Trophos Announces that TRO40303 Significantly Reduces Myocardial Infarct Size and Improves Cardiac Function
News Sep 08, 2009
Trophos SA has announced demonstration of proof of principle that its proprietary compound, TRO40303 significantly reduces myocardial infarct size and improves cardiac function.
The company presented information on two posters at the European Society of Cardiology (ESC) Congress 2009 held in Barcelona, Spain from 29 August to 2nd September.
Trophos expects the new presentations to help identify and obtain partners for this highly promising program for further development and commercialization.
TRO40303 is a novel and promising cardioprotective agent that Trophos is developing to reduce cardiac ischemia-reperfusion injury following a myocardial infarction. This is a process that can be responsible for up to 50 percent of total infarct size, which is a key determinant of morbidity and mortality. TRO40303 is scheduled to enter the clinic in early 2010 followed rapidly by a phase 2 proof of concept clinical trial.
The value of Trophos' approach and the need for such a product is supported by the scientific community and Trophos has received a significant grant to fund the program from the French Agence Nationale de la Recherche.
"These new data demonstrate that TRO40303 protects the myocardium against ischemia-reperfusion injury. This protection is at least in part mediated by prevention of opening of the mitochondrial permeability transition pore, recently validated in the clinic as a target for myocardial protection. Despite the use of treatments such as thromobolytics and stents, there is still a great need to reduce morbidity and mortality following myocardial infarction. TRO40303 could represent a new approach and we are actively seeking partners to help us exploit this promise," said Trophos CEO, Damian Marron.
The posters presented at the ESC were entitled:
TRO40303 reduces myocardial infarction size and promotes functional recovery after cardiac ischemia-reperfusion in mice (Augeul et al.), which demonstrated the activity of TRO40303 in a well characterized mouse model of cardiac ischemia-reperfusion injury. TRO40303 administered at a dose of 1mg/kg significantly reduced myocardial infarct size by 44 percent and 52 percent versus control and vehicle treated animals respectively (p<0.05).
The TRO40303 treatment also resulted in improvements to important parameters of left ventricular cardiac function. Both infarct size and left ventricular function are known to be important determinants of morbidity and mortality post myocardial infarction.
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