DG041 Blocks Platelet Aggregation Through a Novel Mechanism and does not Increase Bleeding Time When Given Alone or with Plavix™ or Aspirin
Reykjavik, ICELAND, June 30, 2008 – deCODE genetics (Nasdaq:DCGN) today announced positive topline results from its latest clinical pharmacology study of DG041, the company’s first-in-class antagonist of the EP3 receptor for prostaglandin E2, developed as a next-generation oral anti-platelet therapy for preventing arterial thrombosis without increasing bleeding risk. The prospective, randomized, blinded, crossover study compared the effects on platelet activation and bleeding time of DG041 alone and in combination with the mainstays of current antiplatelet treatment, Plavix™ (clopidogrel) and aspirin. The results confirm previous clinical findings that DG041 inhibits platelet aggregation without increasing bleeding time as monotherapy, and further demonstrated that in combination with clopidogrel alone, as well as with clopidogrel and aspirin, DG041 provided additional antiplatelet effect without prolonging bleeding time.
deCODE’s product development team will discuss the results of this study in detail at the company’s annual R&D event,to be webcast live today beginning at 1pm Eastern Time through the investor’s page of the company’s website, www.decode.com.
“These findings underscore the potential of DG041 as a next-generation oral anti-platelet: a compound that can reduce the risk of thrombi formation without increasing overall bleeding risk. While the current standard of care, clopidogrel and aspirin, has been shown to be effective in decreasing the risk of blood clots leading to heart attack and stroke, they do so in an untargeted manner and thus raise the likelihood of unwanted bleeding. By targeting EP3, which we identified through our human genetics work in peripheral artery disease, stroke and heart attack, DG041 has been shown to offer a novel approach to inhibiting platelet aggregation where it is needed – at the site of lesions in the vasculature. One of the most compelling results coming out of this study is that DG041 was shown to substantially inhibit EP3 mediated platelet activation that is not being addressed by current therapy. This suggests that DG041 may have a favourable profile not only as a first-line therapy, but also as a combination therapy with existing standard of care. We are encouraged by these results and look forward to advancing DG041 into later stage trials with a strategic partner,” said Kari Stefansson, CEO of deCODE.
deCODE’s medicinal chemistry group discovered DG041 as a means to prevent arterial thrombosis by inhibiting the activity of EP3. In Phase I and Phase IIa clinical trials and follow-on clinical pharmacology studies, DG041 has been shown to dramatically inhibit platelet aggregation as well as platelet activation mediated specifically through vasodilator-stimulated phosphoprotein (VASP), a biomarker useful for measuring platelet activity. Following deCODE’s gene discovery work linking this pathway with arterial disease, work by leading international scientists demonstrated in mice that PGE2 is produced in atherosclerotic plaques, promoting the formation of clots immediately at the sites of plaque but not over normal blood vessels. The formation of these thrombi is dependent on signaling through EP3. This pathway is left largely unaffected by existing anti-platelet drugs such as aspirin and Plavix™. deCODE is actively pursuing partnership opportunities for the latter phases of the clinical development of DG041.