Archives of Pharmacal Research最新文献

{"title":"NRF2 activation in cancer and overview of NRF2 small molecule inhibitors","authors":"Hoang Hai Ngo,&nbsp;Bo-Yeong Yu,&nbsp;Jeong-Eun Lee,&nbsp;Hyunwoo Kim,&nbsp;Young-Sam Keum","doi":"10.1007/s12272-025-01557-x","DOIUrl":"10.1007/s12272-025-01557-x","url":null,"abstract":"<div><p>NRF2 is a redox-sensitive transcription factor that activates the expression of phase II detoxifying and antioxidant enzymes. In addition to maintaining redox homeostasis, NRF2 regulates various other processes, including metabolism, stem cell renewal, mitochondrial function, and proteostasis. NRF2 is considered a tumor suppressor because its activation by chemopreventive phytochemicals contributes to the detoxification of oxidants and electrophiles in normal cells. However, aberrant NRF2 activation occurs in cancer due to mutations in the KEAP1/NRF2 pathway, and it contributes to the generation of a tumor microenvironment that favors the proliferation, survival, and chemoresistance of cancer cells. In this review, we present the regulatory mechanisms of NRF2 and discuss how NRF2 activation contributes to chemoresistance. We also explain therapeutic strategies that exploit the vulnerabilities of NRF2-addicted cancer cells, providing NRF2 small-molecule inhibitors along with their mechanisms of action.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"676 - 705"},"PeriodicalIF":7.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144854362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel multi-target compound mitigates amyloid plaques, synaptic deficits, and neuroinflammation in Alzheimer’s disease models","authors":"Yeongyeong Lee,&nbsp;Sukmin Han,&nbsp;Jeongmi Lee,&nbsp;Yongeun Cho,&nbsp;Jun-Sik Kim,&nbsp;Yeji Jeon,&nbsp;Heewon Cho,&nbsp;Heejin Yoo,&nbsp;Yujung Byun,&nbsp;Tai Kyoung Kim,&nbsp;Ju-Mi Hong,&nbsp;Hyunwook Kim,&nbsp;Sang Yoon Park,&nbsp;Joung Han Yim,&nbsp;Sung Hyun Kim,&nbsp;Dong-Gyu Jo","doi":"10.1007/s12272-025-01562-0","DOIUrl":"10.1007/s12272-025-01562-0","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is characterized by progressive cognitive decline, amyloid plaque accumulation, synaptic dysfunction, and neuroinflammation. This study reports the therapeutic potential of (S)-4-amino-5,5-difluoro-N′-methyl-N′-phenylpentanehydrazide hydrochloride (RA-058HM), a novel compound, in ameliorating these pathological features of AD in the 5xFAD mouse model. RA-058HM was administered orally for 8 weeks, and its multi-target effects – including relief from neuroinflammation, normalization of synaptic transmission, reduction of amyloidogenesis (plaque and soluble oligomers, as well as BACE1 levels), and rescue of cognitive function—were evaluated. To our knowledge, RA-058HM is the first compound to demonstrate simultaneous modulation of these key pathways in the 5xFAD model, highlighting its potential as a comprehensive disease-modifying therapy for AD. Behavioural tests revealed marked improvements in spatial and recognition memory in RA-058HM-treated 5xFAD mice, suggesting a reversal of cognitive deficits. At the molecular level, RA-058HM treatment reduced amyloidogenesis, as evidenced by decreased levels of amyloid precursor protein (APP) and β-secretase (BACE1) in the hippocampus, accompanied by reduced plaque formation, as detected by Thioflavin-S staining. Furthermore, synaptic transmission was restored to near-normal levels in RA-058HM-treated neurons, indicating that RA-058HM effectively rescues synaptic deficits without altering synaptic protein levels of PSD95 and synaptophysin. In addition, treatment of RA-058HM downregulated hippocampal levels of the NLRP3 inflammasome, TNF-α, and GFAP, suggesting a decrease in neuroinflammatory signaling and a modulation of glial activity. Restoration of mitochondrial motility in hippocampal neurons further suggests that RA-058HM may improve cellular energy dynamics. Collectively, these findings indicate that RA-058HM has multifaceted effects on AD pathology, targeting amyloid accumulation, synaptic transmission, neuroinflammation, and mitochondrial function. This study highlights RA-058HM as a promising candidate for AD therapy and underscores the potential of multi-targeted approaches in addressing the complex mechanisms underlying AD progression.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"745 - 764"},"PeriodicalIF":7.5,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into biological activities profile of gingerols and shogaols for potential pharmacological applications","authors":"Anis Najwa Abdul Rani,&nbsp;Anand Gaurav,&nbsp;Vannajan Sanghiran Lee,&nbsp;Nadiah Mad Nasir,&nbsp;Sharifuddin Md Zain,&nbsp;Vaishali M. Patil,&nbsp;Ming Tatt Lee","doi":"10.1007/s12272-025-01559-9","DOIUrl":"10.1007/s12272-025-01559-9","url":null,"abstract":"<div><p>Ginger (<i>Zingiber officinale</i>) rhizome has been widely used in traditional medicine for centuries to promote good health and well-being, treating conditions such as diarrhea, stomach discomfort, nausea, cholera, asthma, and respiratory diseases. Gingerol and shogaol are essential bioactive phenolic compounds abundantly found in fresh and dried ginger and have been extensively studied using modern technology to evaluate their therapeutic effects. These phenolic compounds demonstrate a wide range of properties, including antioxidant, anti-inflammatory, antidiabetic, and anticancer effects, which operate through various mechanisms. Furthermore, researchers have utilized the chemical structures of gingerol and shogaol as templates to develop novel, safer, and more effective drugs for treating multiple illnesses. This review article focuses on previous literature assessing the potential efficacy of these compounds as therapies based on their antioxidant, anti-inflammatory, antidiabetic, anticancer, and neuroprotective properties.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"638 - 675"},"PeriodicalIF":7.5,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effects of taurine in a rodent model of parkinson’s disease involve modulating astrocyte-mediated inflammation","authors":"Sung Min Moon,&nbsp;Jaehoon Kim,&nbsp;Jaeheon Seol,&nbsp;Seonguk Yang,&nbsp;Duwon Jung,&nbsp;Chang Yup Kim,&nbsp;Chang Seok Kim,&nbsp;Ki Wung Chung,&nbsp;Young-Suk Jung,&nbsp;Seung-Cheol Chang,&nbsp;Hae Young Chung,&nbsp;Jaewon Lee","doi":"10.1007/s12272-025-01563-z","DOIUrl":"10.1007/s12272-025-01563-z","url":null,"abstract":"<div><p>Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons due to oxidative stress and inflammation. Targeting inflammation and oxidative stress offers a promising means of slowing PD progression. Taurine, a naturally occurring amino sulfonic acid, has demonstrated potent antioxidant properties, thereby preventing cell death. While taurine has been studied for its potential to restrain the progression of Alzheimer’s disease and mitigate microglial activation, its impact on astrocyte activation in PD models remains underexplored. Here, we found that taurine significantly reduces astroglial activation in MPP⁺-induced primary astrocytes by inhibiting the NF-κB pathway. Additionally, in vivo experiments in MPTP-induced PD models using male C57BL/6 mice showed that taurine improved motor function, protected against dopaminergic neuronal loss, and reduced glial activation in the striatum and substantia nigra. These findings highlight that the anti-inflammatory effects of taurine involve the inhibition of astroglial activation, suggesting that taurine has therapeutic potential in PD.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"814 - 829"},"PeriodicalIF":7.5,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"9H-carbazole derivatives from a Streptomyces species under potassium iodide stress and their anti-inflammatory properties","authors":"Pengcheng Yan,&nbsp;Yunlong Liu,&nbsp;Jibin Liu,&nbsp;Linmeng Chen,&nbsp;Ning Li,&nbsp;Weiming Zhu","doi":"10.1007/s12272-025-01556-y","DOIUrl":"10.1007/s12272-025-01556-y","url":null,"abstract":"<div><p>By continuously activating silent gene cluster of the marine-derived <i>Streptomyces</i> strain OUCMDZ-5511 under high salt stress, three new iodinated 9<i>H</i>-carbazole derivatives (<b>1</b>–<b>3</b>) and a novel oxazole-fused chlorinated 9<i>H</i>-carbazole derivative (<b>4</b>), along with five previously reported analogues (<b>5</b>–<b>9</b>), were obtained from the cultures grown with 7.5% potassium iodide (KI). The structures of these previously undocumented compounds were elucidated as 4-iodo-3-methoxy-9<i>H</i>-carbazole (<b>1</b>), 4-iodo-3-methoxy-9<i>H</i>-carbazole-6-ol (<b>2</b>), 4-iodo-3-methoxy-9<i>H</i>-carbazole-8-ol (<b>3</b>), and 10-chloro-9-methoxy-6<i>H</i>-oxazolo[5,4-<i>c</i>]carbazole (<b>4</b>), using MS and NMR spectroscopic techniques. Notably, compound <b>3</b> demonstrated a more potent anti-inflammatory effect than the positive control in a CuSO₄-induced inflammation zebrafish model, likely by modulating the Myd88/NF-κB signaling pathway to exert its anti-inflammatory activity.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"736 - 744"},"PeriodicalIF":7.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silybin inhibits succinate production and secretion in hepatocytes to reverse liver fibrosis","authors":"Xule Yang,&nbsp;Yunge Lou,&nbsp;Huan Li,&nbsp;Yuanyuan Ma,&nbsp;Zihan Wang,&nbsp;Jiye Aa,&nbsp;Guangji Wang,&nbsp;Yuan Xie","doi":"10.1007/s12272-025-01560-2","DOIUrl":"10.1007/s12272-025-01560-2","url":null,"abstract":"<div><p>Silybin has been used as a therapeutic agent in treating liver fibrosis worldwide with unclear mechanisms. In this study, mice were fed a CDAHFD for six weeks to induce liver steatosis and mild liver fibrosis. Metabolomic analysis of mouse liver mitochondria revealed that silybin reversed metabolic abnormalities and diminished succinate accumulation within the mitochondria. Lipidomic profiling revealed marked decreases in mitochondrial membrane phospholipids (PE, PS, PC, and PI) in CDAHFD-fed mice, along with a substantial reduction in cardiolipin (CL)—a critical component for succinate dehydrogenase (SDH) complex assembly. Silybin restored mitochondrial membrane phospholipids, enhanced CRLS1 expression, facilitated the assembly of SDHA and SDHB, and rejuvenated SDH activity. CRLS1 knockdown via siRNA significantly impaired SDH function, leading to mitochondrial succinate accumulation. Moreover, silybin inhibited succinate efflux by downregulating the expression of the MCT1 transporter. Conditioned medium from palmitic acid/silybin-treated hepatocytes, containing reduced succinate levels, effectively suppressed LX-2 activation. This research indicates that silybin alleviates MASH-induced liver fibrosis by inhibiting succinate generation and its extracellular release, thereby inactivating hepatic stellate cells. These results suggest that targeting succinate production or secretion may represent a promising therapeutic strategy against liver fibrosis progression.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"782 - 797"},"PeriodicalIF":7.5,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin monoglucuronide protects cartilage from progressive degeneration by blocking MMP-13","authors":"Himadri Shekhar Roy,&nbsp;Chirag Kulkarni,&nbsp;K. M. Neethu,&nbsp;Anand Babu,&nbsp;Malika Arora,&nbsp;Govindasamy Jayamurugan,&nbsp;Dipankar Mandal,&nbsp;Rajdeep Guha,&nbsp;Naibedya Chattopadhyay,&nbsp;Deepa Ghosh","doi":"10.1007/s12272-025-01558-w","DOIUrl":"10.1007/s12272-025-01558-w","url":null,"abstract":"<div><p>Collagenases (MMP-1, MMP-8, and MMP-13) play significant roles in the pathophysiology of osteoarthritis. Among these proteins, MMP-13 and MMP-8 are known for their catabolic roles in the degradation of the articular cartilage matrix. Using computational studies, we had previously observed that a metabolite of curcumin, Curcumin monoglucuronide (CMG), binds to MMPs involved in cartilage matrix destruction. The purpose of this study was to confirm the ability of CMG to protect cartilage by blocking the activity of these enzymes. The ability of CMG to bind and block the activities of MMP-13 and MMP-8 was established using several physicochemical methods. First, the protective effect of CMG on MMP-mediated cartilage destruction was demonstrated using cartilage explants in vitro. Second, the in vivo efficacy of CMG was tested by comparison with BI-4394, a specific MMP-13 inhibitor, using a rat anterior cruciate ligament transection (ACLT) model. These studies demonstrated that CMG was more effective than BI-4394 at preventing cartilage degeneration. In separate in vitro studies, CMG did not affect chondrocyte proliferation or the expression of NF-κB-mediated proinflammatory genes. Together, these findings demonstrate the therapeutic potential of CMG and emphasize the importance of inhibiting both MMP-13 and MMP-8 to achieve improved clinical outcomes.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"765 - 781"},"PeriodicalIF":7.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting NF-κB in diabetic nephropathy: exploring the therapeutic potential of phytoconstituents","authors":"Beena Levakumar Abhirami,&nbsp;Anithakumari Aswathy Krishna,&nbsp;Alaganandam Kumaran,&nbsp;Chun-Hui Chiu","doi":"10.1007/s12272-025-01555-z","DOIUrl":"10.1007/s12272-025-01555-z","url":null,"abstract":"<div><p>The growing epidemic of diabetes mellitus and its associated complications presents a major global health challenge. Diabetic nephropathy (DN) is a critical microvascular complication of diabetes, accounts for approximately one-third of all related cases worldwide and frequently progresses to end-stage renal disease (ESRD) and premature mortality. Extensive experimental evidence underscores the pivotal role of chronic inflammation driven by the activation of the nuclear transcription factor NF-κB in the pathogenesis of DN. Triggered by various factors including hyperglycemia, NF-κB activation leads to the expression of numerous pro-inflammatory cytokines, chemokines and cell adhesion molecules, resulting in the pathological hallmarks of DN: podocyte injury, excessive extracellular matrix accumulation, glomerulosclerosis, epithelial-mesenchymal transition, renal tubular atrophy and increased proteinuria. Consequently, NF-κB emerges as a promising therapeutic target for DN. Naturally occurring phytoconstituents, as inhibitors of the NF-κB pathway and are gaining significant attention due to their lower toxicity, enhanced safety, greater efficacy and cost-effectiveness. This review summarizes the role of NF-κB in the pathophysiology of DN and examines recent research on medicinal plants and phytoconstituents that target the NF-κB signaling pathway in both in vitro and in vivo and in silico models. Furthermore, we elucidate their mechanisms of action and evaluate their potential as effective therapeutic agents for mitigating DN-related inflammation and complications. This provides a theoretical framework for the development of novel anti-nephropathic drugs that may overcome the limitations of current medications.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"577 - 637"},"PeriodicalIF":7.5,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sphingolipid modulation and anti-tumor activity of Jaspine B in HepG2 bearing mice","authors":"Jihoon Lee,&nbsp;Ji-Hyeon Jeon,&nbsp;Minyeong Pang,&nbsp;Min-Koo Choi,&nbsp;Dongjoo Lee,&nbsp;Im-Sook Song","doi":"10.1007/s12272-025-01554-0","DOIUrl":"10.1007/s12272-025-01554-0","url":null,"abstract":"<div><p>The cytotoxicity of Jaspine B was evaluated across a concentration range of 0.5–50 μM, yielding a half maximal inhibitory concentration (IC₅₀) of 2.6 μM for HepG2 human hepatocellular carcinoma cells. To explore the mechanisms of Jaspine B, we investigated the expression of sphingosine kinase 1 (SphK1), a rate-limiting enzyme involved in the production of sphingosine-1-phosphate (S1P) from sphingosine, and the modulation of sphingolipids in HepG2 cells. Jaspine B reduced SphK1 expression and S1P levels in a dose-dependent manner. Additionally, flow cytometry analysis indicated that Jaspine B induces apoptosis in HepG2. In HepG2-xenografted mice, Jaspine B treatment (20 mg/kg/every other day for four weeks) reduced tumor size without significant changes in either body or organ weight. The anti-cancer effect in these mice was linked to reduced SphK1 expression in tumor tissue and lower plasma S1P levels. The concentration of Jaspine B in tumor tissue was 4.64 ± 2.05 μM, which exceeded its IC₅₀ value (2.6 μM for cytotoxicity and 1.4 μM for SphK1 inhibition), further supporting its efficacy through SphK1inhibition. The anti-cancer effect and reduced plasma S1P levels induced by Jaspine B were comparable to PF543, a selective SphK1 inhibitor, in HepG2-xenografted mice. In conclusion, this study provides in vitro and in vivo evidence that Jaspine B is a promising anti-cancer agent for hepatocellular carcinoma, acting through SphK1 inhibition, with favorable pharmacokinetic and tumor distribution properties. This study also suggested that reduced plasma S1P levels may serve as a therapeutic biomarker for SphK1 inhibitors in hepatocellular carcinoma treatment.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"798 - 813"},"PeriodicalIF":7.5,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging concepts and challenges in the development of disease-modifying osteoarthritis drugs – a more refined perspective","authors":"Zsuzsa Jenei-Lanzl,&nbsp;Svenja Maurer,&nbsp;Rolf E. Brenner,&nbsp;Frank Zaucke,&nbsp;Michael Fuchs,&nbsp;Jana Riegger","doi":"10.1007/s12272-025-01551-3","DOIUrl":"10.1007/s12272-025-01551-3","url":null,"abstract":"<div><p>Osteoarthritis (OA) is the most common joint disease worldwide. Despite significant efforts byresearchers, no disease-modifying osteoarthritis drugs (DMOADs) have been approved yet. This review compares preclinical and clinical studies of promising therapeutic approaches to gain insights into the potential reasons for their failure in clinical trials. For this purpose, prime examples of different therapeutic groups, including the antioxidant NAC, senotherapeutic UBX0101, anti-inflammatory drug Anakinra®, Wnt inhibitor Lorecevivint®, chondroanabolic growth factor Sprifermin™, and various protease inhibitors, are discussed in detail. The limitations of commonly used OA animal models are elaborated to understand this failure better. Moreover, this review addresses the challenges of patient stratification into different endotypes and phenotypes, the consideration of subgrouping in clinical trials, and the lack of suitable clinical outcome parameters. In summary, this review highlights potential reasons for the high failure rate of DMOADs in clinical trials and outlines key points for future improvement.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 6","pages":"467 - 494"},"PeriodicalIF":7.5,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12241195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}