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In this study, activated platelet‐derived vesicles (Act‐VEs) are developed as a novel hemostatic biomaterial. Spherical Act‐VEs (114.40 ± 11.69 nm in size) with surface charges of −24.73 ± 1.32 mV are successfully prepared from thrombin‐activated murine platelets with high surface expression of active glycoprotein IIb/IIIa (GP IIb/IIIa, also known as αIIbβ3) and P‐selectin. Although nanosized vesicles from resting platelets (VEs) and Act‐VEs showed similar sizes and surface charges, Act‐VEs formed much larger aggregates in the presence of thrombin and CaCl2, compared to VEs. After incubation with fibrinogen, Act‐VEs formed much denser fibrin networks compared to platelets or VEs, probably due to active αIIbβ3 on the surfaces of the Act‐VEs. After intravenous injection of the Act‐VEs, tail bleeding time and the blood loss are greatly reduced by Act‐VEs in vivo. In addition, Act‐VEs showed approximately sevenfold lower release of pro‐inflammatory interleukin‐1β (IL‐1β) during incubation for 4 days, compared to platelets. Taken together, the formulated Act‐VEs can serve as a promising hemostatic biomaterial for the efficient formation of fibrin clots without releasing pro‐inflammatory cytokine.

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Here, as a proof of concept, hybrid vesicles (VEs) are developed from two types of cancer cells, MCF-7 and HeLa, for the dual targeting of the anticancer drug doxorubicin (Dox) to cancer cells via homotypic interactions. Hybrid VEs with a size of 181.8 ± 28.2 nm and surface charge of −27.8 ± 1.9 mV are successfully prepared by the fusion of MCF-7 and HeLa VEs, as demonstrated by the fluorescence resonance energy transfer assay. The hybrid VEs exhibit enhanced intracellular uptake both in MCF-7 and HeLa cells. Dox-encapsulated hybrid VEs (Dox-hybrid VEs) also exhibit promising anticancer and antiproliferative activities against MCF-7/multidrug-resistant cells and HeLa cells. In addition, compared to free Dox, the Dox-hybrid VEs exhibit low intracellular uptake and reduced cytotoxicity for RAW264.7 cells. Thus, hybrid VEs with dual-targeting activity toward two types of cancer cells may be useful for the specific targeting of anticancer drugs for improved anticancer effects with reduced nonspecific toxicity.