | Cardioprotective and pro-angiogenic exosomes for myocardial infarction recovery, heart failure, and cardiac fibrosis reduction
FOR RESEARCH USE AND INTERNATIONAL USE ONLY
| Source & Manufacturing |
|---|
| 110 Billion Exosomes / 1 mL vial |
| VEGF and miR-21 / miR-146a confirmed by ELISA and qPCR |
| NTA mean size 80–115 nm |
| Stored at −80°C. |
Definition
What Are Exosomes?
Exosomes are nanoscale extracellular vesicles (40–150 nm) formed by inward budding of endosomal multivesicular bodies (MVBs) and released upon MVB fusion with the plasma membrane. They carry a protected cargo of mRNAs, miRNAs, proteins, lipids, and signaling molecules from their parent cell, delivering this molecular payload to recipient cells with high specificity and efficiency. Unlike the parent cell, exosomes carry no nuclear material and cannot self-replicate — providing a cell-free therapeutic profile with superior safety and stability characteristics.
Process
Mechanism of Action & Molecular Cargo
Anti-Apoptotic Protection: miR-21 activates PI3K/Akt in cardiomyocytes, directly suppressing PTEN-driven apoptosis and reducing ischemia-reperfusion injury cell death in the infarct border zone by 40–60%.
Angiogenesis: VEGF, miR-132, and FGF-2 cargo stimulates endothelial proliferation and capillary formation in ischemic myocardium — increasing neovascular density and oxygen delivery.
Anti-Fibrosis: miR-146a and miR-21 suppress TGF-β1-driven cardiac fibroblast activation, reducing collagen deposition and preventing adverse ventricular remodeling post-MI.
Cardiomyocyte Survival: IGF-1 mRNA and HGF protein in exosomal cargo activate Met and IGF-1R receptors on cardiomyocytes — suppressing caspase-3 and preserving sarcomere integrity.
Electrical Remodeling: Connexin-43 mRNA delivery restores gap junction communication disrupted by ischemia, supporting electrical synchrony restoration.
Biomarkers
Key Molecular Cargo
| Molecule / miRNA | Therapeutic Function |
|---|---|
| miR-21 | PI3K/Akt activation; anti-apoptotic cardiomyocyte protection |
| miR-146a | TGF-β1 suppression; anti-fibrotic cardiac remodeling |
| VEGF / FGF-2 mRNA | Angiogenesis in ischemic myocardium |
| IGF-1 / HGF protein | Cardiomyocyte survival signaling |
| miR-132 / miR-21 | Pro-angiogenic miRNAs |
| Connexin-43 mRNA | Gap junction restoration; electrical synchrony |
Applications
Therapeutic Applications
- Post-MI Myocardial Repair — anti-apoptotic, anti-fibrotic, pro-angiogenic
- Congestive Heart Failure — ejection fraction support
- Ischemic Cardiomyopathy — neovascularization
- Cardiac Fibrosis — ECM remodeling
- Arrhythmia Prevention Post-MI — connexin restoration
- Coronary Artery Disease — microvascular repair adjunct
Evidence
Clinical & Preclinical Evidence
A 2023 meta-analysis of HUC-MSC therapy in heart failure/MI confirmed significant LVEF improvement and reduced adverse cardiac events — providing the parent cell evidence base directly applicable to the exosome product.[1]
In preclinical MI models, CPC-derived exosomes (IV delivery, 100 μg protein) improved LVEF by 8–12%, reduced infarct scar size by 30–35%, and increased capillary density in border zone by 2.3× at 4 weeks — reproducing the parent cell's therapeutic effects in a cell-free format.
miR-21-enriched exosomes from cardiac progenitor cells demonstrated 55% reduction in cardiomyocyte apoptosis (TUNEL assay) and 3× increase in survival signaling (p-Akt) in in vitro hypoxia models — confirming the primary anti-apoptotic mechanism.[2]