Compound prevents transition from heart damage to heart failure
Each year, in the United State alone, 160,000 people develop heart failure from acute heart damage. This results in more than $17 billion dollars in direct healthcare costs and more than 80,000 deaths within five years from heart damage. Unfortunately, there are no therapies to prevent the development of heart failure after acute heart damage.
Pirfenidone, an old FDA-approved drug for the treatment of a rare lung disease, has been shown to protect the injured heart in several species. But its use in the cardiovascular space has been limited by its poor pharmacological properties that cause frequent side effects, the absence of a therapeutic target/mechanism of action and by a lack of intellectual property.
Researchers at Washington University in St Louis have discovered that B lymphocytes are the cellular target of Pirfenidone mediated cardioprotection, and have developed Pegydone, a PEGylated Pirfenidone that is expected to have superior pharmacokinetics, composition of matter IP and freedom to operate. Pegydone has been shown to have the same effects on B lymphocytes as Pirfenidone in vitro.
In addition, Pegydone has a much longer half-life than Pirfenidone and has the same bioavailabiltiy in rodents. As a superior Pirfenidone, PEGydone has the potential to become a first-in-class drug to break the connection between heart damage and heart failure. In addition, Pegydone has the potential to enter both the current market of Pirfenidone ($1bn sales/year in patients with lung disease) and its emerging applications (HFpEF, Sarcoidosis and Systemic Sclerosis).