A total of 96 patients received DX-9065a, 23 received UFH in this five-center trial.
In terms of side effects, both agents were very similar, Alexander said. The DX-9065a acted in a predictable fashion and as we expected. This trial involved a small number of patients, so obviously more studies are necessary, especially to determine the optimal dosing for patients.
A second Phase II trial, known as XaNADU-ACS (acute coronary syndrome), is currently enrolling an anticipated 400 high-risk heart patients in a comparison with UFH. The results of these two Phase II trials will form the basis for the design of future Phase III trials.
When Factor Xa is activated, it converts a precursor chemical circulating in the blood known as prothrombin into the enzyme thrombin. Once activated, thrombin then converts circulating fibrinogen (Factor I) into the protein fibrin, the primary building block of a blood clot.
The advantages of interrupting the clotting cascade at the point of Factor Xa activation is that it sits at the intersection of the two classical pathways for blood clot formation and limits the generation of thrombin, Alexander said.
Heparin works by inhibiting the action of circulating thrombin, meaning that thrombin is produced, but is then inhibited, Alexander said. The new agent will stop the process even before the formation of thrombin, which theoretically should make it a more effective anti-coagulant.
Unlike other available anti-coagulants, including UFH and the low-molecular-weight heparin, DX-9065a is not dependent on the action of anti-thrombin III and is able to inhibit Factor Xa within clots that have already formed.