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Forcefield Therapeutics

The startup develops therapeutics that protect heart function by preventing the loss of cardiomyocytes after myocardial infarction. This approach enables healthcare providers to minimize heart muscle damage during heart attacks, improving patient outcomes.

London, United Kingdom71K+ followers
Updated 2 months ago

Funding

$8.5M raised to dateRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.

Funding rounds are not available yet.

Founders

Product

Problem

Following a myocardial infarction (MI), or heart attack, patients experience irreversible damage due to the death of cardiomyocytes, the heart's muscle cells, which the body cannot replace. Current treatments often fail to prevent significant cardiomyocyte loss, leading to heart failure and reduced lifespan for many patients. The median time from MI symptoms to treatment is often too long, resulting in inevitable and irreversible damage.

Solution

Forcefield Therapeutics is developing first-in-class therapeutics designed to protect cardiomyocytes and preserve heart function following a heart attack. Their approach centers on naturally occurring cardioprotectant proteins that stimulate cellular repair, prevent cell death, and inhibit scarring within the heart tissue. These proteins are intended to be administered acutely post-MI, working in combination with the existing standard of care to minimize damage and prevent progression to heart failure. Preclinical studies have demonstrated that these proteins outperform existing treatments by preserving left ventricular function and preventing pathological remodeling.

Target Audience

The primary target audience includes patients who have experienced a myocardial infarction and the healthcare providers, including cardiologists and interventional cardiologists, who treat them.

Features

  • Utilizes naturally occurring cardioprotectant proteins to retain heart function after MI.
  • Promotes cellular repair (autophagy) to remove and recycle damaged cardiomyocyte proteins.
  • Prevents cardiomyocyte death (apoptosis) to keep damaged/dying cells healthier for longer.
  • Inhibits scarring (fibrosis) through suppression of TGF-beta mediated pathology.
  • Aims for short-term treatment with a formulation enabling rapid administration post-MI.
  • Designed for use in combination with the existing Standard of Care (SOC).
  • Biopharmaceutical development based on well-established protein science and CMC development approaches.
  • Exclusive IP license for the application of these proteins in the treatment of cardiac disease.
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