Disease Condition
Revolutionary Treatment
Restorative Actions
Responding to the urgent need to minimise the impact of myocardial infarction and prevent further cardiomyocyte death, we have identified three naturally occurring cardioprotectant proteins, with separate restorative actions.
Revitalise
Revitalise heart function preventing
progression to heart failure
Remove, Recycle & Restore
Remove, recycle and restore damaged cardiomyocyte proteins
Protect
Protect damaged/dying cardiomyocytes keeping them healthier for longer
Cardioprotective Biology
Forcefield’s novel approach stimulates cardioprotective biology as shown in proof-of-principle studies.
Our cardioprotectant proteins prevent cardiomyocytes dying and improve long-term outcomes. They do this via three key mechanisms, namely: promotion of cellular repair (autophagy), prevention of cell death (apoptosis), inhibition of scarring (fibrosis), ultimately leading to less heart failure.
Other treatments tested in the clinic have failed to demonstrate these combination of effects (cyclosporine, cardiac ischaemic post-conditioning, sodium nitrite and MYDGF).
In our gold-standard mouse studies, the proteins outperformed existing treatments.
These studies showed that the proteins successfully preserved left ventricular function compared to control treated animals at d15 post-MI, with significantly larger diastolic volume at d60 post-MI when heart failure occurs in controls.
There was no evidence of pathological remodelling in treated animals. As early as d2 post-MI the positive cellular effect of these proteins was observed to include prevention of cardiomyocyte apoptosis by TUNEL staining of heart tissue and removal of cellular damage by autophagy shown by LC3 positive autophagosomes and autophagic flux. Lastly, one of the proteins had a profound anti-fibrotic effect, preventing fibroblast activation and scarring through suppression of TGF-beta mediated pathology.
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Our Approach
We intend to develop this therapy as an easily and acutely administered formulation enabling rapid treatment post-myocardial infarction before heart damage becomes irreversible.
Short-term treatment provides both a short- and long-term solution, preserving cardiac function and preventing likely progression to heart failure. This approach is designed to be used in combination with the existing Standard of Care (SOC) in the critical period immediately after MI.
We will develop a biopharmaceutical with a safe and efficacious mode of action (MoA) and ease of manufacturing. The proteins are known but have not previously been applied to treat MI.
Our goal is to improve outcomes after heart attack by retaining cardiomyocyte function
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