EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES欧洲药物科学杂志
EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES(英文缩写 EUR J PHARM SCI),ISSN 0928-0987,eISSN 1879-0720,中文译名:欧洲药物科学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.112 | Q2 |
| 2022 | 4.600 | Q2 |
| 2023 | 4.300 | Q1 |
| 2024 | 4.700 | Q1 |
| 2025 | 5.100 | Q1 |
EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES 最新收录文献
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1. Evaluation of Citicoline-loaded Lutrol 127/Carbopol/Hyaluronic acid-based gels for brain delivery by intranasal administration.
PMID:期刊:日期:2026-11-01The aim of this work was to evaluate two nasal gels specifically designed to meet three essential criteria: a suitable formulation for nasal administration, a pH compatible with the nasal mucosa, and the encapsulation capacity of the antioxidant Citicoline (CIT), which showed beneficial effects in neurological disorders such as Parkinson's disease. Hence, Carbopol 1342 (Carb) at different weights (5 mg or 25 mg), PF-127 and Hyaluronic acid (HA) provided two gelled systems, denoted as PF-127/Carb-5-HA" and "PF-127/Carb-25-HA", respectively. Gel mechanical and microstructural characterization was conducted using rheological tests and SEM observations. Moreover, in vitro CIT release in simulated nasal fluid showed a consistent burst effect for both gels. Ex vivo permeation studies using excised porcine nasal mucosa mounted on Franz cells confirmed that limited extent of CIT permeated from both formulations (7.8-9.5%). Interestingly, none of the gels was cytotoxic against the primary nasal epithelial cells (pNEC) and also when pNEC were co-cultured with the neuronal SH-SY5Y cells in order to provide an in vitro model of nose-brain axis (NBA). Finally, by SIRT1 quantification in the NBA model, the gels evidenced an effective neuronal inflammatory modulation, so being promising for nerve cell protection.
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2. Gold Nanostars: Emerging Plasmonic Nanoplatforms for Lung Cancer Diagnosis and Therapy.
PMID:期刊:日期:2026-11-01Lung cancer comprises two major histological subtypes, non-small cell lung cancer (NSCLC), which accounts for approximately 80-85% of cases, and small cell lung cancer (SCLC), representing 15-20%; this review discusses the theranostic potential of gold nanostars across both subtypes, with particular emphasis on NSCLC. Despite major improvements in surgery, chemotherapy, radiotherapy, and immunotherapy, therapeutic success remains limited by tumor heterogeneity, drug resistance, and the lack of reliable early detection biomarkers. Therefore, nanotechnology-based strategies are being explored as potential approaches for precision oncology. Gold nanostars have attracted considerable interest because of their anisotropic morphology, tunable localized surface plasmon resonance, and efficient photothermal conversion. In this review, we summarize the structural features, synthesis strategies, physicochemical properties, and emerging applications of gold nanostars in lung cancer diagnosis and therapy. Their plasmonic properties enable integration with imaging approaches, including surface-enhanced Raman spectroscopy, photoacoustic imaging, and computed tomography, as well as therapeutic modalities such as photothermal therapy, photodynamic therapy, and gene delivery. Surface functionalization may further enhance cellular uptake, targeting specificity, and therapeutic performance in selected experimental models. However, the available preclinical evidence remains heterogeneous, with outcomes influenced by nanostar size, morphology, surface chemistry, targeting strategy, administration route, and experimental model. Although several studies report enhanced tumor visualization or therapeutic responses, biodistribution remains variable, and a substantial fraction of administered nanoparticles may accumulate in organs such as the liver and spleen. Moreover, limited standardized head-to-head comparisons and insufficient long-term safety and clearance data prevent definitive conclusions regarding their overall superiority or clinical effectiveness. Gold nanostars therefore represent a promising but still investigational theranostic platform for lung cancer, with further standardized preclinical evaluation, long-term safety assessment, reproducible manufacturing, and well-designed clinical studies required to establish their translational potential.
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4. FcBP-HFQ lipid-mediated trastuzumab modification of mRNA-loaded lipid nanoparticles enhances delivery to HER2-expressing cancer cells.
PMID:期刊:日期:2026-11-01Lipid nanoparticles (LNPs) have emerged as a key delivery platform for mRNA therapeutics, as demonstrated by the clinical success of mRNA vaccines against SARS-CoV-2. LNPs are now being investigated for various applications, such as cancer immunotherapy and the treatment of genetic disorders. However, LNPs tend to accumulate predominantly in the liver and lack intrinsic cell-type specificity. Modifying LNPs with antibodies is a promising strategy for enhancing cell-specific delivery. We have previously developed orientation-controlled anti-transferrin receptor and anti-PD-L1 antibody modifications for the targeted delivery of nucleic acids, including mRNA and siRNA. In this study, we newly applied this platform to trastuzumab, a clinically established high-affinity anti-HER2 therapeutic antibody, to develop orientation-controlled trastuzumab-modified mRNA/LNPs for HER2-selective delivery. we evaluated trastuzumab-modified mRNA/LNPs in HER2-overexpressing SKOV-3 ovarian cancer cells and HER2-low MDA-MB-231 breast cancer cells. Trastuzumab-modified mRNA/LNPs exhibited over 100-fold greater cellular association than unmodified LNPs in cultured HER2-overexpressing SKOV-3 cells. Furthermore, after intratumoral administration in a mouse model bearing subcutaneous SKOV-3 tumors, the trastuzumab-modified group showed significantly higher luciferase expression than the unmodified and isotype-controlled antibody-modified groups. These findings support FcBP-HFQ lipid-mediated trastuzumab modification of LNPs as a useful approach for efficient cell-selective mRNA delivery.
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5. Discovery of a Potent and Selective KRAS G12D Degrader based on PROTAC Degradation.
PMID:期刊:日期:2026-11-01KRAS-G12D has long been regarded as an intractable therapeutic target due to the flat binding pocket and its strong affinity for GTP/GDP. Proteolysis-targeting chimera (PROTAC) is a revolutionary drug discovery strategy that, by virtue of its unique pharmacological mode of action, provides more options for targeting undruggable targets. In this study, we designed and synthesized 20 novel KRAS G12D PROTACs based on the MRTX1133 derivative. Through systematic exploration of linker structure-activity relationship and multi-cell line screening, compound VI-1 exhibited significant KRAS G12D degradation activity in PANC-0203 cells, achieving 69% effective degradation at 10 μM. Notably, the preferred compounds exhibited significant selectivity for other KRAS mutations and normal cells. This work provides an important lead compound for developing highly selective KRAS G12D PROTACs and warrants further exploration in the context of drug-likeness optimization.
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6. Differential myocardial responses to indobufen and aspirin across clinical and experimental models of myocardial infarction.
6. 不同临床和实验心肌梗死模型对吲哚布芬和阿司匹林的不同心肌反应PMID:期刊:日期:2026-11-01Aspirin remains the cornerstone of antiplatelet therapy for acute myocardial infarction (AMI); however, its use is limited in patients with aspirin intolerance, hypersensitivity, or high bleeding risk. Indobufen, a reversible cyclooxygenase-1 inhibitor, has emerged as a potential alternative, yet its cardioprotective effects beyond platelet inhibition and the underlying mechanisms remain incompletely understood. Clinical serum samples were collected from patients with ST-segment elevation myocardial infarction (STEMI) receiving aspirin or indobufen therapy. In parallel, myocardial infarction was induced in mice by left anterior descending coronary artery ligation, and neonatal rat cardiac fibroblasts (NRCFs) were subjected to hypoxia in vitro. Cardiac function, fibrosis, autophagy, apoptosis, and oxidative stress were evaluated using echocardiography, histology, immunostaining, western blotting, and transmission electron microscopy. Publicly available single-cell RNA sequencing data were analyzed to explore relevant cellular pathways. In STEMI patients, indobufen treatment was associated with lower circulating levels of cardiac troponin I, thromboxane B₂, IL-1β, and IL-12, along with increased IL-10 levels than aspirin treatment, and these associations remained significant after multivariable adjustment for baseline clinical characteristics. In vivo, indobufen improved cardiac function and attenuated myocardial fibrosis, accompanied by modulation of autophagy-related signaling, reduced apoptosis, and alleviation of oxidative stress. In vitro, indobufen attenuated hypoxia-induced cardiac fibroblast activation, apoptosis, and mitochondrial dysfunction, whereas aspirin exerted limited effects under the same conditions. Mechanistically, indobufen was associated with increased activation of AKT and AMPK signaling pathways and coordinated modulation of autophagy-related proteins. Further pharmacological inhibition of AMPK partially attenuated the autophagy-related effects of indobufen, suggesting that AMPK signaling contributes, at least in part, to the cytoprotective effects of indobufen. These findings suggest that indobufen may exert myocardial protective effects beyond platelet inhibition, potentially through AKT/AMPK-associated regulation of autophagy, apoptosis, and fibroblast activation. These findings provide a rationale for further investigation of indobufen as a potential alternative antiplatelet strategy in myocardial infarction.
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7. {"_":"Synthesis and biological evaluation of Ga-DOTA-PLE: a Plectin-1-targeted radiotracer for PET/MR imaging of pancreatic cancer.","sup":["68"]}
7. {“_”：“Ga-DOTA-PLE:一种用于胰腺癌症PET/MR成像的Plectin-1靶向放射性示踪剂的合成和生物学评价。”，“sup”：[“68”]}PMID:期刊:日期:2026-11-01Pancreatic cancer is characterized by high malignancy and diagnostic challenges. Plectin-1 is a specific biomarker significantly overexpressed in pancreatic ductal adenocarcinoma (PDAC). This study aimed to synthesize a Plectin-1-targeting radiotracer, Ga-DOTA-PLE, and evaluate its potential for pancreatic cancer imaging. The precursor DOTA-PLE was radiolabeled with Ga, followed by radiochemical yield and stability evaluated. In vitro binding affinity and in vivo biological properties were evaluated using cell binding assays, pharmacokinetic analysis, biodistribution studies, and micro-PET/MR imaging in Plectin-1-positive BxPC-3 and Plectin-1-negative β-TC-6 models. Radiochemical analysis by radio-HPLC and TLC confirmed that ⁶⁸Ga-DOTA-PLE was obtained with high radiochemical purity with no detectable free ⁶⁸Ga or colloidal species. The tracer demonstrated excellent in vitro stability, maintaining a radiochemical purity (RCP) of > 90% after incubation in PBS and serum at 37 °C for 2 h. In vitro binding assays revealed specific binding of ⁶⁸Ga-DOTA-PLE to Plectin-1, as evidenced by significantly higher uptake in Plectin-1-positive BxPC-3 cells than in Plectin-1-negative β-TC-6 cells (P<0.001). Pharmacokinetic evaluation indicated rapid blood clearance, with distribution (T₁/₂α) and elimination (T₁/₂β) half-lives of 2.99 min and 18.99 min, respectively. Biodistribution studies performed prominent tumor accumulation (4.41 ± 1.05%ID/g) at 30 min post-injection. while the radiotracer was primarily excreted via the renal pathway (8.65 ± 1.61%ID/g), exhibiting low hepatic and intestinal background. Micro-PET/MR imaging clearly delineated tumor lesions, and identified 15-30 min post-injection as the optimal imaging window, during which the tumor-to-muscle (T/M) ratio reached its maximum (2.91 ± 0.38).
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8. A new rational model for tablet strength-pressure relation.
PMID:期刊:日期:2026-11-01Excipients with a dominating or substantial elastic recovery are characterised by a convex curvature in contrast to the linear association observed for inorganic materials or organic monomers. A model is proposed combining two synchronous processes, a positive linear effect, representing the increase in strength with pressure and a curved component characterising the adverse effect of elastic expansion. Three models are investigated where the negative elastic effect is either exponential (exp(P)), power-function (x) or a simple quadratic form (P). The three models are evaluated on their fitness ability, internal correlation and relation between parameters and elastic recovery. The elementary polynomial model, TS = aP - b*P + c was preferred due to fitness ability and simplicity in calculation. Furthermore a noteworthy linear relationship was observed between the elastic recovery of tablets from 8 polymer materials and a combination of the linear coefficient a and the quadratic coefficient b as b/a.For brittle materials, like lactose or dicalcium phosphate without significant elastic deformation, the equation reduces to a straight line.
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10. GW0742 prevents neointima formation by upregulating FABP3 expression.
PMID:期刊:日期:2026-11-01Phenotypic switching of vascular smooth muscle cells (VSMCs), leading to neointima formation, is a main cause of in-stent restenosis after coronary stent implantation, resulting in poor patient prognosis. Inhibition of VSMC proliferation, migration, and synthetic phenotype transition holds promise for preventing and treating neointimal hyperplasia and restenosis. GW0742, a peroxisome proliferator-activated receptor (PPAR)-β/δ agonist, has been reported to suppress atherosclerosis and myocardial ischemia-reperfusion injury. However, its role in neointima formation has not been previously studied. In this study, we found that GW0742 significantly inhibited carotid artery injury-induced neointimal hyperplasia in mice. In vitro experiments including cell counting, EdU staining, and proliferation marker detection revealed that GW0742 markedly suppressed Platelet-derived growth factor-BB (PDGF-BB)-induced proliferation of human aortic smooth muscle cells (HASMCs). Flow cytometry analysis showed that GW0742 treatment arrested cells in the G2/M phase. Transwell assays demonstrated that GW0742 inhibited HASMCs migration. Moreover, GW0742 reduced the expression of migration-associated proteins matrix metalloproteinases 2 (MMP2) and matrix metalloproteinases 9 (MMP9), while increasing contractile markers alpha-smooth muscle actin (α-SMA) and calponin 1 (CNN1), suggesting that GW0742 suppresses HASMC proliferation, migration, and phenotypic switching, thereby preserving the contractile phenotype. RNA sequencing revealed that GW0742 regulates fatty acid metabolism by upregulating fatty acid binding protein 3 (FABP3) expression to counteract PDGF-BB-induced VSMC phenotypic switching. Knockdown of FABP3 significantly abrogated the inhibitory effects of GW0742 on VSMC proliferation, migration, and synthetic phenotype transition. Taken together, our findings demonstrate that GW0742 upregulates FABP3 expression, leading to the inhibition of VSMC proliferation, migration, and phenotypic switching, and ultimately suppressing neointima formation. These results underscore the therapeutic potential of GW0742 for the prevention and treatment of vascular restenosis.