A mechanism of action targeting the IRI cascade
Reducing reactive oxygen species (ROS) damage and inflammation
FDY-5301’s unique properties are well-suited to mitigate ischemia-reperfusion injury (IRI).
In preclinical IRI models FDY-5301, a formulation of sodium iodide, reduced tissue damage, infarct size, and inflammation. Iodide functions as a catalytic neutralizer of hydrogen peroxide (H2O2), a prominent reactive oxygen species (ROS) implicated in the IRI cascade leading to cardiomyocyte death. Iodide also acts as an immunomodulating agent.
A potentially powerful intervention
Iodide naturally redistributes in humans following stress. FDY-5301 enhances this response by increasing the body’s natural blood iodide levels by 1000-fold.
Sodium iodide catalytically destroys hydrogen peroxide and beneficially modulates inflammatory pathways by reducing ROS damage and inflammation. These characteristics enable FDY-5301 to potentially target the multiple pathways that cause ischemia-reperfusion injury simultaneously.
Prior to reperfusion
FDY-5301 is easy to deliver prior to reperfusion and rapidly reaches anticipated therapeutic levels.
In seconds
FDY-5301 catalytically destroys hydrogen peroxide (H2O2) to reduce cell death due to ROS burst upon reperfusion.
In minutes to hours
FDY-5301 reduces migration of neutrophils into the damaged tissue.
In hours to days
FDY-5301 reduces the cardiac inflammatory response.
A multi-faceted strategy for limiting IRI
By attenuating ROS, reducing neutrophil migration, and modulating the immune response, FDY-5301 is a multi-faceted strategy for limiting IRI, potentially reducing infarct size following myocardial infarction treated by PCI.
Anterior STEMI typically represents an acute occlusion of the most vital coronary artery, the left anterior descending, and its reperfusion by PCI is believed to have the most IRI-mediated damage among heart attacks as well as risk of subsequent heart failure. The potential clinical impact of IRI in anterior STEMI is being investigated in a Phase 3 clinical trial, Iocyte AMI-3.