About Us

Scientific background

When an organ loses blood flow (during a heart attack, an organ transplant, or a major medical procedure) it becomes starved of oxygen and nutrients. This deprivation is called ischemia, and it places cells under severe stress.

But surprisingly, the greatest damage often occurs not during the loss of blood flow, but when blood flow is restored. This moment, known as reperfusion, unleashes a rapid surge of inflammation, oxidative stress, and cell death. Restoring blood flow is essential and lifesaving, yet the body’s intense reaction to reperfusion can harm the very organs we are trying to protect.

In heart attacks, this can limit heart muscle recovery. In organ transplantation, it can impair the function of the newly transplanted organ.

And during major medical procedures such as long cardiac surgeries or complex tumor resections, it can cause impaired kidney function or acute kidney injury (AKI).  Reduced kidney blood flow during lengthy operations can trigger the same damaging cycle of ischemia followed by reperfusion injury.

Current treatments focus on restoring circulation, supporting organ function, or preventing immune rejection, but none address the harmful cellular cascade triggered when blood flow returns. This gap leaves organs vulnerable during a critical window.

Our lead therapeutic candidate, DMX-5804, is designed to protect organs at the exact moment reperfusion occurs, when they are most at risk. By reducing the inflammatory and stress-response signals that drive reperfusion injury, DMX-5804 aims to preserve tissue, enhance recovery, and improve long-term organ function.

Because the biology of reperfusion injury is similar across the heart, kidney, and transplanted organs, this approach provides a unified therapeutic solution for multiple, high-impact medical needs. Altogether, our therapy is Aiding Ischemic Reperfusion Recovery.