RSC medicinal chemistry最新文献

{"title":"Synthetic pancreatic lipase inhibitors in obesity treatment: current updates on <i>in silico</i> design, synthesis, bioactivity, and SAR.","authors":"Utkarsh A Jagtap, Atish T Paul","doi":"10.1039/d5md00373c","DOIUrl":"10.1039/d5md00373c","url":null,"abstract":"<p><p>Taking a stand against obesity is an urgent priority, as it significantly impacts both the global economy and public health. Synthetic pancreatic lipase (PL) inhibitors represent one of the most effective therapeutics in the management of obesity. PL is a triacylglycerol acyl hydrolase from the family of serine hydrolases that play a key role in the hydrolysis of dietary fat into monoglycerides and fatty acids. Further, fatty acids get deposited in adipose tissue, which progressively results in weight gain. Over the last decade, various new drugs have been studied; however, orlistat still remains the first-line FDA-approved drug for obesity management. However, long-term use of orlistat can lead to serious health complications, including liver toxicity, osteoporosis, and gastrointestinal issues. Notably, the formation of an irreversible covalent bond of the β-lactone moiety of orlistat with the active serine site of HPL and PPL enzyme has been considered to be responsible for these complications. A deeper understanding of the crystal structure of HPL indicates that repositioning the hydrophobic lid domain, also known as the flap, opens access for designed inhibitors to interact with the active site residues: Ser152, His263, and Asp176. Additionally, predicting the mode of inhibition and the inhibition constant (<i>K</i> _i) value through enzyme kinetic study is helpful. This review presents a comprehensive overview of the <i>in silico</i> design, synthetic strategies, <i>in vitro</i> assays using human (HPL) and porcine (PPL) enzymes, <i>in vivo</i> activity, and structure-activity relationship (SAR) studies of synthetic PL inhibitors reported since 2014, aimed at the development of anti-obesity agents. Additionally, we propose the challenges to overcome and a potential path for future development in this field.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12498147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145245022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design, synthesis, and structure-activity relationship studies of 4-substituted phenylpyrazolidinone derivatives as potent Ku70/80 targeted DNA-PK inhibitors.","authors":"Narva Deshwar Kushwaha, Pamela VanderVere-Carozza, Tyler L Vernon, Pamela L Mendoza-Munoz, Jitender D Gaddameedi, Karim Ben Ali Gacem, Joseph Engel, Jean-Baptiste Charbonnier, Navnath S Gavande, John J Turchi","doi":"10.1039/d5md00263j","DOIUrl":"10.1039/d5md00263j","url":null,"abstract":"<p><p>The Ku70-Ku80 (Ku) heterodimer complex plays a central role in the non-homologous end joining (NHEJ) double-strand break (DSB) repair pathway and the DNA damage response (DDR). Like DNA-PK, Ku is a promising drug target for cancer treatment when combined with radiotherapy or DSB-inducing agents. We have previously reported the first-in-class, early-generation, highly potent, and specific Ku-DNA binding inhibitors (Ku-DBi's) that block the Ku interaction with DNA and inhibit DNA-PK kinase activity. These early-generation Ku-DBi's also inhibit cellular DNA-PK, NHEJ-catalyzed DSB repair, sensitize non-small cell lung cancer (NSCLC) cells to DSB-inducing agents, and potentiate the cellular effects of these agents <i>via</i> p53 phosphorylation through the activation of the ATM pathway. In this study, we report a comprehensive structure-activity relationship (SAR) analysis around the initial X80 hit molecule to develop highly potent Ku-DBi's. Early generation Ku-DBi's display a potent Ku-DNA binding inhibitory activity with a range of 2 to 6 μM, and DNA-PK inhibitory activity in the nanomolar range of approximately 110 nM. Microscale thermophoresis assay shows that these compounds inhibit Ku70-Ku80 binding to DNA with a Kd value of 0.4-6.4 μM. The thermal stability analysis also supports the notion that these Ku-DBi's bind to the Ku as measured by nanoDSF (Differential Scanning Fluorimetry), which is consistent with the observed SAR trends. These Ku-DBi's may serve as candidate compounds for further modification and development as anticancer therapeutics in combination with radiotherapy or DSB-inducing agents to treat certain DNA repair-deficient cancers.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in structural modifications of natural products for anti-leishmaniasis therapy (2010-2024).","authors":"Fu-Qun Sun, Yin-Sheng Quan, Qing-Kun Shen, Hong-Yan Guo, Xiu-Mei Yin, Zhe-Shan Quan","doi":"10.1039/d5md00534e","DOIUrl":"10.1039/d5md00534e","url":null,"abstract":"<p><p>Leishmaniasis represents a significant threat to global health as a neglected tropical disease. While therapeutic options exist, their high cost, safety concerns, and significant adverse effects necessitate the discovery of safer and more efficacious alternatives. Natural products, possessing diverse biological activities including inherent anti-leishmanial properties, constitute a vital resource for drug development. However, the intrinsic activity of these compounds is frequently suboptimal. Structural modification offers a potent strategy to significantly enhance their efficacy. This comprehensive review summarizes advances from 2010 to 2024 in the structural modification of natural products to improve anti-leishmanial activity, with particular emphasis on phenylpropanoid derivatives and other natural product classes, and provides detailed synthetic routes for each derivative. The findings demonstrate that strategic structural modifications can substantially increase potency, achieving IC₅₀ values in the nanomolar range for some derivatives. Furthermore, these optimized compounds exhibit promising safety profiles and favorable pharmacokinetic properties, underscoring their considerable potential for further development. These advancements not only offer promising avenues for novel anti-leishmanial drug discovery but also provide valuable insights applicable to natural product-based therapies for other diseases. Future research should prioritize elucidating mechanisms of action and conducting further structure-activity relationship optimization to develop more potent and less toxic anti-leishmanial agents.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyphenolic compounds as protective agents against cisplatin-induced ototoxicity with molecular mechanisms and clinical potential.","authors":"Tong Wei, Jing Nie, Dongbo Wang, Huina Wu, Lijiao Guan, Jiyong Wu","doi":"10.1039/d5md00426h","DOIUrl":"10.1039/d5md00426h","url":null,"abstract":"<p><p>Cisplatin remains a cornerstone in the treatment of various solid tumors due to its exceptional antineoplastic efficacy. However, its clinical utility is significantly constrained by severe adverse effects, with ototoxicity emerging as particularly problematic due to its potential to cause permanent hearing impairment and substantially diminish patient quality of life. Recent investigations into mitigating cisplatin-induced ototoxicity have identified natural polyphenolic compounds as promising protective agents, attributable to their diverse biological activities and potent antioxidant properties. This review critically examines the molecular mechanisms underlying cisplatin-induced cochlear damage and systematically evaluates recent advances in employing polyphenolic compounds as otoprotective interventions. Evidence indicates these bioactive molecules attenuate cisplatin-mediated hearing loss through multiple complementary pathways, including modulation of oxidative stress, inflammatory responses, and apoptotic cascades within the cochlear architecture. However, significant challenges, such as low bioavailability and potential interference with cisplatin's antitumor efficacy, hinder their clinical translation. Based on evidence from studies published between 2010 and 2025, with a focus on advances from the last five years, this review systematically outlines protective mechanisms while critically addressing current research limitations. It further proposes future directions, highlighting advanced drug delivery systems and innovative therapeutic strategies. These insights provide a robust mechanistic framework for the rational design and development of novel otoprotective strategies that preserve cisplatin's antitumor efficacy while minimizing its ototoxic potential.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12423776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of long-term TNF-alpha induced EGFR tyrosine kinase inhibitor resistance in chordoma.","authors":"HaoShuai Tang, QingRun Zhu, JinHong Fan, XinAo Li, ZhenYe Yan, Feng Wang, HaiFeng Wang, DaChuan Wang","doi":"10.1039/d5md00258c","DOIUrl":"10.1039/d5md00258c","url":null,"abstract":"<p><p>Chordoma is a special malignant tumor that lacks effective therapeutic targets, which can lead to incomplete treatment and metastasis. Inflammation plays an important role in chordoma progression and malignant phenotype. Inflammatory factors such as NF-kappaB and STAT3 are continuously activated in many tumors and contribute to the malignant phenotype of tumors and are potential therapeutic targets. This study suggest TNF-alpha and NF-kappaB signaling pathways were consistently activated in chordomas. Long-term TNF-alpha treatment induces chordoma resistance to EGFR family inhibitors. The underlying mechanism is realized by the key molecules HS3ST3A and HS3ST3B1. These two enzymes are potential targets for chordoma treatment, as well as for combination drugs treatment. It should be emphasized that the above analysis lacks experimental verification.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design and synthesis of 4-(2,4-dihydroxyphenyl)thiazole-2-carboxamide derivatives as novel tyrosinase inhibitors: <i>in vitro</i> and <i>in vivo</i> validation.","authors":"Wei Zou, Yijian Li, Zhaohang Xue, Chen Zhang, Hua Cao, Yan-Long Ma","doi":"10.1039/d5md00620a","DOIUrl":"10.1039/d5md00620a","url":null,"abstract":"<p><p>Melanin is essential for protecting human skin against harmful ultraviolet (UV) irradiation and environmental pollutants. However, excessive melanin accumulation in the epidermis can affect aesthetics, cause psychological distress, and reduce quality of life. Despite the development and utilization of several well-known tyrosinase (TYR) inhibitors as skin-whitening agents in cosmetics to address hyperpigmentation concerns, there remains a growing demand in the cosmetics market for safer, more efficient, and diverse skin-whitening agents. Guided by the binding model of thiamidol with TYR, this study synthesized and characterized 26 4-(2,4-dihydroxyphenyl)thiazole-2-carboxamide derivatives, evaluating their anti-TYR activities. Among these compounds, compound 4 exhibited the strongest anti-TYR activity (IC₅₀ = 1.51 μM) and effectively inhibited melanogenesis in the <i>in vitro</i> B16 cell model. Although its anti-TYR activity and anti-melanogenic effect <i>in vitro</i> were less than those of thiamidol (IC₅₀ = 0.72 μM), its depigmenting effect on the <i>in vivo</i> zebrafish embryo model was comparable to thiamidol. Additionally, compound 4 demonstrated excellent biocompatibility and exhibited lower toxicity compared to thiamidol. Overall, these results suggest that compound 4 holds potential as a promising candidate for application as a skin-whitening cosmetic ingredient.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12462781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Profile of NT-0527, a brain penetrant NLRP3 Inflammasome inhibitor suitable as an <i>in vivo</i> tool compound for neuroinflammatory disorders.","authors":"David Harrison, Andy Billinton, Mark G Bock, Nicholas P Clarke, Zsofia Digby, Christopher A Gabel, Nicola Lindsay, Valérie Reader, Jane Scanlon, Pamela Smolak, Peter Thornton, Heather Wescott, Alan P Watt","doi":"10.1039/d5md00639b","DOIUrl":"10.1039/d5md00639b","url":null,"abstract":"<p><p>Inhibition of the NLRP3 inflammasome has emerged as a high potential treatment paradigm for the treatment of neuroinflammation, with demonstrated anti-neuroinflammatory effects in Parkinson's disease patients and a strong rationale in Alzheimer's disease and amyotrophic lateral sclerosis. To facilitate further progress in this field, brain penetrant NLRP3 inflammasome inhibitors as leads and tool compounds are required. We discovered a small molecule NLRP3 inflammasome inhibitor, NT-0527 (11), and extensively profiled this to reveal a highly potent, selective and brain penetrant compound. This was shown to be orally bioavailable, efficacious in an <i>in vivo</i> model of inflammation, and with good developability characteristics. However, NT-0527 exhibited CYP 2C19 time-dependent inhibition, which halted development, but this molecule could be employed as a valuable tool compound for the investigation of neuroinflammatory conditions where NLRP3 inflammasome activation is implicated.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12409668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Olefinic side chain modification of fusidic acid enhances anti-MRSA activity and mitigates resistance development.","authors":"Wu-He Wu, Li-Juan Song, Kai-Yuan Bai, Fu-Huan Luo, Ya-Xin Li, Jing Luo, Xing-Fu Liu, Shang-Gao Liao, Jun-Li Ao, Guo-Bo Xu","doi":"10.1039/d5md00652j","DOIUrl":"10.1039/d5md00652j","url":null,"abstract":"<p><p>The escalating prevalence of antibiotic resistance underscores the urgent need for innovative antimicrobial agents. Fusidic acid (FA), a fungal-derived tetracyclic triterpene clinically employed against methicillin-resistant <i>Staphylococcus aureus</i> (MRSA), is limited by rapid resistance development and elevated MIC values in resistant strains. While previous olefinic side chain (Δ^24,25) modifications yielded FA derivatives with retained anti-MRSA activity, most analogs exhibited compromised efficacy against Gram-positive bacteria. To address this limitation, we systematically engineered the olefinic side chain through Wittig and olefin metathesis reactions, synthesizing 26 novel FA derivatives. Compound 10a emerged as a standout candidate, demonstrating MIC value lower than FA against MRSA (0.125 μg mL^-1) as well as low resistance. It also exhibited biofilm disruption capability of reducing MRSA biofilm formation by 61.4% at 0.5 × MIC, along with downregulation of biofilm-related regulators (<i>e.g. clfA, cna, agrA</i>, <i>agrC</i>). In a murine skin infection model, compound 10a significantly inhibited bacterial growth and accelerated wound healing at 2 mg kg^-1. Given these advantages, compound 10a represents a promising candidate molecule for combating multidrug-resistant Gram-positive infections.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145076277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a nitric oxide-releasing cephalexin-based hybrid compound for enhanced antimicrobial efficacy and biofilm disruption.","authors":"Sumit Kumar, Myddelton C Parker, Yi Wu, Anastasia Marx, Hitesh Handa, Elizabeth J Brisbois","doi":"10.1039/d5md00602c","DOIUrl":"10.1039/d5md00602c","url":null,"abstract":"<p><p>Biofilm formation on medical devices and the rise of antibiotic resistance have undermined conventional antibiotics such as cephalexin (CEX), which is effective against Gram-positive infections but has limited activity against Gram-negative pathogens and biofilms. To overcome these limitations, we developed a hybrid nitric oxide (NO)-releasing conjugate (SNAP_CEX) by covalently attaching the NO donor <i>S</i>-nitroso-<i>N</i>-acetylpenicillamine (SNAP) to CEX. SNAP_CEX exhibited a sustained NO release profile over 30 days, indicating enhanced stability compared to SNAP's rapid degradation, even though the Griess assay showed NO release from SNAP over 30 days. The hybrid maintained strong antibacterial activity against <i>Staphylococcus aureus</i> (<i>S. aureus</i>; MIC₅₀ = 7 μM <i>vs.</i> 2.5 μM for CEX) and dramatically improved efficacy against <i>Pseudomonas aeruginosa</i> (<i>P. aeruginosa</i>; MIC₅₀ = 3 mM <i>vs.</i> 16 mM for CEX). SNAP_CEX also significantly disrupted established biofilms, reducing <i>S. aureus</i> biofilm biomass by ∼75% (<i>vs.</i> ∼33% by CEX) and viable cells by ∼99%, and achieving ∼67% biomass reduction and 77% killing in <i>P. aeruginosa</i> biofilms (<i>vs.</i> ∼25% and 18% by CEX). These effects demonstrate that SNAP_CEX combines NO's biofilm-disruptive action with antibiotic therapy to combat biofilm-associated resistant infections, while remaining cytocompatible at therapeutic concentrations.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145076206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How to spare gut microbiota from antibiotic effects? PK-PD based innovative strategies, target specificity, and molecule-to-medicinal properties.","authors":"Abhishek Rai, Vaishnavi Newaskar, Nibedita Roy, Sankar K Guchhait","doi":"10.1039/d5md00591d","DOIUrl":"10.1039/d5md00591d","url":null,"abstract":"<p><p>Conventional broad-spectrum antibiotics often disrupt gut microbiota, causing a range of health issues like inflammatory bowel disease (IBD), secondary infections, colorectal cancer, liver disease, cognitive impairment, diabetes, and obesity. While the 'one drug treats all' strategy offers convenience, the long-term consequences of microbiota imbalance caused by such antibiotics can no longer be ignored. Modern antibiotic discovery and development programs must consider the strategies that minimize microbiota disruption to prevent long-term dysbiosis. This article presents, for the first time, a critical analysis of emerging microbiota-sparing pharmacokinetic-pharmacodynamic (PK-PD) based innovative antibacterial therapeutic strategies, such as transporter (BmpD)-mediated selective uptake, selective accumulation driven by efflux deficiency, pathogen-specific and pH-dependent selective cellular absorption, adjuvant facilitated therapy, β-lactamase-directed selectivity, microbiota-conserving immunotherapy, and CRISPR-based phage therapy. It highlights target-specific antibacterial approaches aimed at distinct bacterial pathways, such as lipoprotein transport, fatty acid biosynthesis, protein biosynthesis <i>via</i> methionyl-tRNA synthetase (MetRS), and DNA replication through DNA polymerase IIIC, which can minimize microbiota disruption and antibiotic-associated dysbiosis. Additionally, the discovery of antibacterial clinical candidates, such as afabicin, lolamicin, hygromycin A, cadazolid, and ribaxamase, that exhibit pathogen-specific efficacy with limited gut exposure, has been discussed with an in-depth analysis of their mechanism of actions (MoAs) and specific bacterial targets, molecular structure-to-medicinal insights, and strategic innovations. Collectively, this article provides a perspective for next generation antibacterial drug design and discovery, focusing on innovative strategies, specific biological pathways, and key molecular features that spare gut microbiota while maximizing antibacterial treatment efficacy.</p>","PeriodicalId":21462,"journal":{"name":"RSC medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}