Nanoparticle-based drug delivery systems hold great promise for improving the effectiveness of anti-tumor therapies. However, their clinical translation remains hindered by several significant challenges, including intricate preparation processes, limited drug loading capacity, and concerns regarding potential toxicity. In this context, pure drug-assembled nanosystems (PDANSs) have emerged as a promising alternative, attracting extensive research interest due to their simple preparation methods, high drug loading efficiency, and suitability for large-scale industrial production. This innovative approach presents new opportunities to enhance both the safety and therapeutic efficacy of cancer treatments. This review comprehensively explores recent progress in the application of PDANSs for cancer therapy. It begins by detailing the self-assembly mechanisms and fundamental principles underlying PDANS formation. The discussion then advances to strategies for assembling single pure drug nanoparticles, as well as the co-assembly of multiple drugs. Subsequently, the review addresses the therapeutic potential of PDANSs in combination treatment modalities, encompassing diagnostic and therapeutic applications. These include combinations of chemotherapeutic agents, phototherapeutic approaches, the integration of chemotherapy with phototherapy, and the synergistic use of immunotherapy with other treatment methods. Finally, the review highlights the potential of PDANSs in advancing tumor therapy and their prospects for clinical application, providing key insights for future research aimed at optimizing this technology and broadening its utility in cancer treatment.

Background: Cardiovascular disease is the leading cause of death in most of the world. Previous meta-analyses of generic drugs for the treatment of cardiovascular disease have not provided sufficient evidence to demonstrate the true efficacy and safety of the drugs. Subsequently, concern exists regarding whether the use of generic drugs can fully substitute brand-name drugs in clinical treatment. To enhance the evidence for generic drugs, this meta-analysis compares the actual effectiveness of generic drugs with brand-name drugs in preventing and treating cardiovascular diseases. This study aimed to resolve the controversy over whether generic drugs in cardiovascular disease can replace brand-name drugs, fully evaluating the best evidence on the clinical equivalence of generic drugs. Methods: The PubMed, Embase, The Cochrane Library, and Clinicaltrials.gov databases were searched. The search period included articles published before December 2023. Studies on generic and branded cardiovascular drugs were collected, and two independent reviewers screened eligibility, extracted study data, and assessed the risk of bias. Safety outcomes included major adverse cardiovascular events and other adverse events. Efficacy outcomes included relevant vital signs (e.g., blood pressure, heart rate, urine volume) and laboratory measures (e.g., international normalized ratio, low-density lipoprotein cholesterol, platelet aggregation inhibition). A meta-analysis and subgroup analysis were conducted using the Rev Man software. Results: A total of 4238 studies were retrieved, and 87 studies (n = 2,303,818) were included in the qualitative analysis. There were 57 quantitatively assessed studies (n = 560,553), including angiotensin II receptor blockers, beta-blockers, calcium channel blockers, antithrombotic drugs (anticoagulants or antiplatelet agents), diuretics, statins, and other classes of cardiovascular medications. Regarding clinical safety, 19 studies assessed the occurrence of major adverse cardiovascular events (MACEs) (n = 384,640), and 35 reported secondary adverse events (n = 580,125). In addition to the MACEs for statins (risk ratio (RR) 1.13 [1.05, 1.21]) and adverse events (AEs) for calcium channel blockers (RR 0.90 [0.88, 0.91]), there were no significant differences in the overall risk of MACEs (RR = 1.02 [0.90, 1.15]) and minor adverse events (RR = 0.98 [0.91, 1.05]) between generic and brand-name cardiovascular drugs. In terms of effectiveness, there were no significant differences observed between the two groups in blood pressure (BP), platelet aggregation inhibition (PAI), international normalized ratio (INR), low-density lipoprotein (LDL), and urinary sodium levels. Subgroup analyses for the region, study design, duration of follow-up, and grant funding revealed no significant differences in the risk of MACEs. However, the risk of AE was significantly higher in the Asian region for brand-name cardiovascular drugs than for generics. There was no statistically significant difference in risk between generic and brand-name drugs in the remaining subgroup analyses. Conclusions: Cardiovascular drugs encompass many types; a minority of generic and brand-name drugs have discrepancies. Given the overall development trend of multi-manufacturer generic drugs in the future, this study provides a strong basis for the global application of generic drugs. The feasibility of generic drugs in terms of efficacy and safety in cardiovascular diseases is clarified. However, some drugs still need to be improved to replace the original drugs used in clinical practice completely. Therefore, large-sample, multicenter, high-quality studies are still required to guide the clinical use of cardiovascular drugs. The PROSPERO registration: CRD42023481597, https://www.crd.york.ac.uk/PROSPERO/view/CRD42023481597.

To investigate the potential targets and underlying mechanisms of coptisine in regulating platelet activation and thrombosis by integrating an approach combining network pharmacology and experimental validation. An in vivo carotid artery thrombosis model induced by FeCl ₃ ‐mediated endothelial injury was established in mice to evaluate the antithrombotic effects of coptisine. A combination of network pharmacology prediction and both in vivo and in vitro experimental validation was employed to elucidate the antithrombotic mechanisms of coptisine. Molecular docking simulations were performed using AutoDock Vina to assess the binding interactions between coptisine and its targets. The in vitro antiplatelet effects of coptisine were assessed using platelet aggregation assays induced by thrombin, ADP, and collagen, as well as a thrombin‐induced platelet activation model. Administration of coptisine significantly reduced thrombus formation in the mouse model of carotid artery thrombosis. Network pharmacology analysis identified four key genes—NFKB1, PTGS2, STAT1, and ACE—as potential core targets contributing to the antithrombotic effects of coptisine. Functional enrichment analysis further indicated the involvement of these targets in pathways relevant to thrombosis and inflammation. Molecular docking studies demonstrated strong binding affinities between coptisine and the identified targets. Both in vivo and in vitro studies confirmed that coptisine treatment markedly attenuated thrombin‐induced platelet activation, as evidenced by reduced platelet inflammation and decreased levels of platelet granule release. This study demonstrates that coptisine exerts significant protective effects against thrombosis‐related diseases through modulation of the NF‐κB and MAPK signaling pathways.