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Updated: Feb 21, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Drug-loaded nanoparticles reduced platelet aggregation and blood coagulation
Sarah Majin1, Afrida Malik1, Pratima Poudel1
1Department of Chemistry and Chemical & Biomedical Engineering, University of New Haven, West Haven, CT, United States.
None:
Surface-induced thrombosis remains a significant limitation of blood-contacting medical devices, driven primarily by platelet activation and rapid clot formation. Nitric oxide (NO), a potent endogenous antiplatelet agent, has therefore inspired the development of targeted NO-delivery strategies to mitigate device-associated thrombosis. In this study, nitric oxide-releasing antiplatelet lipid nanoparticles (anti-PLT LNPs) were formulated and characterized for their physicochemical properties and NO-release kinetics. Their platelet aggregation inhibition was evaluated in vitro, while mammalian cell biocompatibility and effects on whole-blood coagulation were evaluated using activated clotting time (ACT) measurements. Anti-PLT LNPs exhibited sustained and measurable NO release after 22 weeks of storage and demonstrated high mammalian cell biocompatibility. The nanoparticles inhibited platelet aggregation by up to 84.4% (p < 0.01) and significantly prolonged whole-blood clotting time, resulting in up to a threefold increase in ACT (p < 0.05). These findings indicate that NO-releasing anti-PLT LNPs effectively suppress platelet activation and coagulation while maintaining biocompatibility, offering a customizable and targeted approach to mitigate surface-induced thrombosis in blood-contacting medical devices.
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