Drug Research药物研究
Drug Research(英文缩写 DRUG RES),ISSN 2194-9379,eISSN 2194-9387,中文译名:药物研究 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：2025-10-01 至 2026-09-30，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 | 未收录 | N/A |
| 2022 | 2.200 | N/A |
| 2023 | 1.700 | Q3 |
| 2024 | 2.100 | Q3 |
| 2025 | 2.400 | Q3 |
Drug Research 最新收录文献
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1. Shikonin inhibits Vascular Smooth Muscle Cell Phenotypic Modulation and attenuates Neointimal Hyperplasia.
PMID:日期:2026-09-15Enhanced glycolytic activity drives vascular smooth muscle cell proliferation and migration. Pyruvate kinase M2, a key glycolytic enzyme, modulates cancer cell proliferation. Shikonin, an inhibitor of pyruvate kinase M2, exerts anti-proliferative effects on cancer cells; still, its involvement in vascular smooth muscle cell proliferation and neointimal hyperplasia is not established. We investigated the effects of shikonin on platelet-derived growth factor-BB-induced changes in vascular smooth muscle cell function and neointimal hyperplasia. Methods: Murine aortic vascular smooth muscle cells were pretreated with shikonin and stimulated with platelet-derived growth factor-BB. Wire injury of the carotid artery was performed in C57Bl/J6 mice to induce neointimal hyperplasia. Results: Our study observes a marked upregulation of pyruvate kinase M2 in platelet-derived growth factor-BB stimulated vascular smooth muscle cells. Shikonin inhibited pyruvate kinase M2 expression and effectively reduced platelet-derived growth factor-BB-induced vascular smooth muscle cell proliferation and migration and also favoured the contractile vascular smooth muscle cell phenotype. Expression of matrix metalloproteinase-2 and interleukin-6 messenger RNAs was significantly lower in shikonin-treated vascular smooth muscle cells as compared to platelet-derived growth factor-BB-treated control. Pyruvate kinase M2 translocated to the mitochondria and pyruvate kinase M2 inhibition via shikonin promoted mitochondrial reactive oxygen species levels, increased oxidative stress and induced vascular smooth muscle cell apoptosis. Perivascular application of shikonin suppressed neointimal hyperplasia. Conclusion: Our findings indicate that shikonin suppresses vascular smooth muscle cell proliferation and migration, thereby limiting neointimal hyperplasia and potentially serving as a novel therapeutic strategy for atherosclerosis and restenosis.
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2. Nortrachelogenin Inhibits Receptor Activator of Nuclear Factor Kappa-B Ligand-Induced Nuclear Factor Kappa-B Signaling and Osteoclastogenesis.
PMID:日期:2026-09-03Nortrachelogenin is a dibenzylbutyrolactone lignan associated with redox-sensitive signaling. We examined its effects on receptor activator of nuclear factor kappa-B ligand (RANKL)-induced nuclear factor kappa-B (NF-κB) activation in osteoclast precursors. Nortrachelogenin attenuated IκB phosphorylation and degradation and reduced p65 phosphorylation. Consistently, it markedly decreased the formation of tartrate-resistant acid phosphatase (TRAP) -positive multinucleated osteoclasts. These findings identify nortrachelogenin as a lignan scaffold that suppresses nuclear factor kappa-B signaling and osteoclastogenesis in vitro.
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3. A Review of the Current Status of Antiviral Drugs Targeting Human Immunodeficiency Virus, Hepatitis and Others.
PMID:日期:2026-08-19Antiviral drugs are pivotal in the prevention and management of infections caused by viruses, ranging from common cold viruses to life-threatening pathogens like human immunodeficiency virus, hepatitis viruses, Ebola virus, etc. Furthermore, antiviral therapy is increasingly being integrated into the management of chronic viral infections to restrain their replication, avert disease progression, and minimize the risk of complications. The availability of newer generations of antiviral drugs, particularly direct-acting antivirals, and combination therapies have significantly improved treatment outcomes, offering better cure speed, shorter treatment time, and reduced side effects as compared to older-generation antivirals. This comprehensive review provides an in-depth analysis of the diverse classes of antiviral drugs, their mechanisms of action, clinical applications, challenges, and future directions. With a focus on recent advancements and emerging trends, the current landscape of antiviral drug development and its implications for global public health are also discussed.
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4. A Novel Transcriptome-Wide Association Study Identifies USP36 as a Potential Therapeutic Target for Heart Failure.
PMID:日期:2026-08-17Heart failure is a significant global health burden. This study aims to identify heart failure-associated genes through transcriptome-wide association studies combined with genome-wide association studies. A transcriptome-wide association study was conducted using Functional Summary-based Imputation, integrating heart failure genome-wide association study summary data (47,309 cases and 930,014 controls) with Genotype-Tissues Expression Project V8 expression quantitative trait loci data from 49 tissues. Gene-level analysis was performed using Multi-marker Analysis of Genomic Annotation, followed by mendelian randomization and Bayesian colocalization. The functional implications of candidate genes were explored using GeneMANIA, and the druggability of the top gene, , was evaluated via molecular docking simulations. Functional Summary-based Imputation and Multi-marker Analysis of Genomic Annotation analyses identified 26 candidate genes. Further investigation highlighted as significant, particularly in left ventricular tissue, where it confers protection against heart failure. GeneMANIA showed that interacts with genes involved in oxidative stress-induced apoptosis, suggesting its role in heart failure pathogenesis. Molecular docking simulations confirmed USP36's binding affinity with heart failure therapeutics, supporting its potential as a therapeutic target. is a novel heart failure susceptibility gene and a promising therapeutic target. Its involvement in oxidative stress-related pathways offers new insights into heart failure risk and warrants further investigation for disease development and treatment.
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5. Walnut (Juglans regia L.) as a Promising Antidiabetic Agent: Mechanistic, Preclinical, and Clinical Evidence.
PMID:日期:2026-08-13Diabetes mellitus (DM) is a chronic metabolic disorder that continues to pose a major healthcare challenge worldwide. Despite the availability of several therapeutic options, achieving sustained glycaemic control and preventing long-term complications remain difficult in many patients. Walnut () has gained attention as a potential complementary approach because of its diverse bioactive constituents and reported metabolic benefits. This review discusses the mechanistic, preclinical, and clinical evidence supporting the role of in diabetes management. The available studies indicate that walnut contains several phytochemicals, including juglone, flavonoids, polyphenols, and polyunsaturated fatty acids, which may contribute to antioxidant, anti-inflammatory, and insulin-sensitizing activities. Experimental findings suggest that these constituents help improve glucose homeostasis, protect pancreatic β-cells, and regulate insulin-signalling pathways. Preclinical studies consistently demonstrate beneficial effects on glycaemic parameters and pancreatic function, while clinical investigations report modest improvements in fasting blood glucose, HbA1c, and lipid profiles with good tolerability. However, differences in extract preparation, dosage, study design, and duration limit direct comparison among studies and highlight the need for further standardization. Future research should focus on well-designed clinical trials, optimized dosing strategies, and the evaluation of walnut preparations as adjuncts to conventional antidiabetic therapy. Overall, the current evidence supports as a promising complementary candidate for diabetes management and provides a basis for its further clinical development.
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6. The Real-World Safety Profile of Hydroxyprogesterone: A Pharmacovigilance Study Based on the Food and Drug Administration's Adverse Event Reporting System Database.
PMID:日期:2026-08-04This study aimed to explore the spectrum of adverse events associated with hydroxyprogesterone and provide a comprehensive understanding of the drug's safety profile based on the Food and Drug Administration's Adverse Event Reporting System database. Adverse events associated with hydroxyprogesterone were extracted from the Food and Drug Administration's Adverse Event Reporting System database, covering the period from the first quarter of 2004 to the second quarter of 2025. Disproportionality analysis methods were used to detect potential safety signals related to hydroxyprogesterone. We further analyzed the demographic characteristics of the population and the onset time of adverse events. A total of 40,450 adverse event reports related to hydroxyprogesterone were included, corresponding to 197 significant preferred terms categorized into 21 system organ classes per Medical Dictionary for Regulatory Activities criteria. In addition to commonly observed adverse events, several clinically relevant adverse events not previously documented were identified, including fetal distress syndrome, abnormal fetal heart rate deceleration, neonatal jaundice, neonatal respiratory distress, and low birth weight infant. The median time to the onset of hydroxyprogesterone-induced adverse events was 20 days (interquartile range: 0-72 d), with 57.8% of adverse events occurring within the initial 30 days following hydroxyprogesterone administration. In this study, we identified both clinically observed adverse events and potential safety signals associated with hydroxyprogesterone. These results provide valuable evidence to support clinical monitoring, safety risk identification, and the development of subsequent safety investigations.
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7. A Novel Ruthenium(II) Complex and its Synergistic Anti-Leukemia Activity with GidA Protein via Dual-Pathway Apoptosis.
PMID:日期:2026-07-27This study demonstrates the effective anticancer activity of a semi-synthetic complex integrating the GidA protein and the ruthenium(II) complex against K562 human leukemia cells. Monotherapy evaluation revealed exceptional cytotoxicity, with half-maximal inhibitory concentration values of 0.058 μg/mL for GidA (a novel topoisomerase II inhibitor) and 14.1 μg/mL for Ru(II). Subsequently, isobologram analysis of six combination ratios identified profound synergy in formulations with elevated Ru(II) concentrations (combinations 4 and 5; sum of the fractional inhibitory concentration=0.17-0.86). All these synergistic complexes induced up to 73.91% apoptosis, exceeding single-agent efficacy (<0.01), while minimizing necrosis (<20%). Besides, mechanistic studies revealed dual pathways: Ru(II) triggered reactive oxygen species-dependent apoptosis (2.8-fold reactive oxygen species surge at 30 min; <0.01), while GidA operated via reactive oxygen species-independent mechanisms. This semi-synthetic complex may involve Ru(II), potentially mediated by transferrin receptor overexpression for targeted uptake. Also, combination 5 (4×Ru(II):1×GidA) emerged as the lead candidate, reducing effective doses and potentially mitigating resistance. Overall, these findings establish GidA-Ru(II) complexes as first-in-class dual-mechanism agents with high translational potential for refractory leukemia, offering a strategic solution to chemotherapy limitations through rational synergy.
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8. Development and Validation of a Liquid Chromatography-Electrospray Ionization-Tandem Mass Spectrometry Method for the Determination of Alpelisib, a Novel Phosphatidylinositol 3-Kinase Inhibitor, and Its Application to a Pharmacokinetic Study in Mice.
PMID:日期:2026-07-14Alpelisib (BY719) is a phosphoinositide-3-kinase inhibitor that specifically targets phosphoinositide-3-kinase-alpha. This enzyme is part of the phosphoinositide-3-kinase/α-serine/threonine-protein kinase/mammalian target of rapamycin signaling pathway, which promotes cell growth and survival. Mutations in the phosphoinositide-3-kinase gene cause the phosphoinositide-3-kinase signaling pathway to become overactive, leading to uncontrolled cell growth and survival, which contributes to tumor development. By inhibiting phosphoinositide-3-kinase-alpha, alpelisib can slow tumor growth and kill cancer cells. The goal of this study was to develop and validate a new, sensitive, specific, and rapid liquid chromatography-tandem mass spectrometry method for measuring alpelisib in dried blood spots from both mice and humans. Filgotinib served as the internal standard, and all procedures adhered to regulatory standards. Alpelisib and the internal standard were measured using a Sciex triple quadrupole mass spectrometer in multiple reaction monitoring mode with positive-ion detection. The focus was on the parent-daughter mass-to-charge transitions of 442.0→327.9 for alpelisib and 426.2→291.2 for the internal standard. The linear range for alpelisib was 0.331-1026 ng/mL (>0.990). This method successfully characterized the in vitro metabolic profiles and in vivo pharmacokinetics of alpelisib in mice. A strong correlation was found between dried blood spots and plasma concentrations, suggesting that dried blood spots can serve as an alternative to plasma for pharmacokinetic analysis.
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9. Astragalus Polysaccharide Alleviates Oxidative Stress Injury through Modulation of the Nrf2/HO-1 Axis in the Striatum of Cerebral Ischemic Rats.
9. 黄芪多糖通过调控脑缺血大鼠纹状体中Nrf2/HO-1轴减轻氧化应激损伤PMID:日期:2026-07-13Astragalus polysaccharide (APS) has therapeutic potential for neurodegenerative diseases; however, its specific mechanism of action against ischemic stroke (IS) requires further elucidation. This study aimed to elucidate the protective effects of APS on neural tissue and to explore the underlying molecular pathways in a rat population subjected to middle cerebral artery occlusion (MCAO). The animals received intraperitoneal (IP) injections of APS. Neurological recovery was assessed using neurobehavioral tests, and neuronal morphology was examined using Nissl staining. Then, we assessed the mRNA levels of IL-1β, IL-6, and TNF-α as well as the concentrations of oxidative stress-related substances. Finally, we evaluated the expression levels of Nrf2, Keap1, HO-1, and GPX4 through Western blotting and immunofluorescence. APS improved neurological function and ameliorated neuronal damage. It concurrently inhibited IL-1β, IL-6, and TNF-α expression while enhancing antioxidative potential. Mechanistically, APS induced an elevation in the levels of Nrf2, HO-1, and GPX4 proteins while concurrently causing a reduction in the protein levels of Keap1 in the striatum. APS effectively mitigated neuronal damage and motor dysfunction after cerebral ischemia. The protective mechanism involves the activation of the Nrf2/HO-1 axis and subsequent suppression of oxidative stress and neuroinflammation.
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10. Comparative Biochemical and Functional Characterization of a Novel Human Fibrinogen Concentrate (BT524) and Established Plasma-Derived Fibrinogen Concentrates.
PMID:日期:2026-06-24Human fibrinogen concentrate is used as replacement therapy for congenital and acquired fibrinogen deficiencies. Despite similar manufacturing principles, compositional differences among products may affect clot quality and hemostatic efficacy. BT524 (Biotest) is a newly developed human fibrinogen concentrate with proven clinical safety and efficacy. The objective of this study was to compare the biochemical composition and in vitro functional characteristics of BT524 with those of two commercially available plasma-derived fibrinogen concentrates (Products I and II). Three independent batches of each human fibrinogen concentrate were analyzed for the total and clottable protein, fibrinogen antigen, fibrinogen activity by Clauss, clotting factors, degradation markers (fibrinopeptide A and D-dimer), sub-visible particles, and aggregates. Maximum clot firmness and dynamics were assessed using rotational thromboelastometry (fibrin-based thromboelastometry). Fibrinogen deficient plasma with low factor XIII content was spiked each fibrinogen concentrate and increasing concentrations of factor XIII (0-0.8 U/mL). BT524 showed consistent fibrinogen content but contained no active factor VIII, factor XIII, or von Willebrand factor, indicating a precisely defined composition. Levels of degradation markers, aggregates, and sub-visible particles were markedly lower than in comparator products, reflecting the superior biochemical purity of BT524. BT524 achieved significantly higher maximum clot firmness than Product I (<0.0001) and demonstrated comparable performance with Product II. Spiking of factor XIII resulted in an additional increase in maximum clot firmness in BT524 and Product II, but not in Product I, proving functional factor XIII susceptibility of BT524. BT524 demonstrates high biochemical purity and robust functional clot formation. These findings highlight that fibrinogen concentrates differ in composition, functionality and molecular integrity, which determines clot quality and hemostatic performance.