MEDICINAL RESEARCH REVIEWS药物研究评论
MEDICINAL RESEARCH REVIEWS(英文缩写 MED RES REV),ISSN 0198-6325,eISSN 1098-1128,中文译名:药物研究评论 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：2025-09-28 至 2026-09-28，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 | 12.388 | Q1 |
| 2022 | 13.300 | Q1 |
| 2023 | 10.900 | Q1 |
| 2024 | 11.600 | Q1 |
| 2025 | 13.600 | Q1 |
MEDICINAL RESEARCH REVIEWS 最新收录文献
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1. Molecular Glue Degraders in Early Development for Cancer Therapy.
1. 用于癌症治疗的早期开发中的分子胶降解剂PMID:日期:2026-09-07Molecular glue degraders are an emerging class of small molecule allosteric modulators that induce or stabilize protein-protein interactions, enabling targeted degradation of previously intractable proteins. By redirecting E3 ligases to recognize neosubstrates, proteins that are not typically recognized by a specific E3 ubiquitin ligase, they expand the scope of drug discovery beyond traditional paradigms. We review mechanistic principles underlying molecular glue activity, including cooperativity, weak affinity interactions, structural degrons, and higher-order complex formation. We discuss discovery strategies, from serendipitous identification to emerging rational and chemoproteomic approaches, and key E3 ligase systems with relevance to oncology. We highlight clinical and preclinical applications, alongside challenges such as resistance mechanisms, context-dependent activity, and limitations in predicting neosubstrates. Molecular glues are transitioning from serendipitous discoveries to a mechanism-driven therapeutic platform. Progress depends on integrating structural biology, proteomics, and computational modeling to enable rational design and improve predictability. Expanding the repertoire of E3 ligases and understanding context-specific degradation will be critical to fully realize their potential in oncology and beyond.
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2. N-Myristoylation: A Central Hub Integrating Tumor Signaling, Metabolism, and Immunity for Precision Therapy.
PMID:日期:2026-09-07Lipid modifications are critical for membrane anchoring and signal transduction. N-myristoylation, catalyzed by NMT1/2, irreversibly attaches myristic acid to N-terminal glycine residues, enabling stable membrane localization and crosstalk with other post-translational modifications. This review traces NMT research from structural characterization to substrate profiling, highlighting the ordered double-substitution catalytic mechanism and variations in substrate recognition. While prior reviews have covered NMT biochemistry and innate immunity, we emphasize underappreciated roles of N-myristoylation in metabolic vulnerability, immune evasion, and acquired resistance to targeted therapies and immunotherapies. We discuss how exogenous myristic acid from dietary sources fuels oncogenic signaling, and how N-myristoylation regulates key signaling pathways (PI3K/AKT, MAPK, ferroptosis) and targets (Src, AMPK, EZH2) to drive immunosuppressive and pro-tumor phenotypes. Antitumor potential of NMT inhibitors (e.g., B-13, Zelenirstat) and allosteric ABL1 inhibitors (asciminib) is evaluated. Recent methodological advances (including metabolic labeling, click chemistry, spatial proteomics, and computational simulations) are reviewed. However, translational challenges such as biomarker absence, blood-brain barrier limitations, and functional redundancy remain. Addressing these will require combination therapies tailored to specific mutational, metabolic, and immune profiles. In summary, N-myristoylation integrates signaling, metabolism, and immunity, offering a rationale for future precision oncology.
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3. Exercise-Induced Exerkines: Multi-Nodal Suppression of the NLRP3 Inflammasome and Translational Potential.
PMID:日期:2026-09-01Chronic low-grade inflammation driven by persistent NLRP3 inflammasome activation is a unifying pathophysiological feature of most non-communicable diseases (NCDs). Whereas single-target pharmacological inhibitors exhibit limited breadth and durability, regular moderate-intensity exercise confers robust multi-system protection through a diverse network of exerkines. This narrative review synthesizes evidence that exercise-released myokines (irisin, Metrnl, context-reprogrammed IL-6), hepatokines/adipokines (FGF21, adropin, adiponectin), metabolites (lactate, β-hydroxybutyrate), microbiota-derived factors (SCFAs, betulinic acid), and extracellular vesicle (EV)-delivered non-coding RNAs converge on every regulatory node of the canonical NLRP3 inflammasome to achieve multi-nodal suppression that is currently unmatched by any single pharmacological approach based on available evidence. Acute high-intensity exercise transiently activates NLRP3 via canonical danger signals, whereas chronic moderate-intensity training (150-300 min·wk, 60%-75% HRmax) induces profound basal suppression through NF-κB attenuation, mitochondrial protection, direct interference with NEK7-NLRP3 interaction and ASC oligomerization, post-transcriptional silencing, and enhanced autophagic clearance. These mechanisms are supported by preclinical structural data and human biomarker studies across cardiovascular, metabolic, neurodegenerative, and musculoskeletal disorders. We propose a precision exercise medicine framework integrating exerkine/genetic/microbiome profiling to minimize non-responders, together with emerging mimetics, RNA therapeutics, and synergistic pharmacology, to deliver scalable systems-level modification of NLRP3-driven metaflammation.
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4. Insights From Spatiality: Accelerating Pharmaceutical Research Using Mass Spectrometry Imaging.
PMID:日期:2026-09-01Mass spectrometry imaging (MSI) has emerged as a transformative technology in pharmaceutical research, offering unprecedented capabilities to visualize drug distribution, metabolism, and target engagement in biological tissues. By combining the molecular specificity of mass spectrometry with spatial imaging resolution, this label-free approach enables simultaneous mapping of drugs, metabolites, and endogenous molecules across tissue sections, providing comprehensive insights into drug absorption, distribution, metabolism, excretion, and toxicity properties. Recent technical advances have dramatically enhanced MSI capabilities, achieving spatial resolutions down to the cellular level. The integration of tandem mass spectrometry, ion mobility separation, and dedicated data analysis tools powered by artificial intelligence has further expanded the analytical power of MSI, enabling robust molecular identification and pattern recognition in complex biological matrices. MSI applications span critical areas of drug development, from characterizing blood-brain barrier permeability and CNS drug distribution to mapping tumor microenvironment heterogeneity and evaluating anticancer drug penetration. This technology has proven invaluable for assessing drug disposition in the heart, liver, kidney, lung, as well as the gastrointestinal tract and skin. As drug research increasingly embraces multimodal approaches and single-cell analysis, MSI continues to evolve as an indispensable tool for understanding drug behavior in complex biological systems, ultimately accelerating drug development and reducing clinical failures.
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5. Targeting ClpP Protease: Emerging Therapeutic Strategies and Small-Molecule Modulators in Drug Discovery.
5. 靶向ClpP蛋白酶：药物发现中的新兴治疗策略与小分子调节剂PMID:日期:2026-09-01The caseinolytic protease P (ClpP) is a conserved serine protease that functions with ATPases associated with diverse cellular activities (AAA+) chaperones to ensure protein quality control in organisms ranging from bacteria to human mitochondria. Its tetradecameric structure and adjustable gating support selective substrate recognition, unfolding, and proteolysis, thereby contributing to proteostasis, metabolic balance, stress responses, and bacterial virulence. Growing insights into human ClpP and ClpX complex (hClpXP) have further underscored its relevance to human disease. This review summarizes current knowledge of ClpP architecture and regulatory mechanisms, with emphasis on its roles in cellular homeostasis and pathophysiology. We highlight advances in small-molecule ClpP modulators, including activators, inhibitors, and emerging heterobifunctional degraders such as bacterial proteolysis-targeting chimeras (BacPROTACs) and mitochondrial-targeted PROTACs (MtPTACs), which harness ClpP activity for targeted protein degradation in antibacterial and anticancer applications. Despite notable progress, challenges remain, particularly in achieving selectivity between bacterial and human ClpP (hClpP), minimizing off-target effects, and preventing resistance. Future opportunities include designing reversible covalent inhibitors, developing novel allosteric modulators, and optimizing degrader architectures to expand therapeutic potential. ClpP-directed therapeutic strategies therefore represent a promising avenue for next-generation antibacterial and anticancer drug discovery.
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6. {"_":"Quantification of B and B in Biological Samples in Translational Science and Clinical Applications for Boron Neutron Capture Therapy (BNCT).","sup":["10","11"]}
6. 硼中子捕获疗法（BNCT）转化科学和临床应用中生物样本中10B和11B的定量PMID:日期:2026-09-01Boron neutron capture therapy (BNCT) is a targeted radiotherapy that exploits the selective accumulation of the B isotope within tumors, followed by irradiation with low-energy neutrons to induce high linear energy transfer particles with short path lengths, resulting in localized tumor cell destruction while sparing surrounding healthy tissue. Achieving optimal therapeutic efficacy requires precise quantification of B and B in biological samples such as blood, tissue, and cells to inform treatment planning, dosimetry, and patient selection. This review provides a comprehensive assessment of analytical methods for boron (isotope) determination in BNCT, covering neutron-based techniques, mass spectrometry, nuclear imaging, and spectroscopic and magnetic approaches. Each method is discussed in terms of analytical principles, sample preparation, sensitivity, isotopic specificity, invasiveness, real-time capability, infrastructure complexity, and clinical applicability. Particular emphasis is placed on spatially resolved and in vivo techniques, as well as emerging theranostic strategies that integrate boron delivery with multimodal imaging. Despite significant technological progress, the lack of widely available, real-time, non-invasive, and B-specific dosimetry remains a key limitation for routine clinical implementation. In particular, while positron emission tomography-based approaches such as 4-borono-2-[F]fluoro-L-phenylalanine provide essential information on boron biodistribution for treatment planning, they reflect tracer-level pharmacokinetics and therefore offer indirect rather than absolute quantification of therapeutic boron concentrations. This review critically assesses current methodologies in the context of clinical readiness and outlines future directions to support the translation of BNCT from bench to bedside.
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7. STING: An Attractive Target for Autoimmune and Inflammatory Diseases.
PMID:日期:2026-09-01Stimulator of Interferon Genes (STING) is a transmembrane homodimer protein located in the endoplasmic reticulum membrane and plays an essential role in human innate immunity. Hyperactivation of STING has been found in many autoimmune and inflammatory diseases. Therefore, STING has been recognized as a promising target for the treatment of these diseases. Many efforts have been devoted to identifying STING inhibitors and degraders. However, development of STING drug candidates is still challenging and in its infancy, and no candidates have been advanced into clinical trials. In this perspective, we comprehensively summarize recent advances in the development of STING inhibitors and degraders and highlight their design strategies. We also discuss the challenges and opportunities of STING inhibition and expect to shed light on future STING drug discovery.
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8. Decoding WDR5-Mediated Interactions in Gliomas: Implications for Targeted Therapy.
PMID:日期:2026-09-01Gliomas are aggressive and treatment-resistant tumors of the central nervous system, characterized by molecular heterogeneity, diffuse infiltration, rapid progression, and persistent poor prognosis despite multimodal therapy. Emerging evidence highlights the role of complex genetic changes (such as IDH1 and H3F3A mutations) and epigenetic interactions in reshaping chromatin structure and activity in gliomas, increasing their reliance on epigenetic regulators for their growth and resistance. The nuclear scaffolding protein WD repeat domain 5 (WDR5), is a core component of the MLL/SET1 (WRAD) methyltransferase complex, which has been recently validated as a molecular target for cancer. WDR5 implication in H3K4 trimethylation (H3K4me3)-mediated gene regulation sustains transcriptional programs linked to proliferation, ribosome biogenesis, stemness, and MYC-driven oncogenic activity. In gliomas, WDR5 expression is increased, promoting proliferation and migration, as well as maintaining the glioma stem cell population, contributing to tumor progression. Targeting of WDR5 through specific WIN-site and WBM-site inhibitors or PROTAC degraders has been shown to impair WRAD assembly, reduce H3K4me3 levels, weaken MYC-associated transcription, and suppress tumor growth. In this review, we highlight the significant role of WDR5 in gliomas as part of a tumor-specific epigenetic vulnerability network, providing a critical update on the major WDR5-targeted inhibitors and degraders for future therapeutic applications.
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9. Designing the Next Generation of Antibiotics: Structure, SAR, and Strategy in Medicinal Chemistry (2000-2025).
PMID:日期:2026-09-01Antibacterial agents remain vital for managing infectious diseases, yet the global escalation of antimicrobial resistance (AMR) continues to compromise their therapeutic effectiveness. Despite decades of discovery and chemical refinement, most recently developed antibacterials belong to existing structural classes, underscoring a pressing need for innovative molecular scaffolds and mechanisms of action. This review provides a comprehensive medicinal-chemistry overview of major antibacterial classes, including β-lactams, glycopeptides, tetracyclines, fluoroquinolones, macrolides, aminoglycosides, oxazolidinones, polymyxins, and lipopeptides. The discussion emphasizes their structural frameworks, key structure-activity relationship (SAR) features, and the chemical strategies used to enhance potency, spectrum, and pharmacokinetic properties while counteracting bacterial resistance mechanisms. In addition, emerging developments in the antibacterial pipeline-covering new, withdrawn, discontinued, and clinically advancing compounds (2000-2025)-are highlighted to reflect the current state of innovation in antibiotic discovery. By integrating chemical, pharmacological, and developmental insights, this review aims to provide a clear and updated perspective on how medicinal chemistry continues to shape the design and evolution of antibacterial therapeutics in the face of rising resistance.
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10. Histone Deacetylase Meets Protein Degradation: Accelerating Anticancer Drug Discovery.
PMID:日期:2026-09-01Histone deacetylases (HDACs) are key epigenetic regulators involved in a variety of cancers, rendering them attractive therapeutic targets. Although several HDAC inhibitors have achieved clinical success, challenges such as poor isoform selectivity, acquired resistance, and off-target toxicity limit their broader application. Proteolysis-targeting chimeras (PROTACs) represent an innovative therapeutic strategy that enables ubiquitin-proteasome-mediated degradation of HDACs. This approach enhances specificity, overcomes resistance mechanisms, including those resulting from point mutations or persistent target activity, and enables sustained suppression at low concentrations, owing to its catalytic and event-driven mode of action. This review summarizes the structural classification and biological functions of HDACs and surveys recent advances in the design of HDAC-directed PROTACs. Key emphasis is placed on rational warhead selection, linker optimization, and the strategic choice of E3 ligase recruiters to guide degradation efficiency and isoform specificity. Representative degraders are evaluated for their pharmacological characteristics and antitumor efficacy across diverse malignancies. Current challenges and future directions for the development of HDAC degraders as clinically viable agents are also discussed.