Cayuga Biotech introduced groundbreaking preclinical findings today on its innovative polyphosphate (polyP)-based therapy aimed at combating life-threatening hemorrhage. The study revealed that the polyP-SNP (silica nanoparticle) complex accelerates thrombin production 12 times faster than conventional methods under both standard and lethal triad conditions in vitro and ex vivo. These results, presented at the Annual Meeting of the International Society for Thrombosis and Haemostasis in Bangkok, showcase the complex’s potential to significantly enhance clotting speed while minimizing the risk of off-target thromboembolism.
Dr. James Morrissey, co-author of the study and Professor of Biological Chemistry and Internal Medicine, Cardiology at the University of Michigan, highlighted the significance: “The ability of exogenous polyP to address noncompressible hemorrhage has historically been hindered by systemic delivery challenges. These findings are particularly exciting as they demonstrate that our novel polyP-SNP complex not only overcomes these obstacles but also exhibits superior clotting efficacy, even in conditions that compromise the body’s natural hemostatic mechanisms like hemodilution, hypothermia, and acidosis.”
Presented in the ISTH session on “New strategies for reversal and prevention of bleeding,” the data underscored the complex’s ability to hasten clot formation both in laboratory settings and in scenarios mimicking severe physiological stress. As an injectable agent inert to healthy tissue, the polyP-SNP complex targets bleeding sites through the bloodstream, facilitating rapid clotting responses without inducing excessive clot formation elsewhere. Importantly, its mechanism of action operates independently of FXII activation, mitigating concerns about unintended clotting complications in non-bleeding tissues.
Detailed abstracts of the studies are available on the ISTH website at isth2024.org.
In the context of hemorrhage, an issue claiming nearly 2 million lives annually worldwide, preventable deaths often stem from non-compressible bleeding sites and delays in achieving effective hemostasis, inadequately addressed by current medical practices.
