Experimental Drug Prevents Cardiac Reperfusion Injury

About 50% of the damage to heart tissue following MI is due to re-oxygenation leading to a burst of reactive oxygen species as energy production by mitochondria is reactivated. The mechanism of action of TRO40303 involves prevention of stress-induced mitochondrial permeability transition, a target implicated in cardiac reperfusion injury.

The objective of the phase I study was to assess the safety, tolerability, and pharmacokinetics of single escalating doses of TRO40303 as an intravenous infusion at different rates compared with placebo in 72 healthy volunteers. The results demonstrated that TRO40303 could be safely administered by the iv route in humans at doses expected to be pharmacologically active.

"We are very pleased with the highly satisfactory results of this rigorous and extensive phase I study of TRO40303. This will allow us to initiate our important phase II proof-of concept trial of TRO40303 in the second half of this year with our consortium partners in the European Union funded MitoCare project,” said Dr. Jean-Louis Abitbol, chief medical officer at Trophos. "A treatment is urgently required globally to prevent cardiac reperfusion injury. This is a major problem in the care of MI patients despite the overall improvements in prognosis in recent years. There is no existing treatment for this problem that contributes to long-term morbidity, progression to heart failure, and death following a MI. The role of mitochondrial permeability transition in cardiac reperfusion injury has recently been validated clinically making this is a tremendous opportunity for our novel mitochondrial pore modulator, TRO40303, discovered and developed in our laboratories to target this mechanism.”

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