Helping cells survive ischemia

Ischemic damage to the heart, whether by acute thrombosis or procedural intervention, can lead to myocardial tissue death and irreversible loss of function, resulting in worse clinical outcomes including cardiac failure and death. By reducing and optimally preventing irreversible ischemic damage, our therapy has the potential to improve outcomes and extend lives. This technology is expected to be especially useful in the older population, which suffers disproportionally from poor outcomes after cardiac ischemia. The technology has the potential to offer notable commercial and health-related benefits to payers, patients, and providers including: 


  • Reduction in the incidence of heart failure with improved quality of life, decreased morbidity and mortality, and resulting in significant reduction of healthcare costs

  • Intravenous delivery for rapid provision of myocardial protection even outside an ER setting, or intracoronary administration for immediate bioavailability

  • Action through an endogenous pathway to augment the body’s normal defense mechanism

  • High-yield, low-cost manufacturing of the drug component in bacteria

  • The opportunity to provide precision medicine to a leading cause of premature death by the use of a rapid point-of-care genetic test, and the opportunity to conduct more cost effective clinical trials in a genetically stratified patient population

MIFCOR's Therapeutic interventions


Also known as D-dopachrome tautomerase (D-DT), is a recombinant protein therapeutic that engages pro-survival pathways.


A small molecule agonist of MIF activity that activates same pro-survival signaling in cells under ischemia.

Indications where ischemia-reperfusion injury occurs:

Heart Attack and percutaneous coronary intervention (PCI)

Coronary Artery Bypass Graft (CABG)

Organ Transplant

Acute Kidney Injury

Peripheral Arterial Disease and Stroke