Drug Development Research最新文献

{"title":"Vitexicarpin Directly Targets RSK2 to Attenuate Migration and Invasion of Triple-Negative Breast Cancer Through Modulating HIF-1α/MMP-9 Pathway.","authors":"Shuhui You, Tianhui Wu, Min Qian, Jiahui Du, Wenbing Sun, Mengyao Li, Xiaocan Zhang, Yuyang Zhou, Liangzhi Li, Min Xiang, Weiqiang Guo","doi":"10.1002/ddr.70291","DOIUrl":"https://doi.org/10.1002/ddr.70291","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with high metastatic potential and lacking effective treatment strategies. Vitexicarpin (VIT) has been reported to have excellent inhibitory effects on several types of cancer, including TNBC. However, its potential mechanisms on metastatic TNBC are not well understood. Herein, we found that VIT inhibited migration and invasion of TNBC through reducing MMP-9 expression in vitro and in vivo. Subsequently, RSK2 was identified as the potential target of VIT in TNBC by pull-down and MS analysis. Moreover, the further validations showed that VIT bound to Asp148 and Asp154 residues of NTKD, and Thr493 of CTKD, thereby inhibiting its phosphorylation and kinase activity. Mechanistically, we found that HIF-1α/MMP-9 was involved in VIT-mediated inhibition of migration and invasion of TNBC, and similar results were observed upon RSK2 knockdown or combined with VIT treatment, which demonstrated that VIT-mediated inhibition of HIF-1α/MMP-9 pathway was dependent on targeting RSK2. Finally, TNBC mouse xenograft models showed that VIT effectively inhibited TNBC metastasis and growth through regulating the RSK2/HIF-1α/MMP-9 axis in vivo. Taken together, our findings demonstrated that VIT downregulated the HIF-1α/MMP-9 pathway to suppress TNBC migration and invasion by directly targeting RSK2. These results suggested that VIT is a potential drug candidate for TNBC treatment.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70291"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FDA-Approved Drugs Containing D-Amino Acids: A Historical and Developmental Perspective.","authors":"Linh Tran, Tien Dung Nguyen, Abdelrahman Gamil Gad, Ethar Shaaban, Tu Ha Tai, Nguyen Thanh Tram, Huynh Nguyen Khanh Tran, Minh-Tri Le, Nguyen Tien Huy","doi":"10.1002/ddr.70293","DOIUrl":"https://doi.org/10.1002/ddr.70293","url":null,"abstract":"<p><p>d-Amino acids, the non-natural enantiomers of l-amino acids, have emerged as powerful tools in peptide drug development due to their unique biochemical properties. Their resistance to proteolytic degradation, enhanced conformational rigidity, and reduced immunogenicity make them especially valuable in designing long-acting and receptor-selective therapeutics. Since the mid-20th century, more than 20 FDA-approved drugs have incorporated at least one d-amino acid into their structure, spanning indications from infectious diseases and endocrine disorders to rare dermatologic conditions and diagnostic imaging. These drugs include both natural products like gramicidin D and synthetic analogs such as desmopressin, leuprolide, bremelanotide, and etelcalcetide, the latter being the first fully d-amino acid peptide to receive FDA approval. This review traces the historical development and clinical adoption of d-amino acid-containing drugs, highlighting their mechanisms of action, therapeutic relevance across disease areas, and the technological innovations, particularly solid-phase peptide synthesis and conceptual advances such as mirror-image phage display, that enabled their advancement. As peptide therapeutics continue to evolve, d-amino acids-containing drugs are poised to play a central role in the next generation of targeted, stable, and high-precision pharmaceuticals.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70293"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design, Synthesis, Biological Evaluation, and Molecular Modeling Studies of Novel 2-Aminothiazole Derivatives as Potential FOXM1 Inhibitors for Triple-Negative Breast Cancer Therapy and Structure-Activity Relationship.","authors":"Khaled A N Abusharkh, Venhar Çınar, Alper Onder, Merve Sıkık, Mustafa Guzel, Zuhal Hamurcu, Bulent Ozpolat, Mehmet Ay, Ferah Comert Onder","doi":"10.1002/ddr.70296","DOIUrl":"10.1002/ddr.70296","url":null,"abstract":"<p><p>Triple Negative Breast Cancer (TNBC) is one of the most aggressive subtypes of breast cancer (BC), which is associated with a very poor prognosis. It is a broad category of tumors with a variety of biological, clinical, and morphological characteristics. FOXM1 is a pivotal transcription factor that modulates proliferation-associated genes through complex protein-DNA and protein-protein interactions, making it a highly attractive target in cancer therapy. However, existing small-molecule inhibitors often suffer from limited specificity and efficacy. In this study, we designed, synthesized, and evaluated novel series of 2-aminothiazole derivatives (C1-C15) as potential FOXM1 inhibitors. Molecular docking and molecular dynamics (MD) simulations were employed to investigate the binding interactions of these compounds with the FOXM1 DNA-binding domain (FOXM1-DBD). Structural analysis highlighted the importance of crucial residues, including Asn283, His287, and Arg286, in mediating inhibitory activity. Among the synthesized compounds, C11 exhibited remarkable structural alignment and interaction patterns with FOXM1-DBD, comparable to the reference inhibitor FDI-6. In vitro studies using TNBC cell lines (MDA-MB-231, BT-549, and BT-20) demonstrated that compound C11 significantly outperformed FDI-6 in potency. Western blot analysis revealed that C11 effectively suppressed FOXM1 transcriptional activity at concentrations of 10 µM in BT-549 cells and 20 µM in MDA-MB-231 cells. These findings underscore the potential of C11 as a potent FOXM1 inhibitor and highlight its promise for further development in TNBC therapy.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70296"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812504","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":"Sustained DNA Hypomethylation Induced by a DNA Methyltransferase 1 Inhibitor Triggers Apoptosis in Thyroid Cancer Cells.","authors":"Chao-Wen Cheng, Wen-Fang Fang, Yuan-Hung Wang, Yea-Mey Yang, Jiunn-Diann Lin","doi":"10.1002/ddr.70299","DOIUrl":"https://doi.org/10.1002/ddr.70299","url":null,"abstract":"<p><p>DNA methylation, is catalyzed by DNA methyltransferases (DNMTs), and its aberrant patterns are implicated in thyroid cancer pathogenesis. The study aimed to investigate the association of DNMTs with thyroid cancer and evaluated the effects of sustained demethylating therapy in a cell-based study. DNMTs expressions in thyroid cancer were analyzed using GEO and TCGA datasets. Additionally, 16 paired and three unpaired papillary thyroid carcinoma (PTC) samples from Taipei Medical University (TMU), along with commercial tissue arrays, were analyzed. Furthermore, the effects of the covalent DNMT inhibitor, 5-azacytidine (5-Aza), and the DNMT1-selective inhibitor, GSK-3484862, on cell viability were evaluated in PTC and follicular thyroid carcinoma (FTC) cell lines. DNMT1 and DNMT3A were upregulated in PTC, with DNMT1 expression correlated with the BRAF mutation and lymph node invasion in TCGA data, findings further confirmed in the TMU cohort and tissue arrays. Short-term (24 h) 5-Aza treatment (1 and 5 µM) induced substantial cell death regardless of the DNA methylation status, whereas short-term GSK-3484862 (5 µM) treatment showed minimal cytotoxicity. In contrast, sustained low-dose GSK-3484862 treatment (approximately 1-3 weeks at 2 µM) effectively reduced global DNA methylation and decreased cell viability of TPC-1 and FTC-236 cells through apoptosis, rather than by inhibiting proliferation. In conclusion, DNMT1 overexpression in PTC suggests its involvement in thyroid carcinogenesis. Sustained inhibition of DNMT1 effectively reduced global DNA methylation and promoted apoptosis, highlighting the potential of prolonged DNMT1-targeted therapy. Further in vitro and in vivo studies are warranted to validate these results and elucidate the underlying mechanisms.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70299"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Discovery of Tetrahydropyrrolo[3,4-c]pyrrole-1,3-dione Derivatives as Novel RIPK1 Inhibitors via Pharmacophore-Based Virtual Screening.","authors":"Xin Zeng, Yanzhen Yu, Yifan Wu, Geng Chen, Rong Sheng","doi":"10.1002/ddr.70290","DOIUrl":"https://doi.org/10.1002/ddr.70290","url":null,"abstract":"<p><p>RIPK1 regulates the pathways in programmed cell death, and is closely associated with inflammatory and immune diseases. Based on the pharmacophore-based virtual screening, compound 15, a tetrahydropyrrolo[3,4-c]pyrrole-1,3-dione derivative, was identified as a hit of RIPK1 inhibitor with an IC₅₀ value of 6.42 μM. Furthermore, a similarity searching was carried out to get more potent RIPK1 inhibitors. Among them, compound 21 showed obvious improvement in RIPK1 inhibitory activity with an IC₅₀ value of 2.21 μM, accompanied with moderate anti-necroptosis activity in HT-29 cells (IC₅₀ = 15.32 μM). Molecular dynamics (MD) simulations indicated that it probably functioned as a type III kinase inhibitor.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70290"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Development of Chemical Probes for Targeting Coactivator Associated Arginine Methyltransferase 1 (CARM1) Inhibitors.","authors":"Kadalipura P Rakesh, Santosh Kumar Verma, Man Vir Singh, Abdulwahab Abuderman, Shekhar Verma, Rameshwari Verma, Sangeeta Soni","doi":"10.1002/ddr.70302","DOIUrl":"https://doi.org/10.1002/ddr.70302","url":null,"abstract":"<p><p>As a transcriptional coactivator and associated arginine methyltransferase 1, CARM1 controls various biological functions. CARM1 was thought to be a prospective therapeutic target, as anomalous appearance of the gene has been linked to the development of several cancer types. Since there aren't any CARM1 inhibitors available for use in clinical trials at the moment, Kindle is interested in the development of human pharmacological treatments that target CARM1. To confirm this PRMT as a therapeutic target, selective inhibitors of CARM1 would be helpful tools. In this review, we discuss the identification, description, and biological use of CARM1 inhibitors, focusing on significant developments in the field.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70302"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DPP4-Driven Ferroptosis Promotes Senescence: Galangin as a Therapeutic Agent for Age-Related Bone Loss.","authors":"Hongming Zhou, Xiaoxi Liu, Hengren Li, Heng Yang, Xingang Cui","doi":"10.1002/ddr.70295","DOIUrl":"https://doi.org/10.1002/ddr.70295","url":null,"abstract":"<p><p>Senile osteoporosis is driven by bone marrow stromal cell (BMSC) senescence. Ferroptosis, an iron-dependent cell death pathway, is implicated in aging. The natural flavonoid galangin possesses anti-aging properties, yet its effects on ferroptosis and BMSC senescence are unknown. Natural aging and d-galactose-induced aging models were used, with galangin supplementation. Bone mass was assessed via micro-computed tomography and histomorphometry. Senescence markers (P21, SA-β-gal, NAD+) and ferroptosis regulators (GPX4, GSH/GSSG) were measured. BMSC senescence was induced by d-galactose or serial passaging. Effects of galangin on senescence, ferroptosis, osteogenic differentiation, and dipeptidyl peptidase-4 (DPP4) signaling were evaluated. Galangin significantly attenuated bone loss and reduced senescence markers in both aging mouse models. Ferroptosis was activated in senescent BMSC. Galangin suppressed ferroptosis, rescued senescence phenotypes, and restored osteogenic differentiation capacity. Mechanistically, galangin inhibited DPP4 nuclear translocation and disrupted its interaction with NADPH oxidase NOX1, thereby blocking reactive oxygen species-dependent ferroptosis signaling without altering total DPP4 expression. Galangin ameliorates Senile osteoporosis by specifically inhibiting DPP4 nuclear translocation and its interaction with NOX1, thereby suppressing ferroptosis, rescuing BMSC senescence, and restoring osteogenic function. This identifies galangin as a promising agent against skeletal aging.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70295"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structure-Guided Design and Mechanistic Elucidation of New Chromene Derivatives as Selective Vascular Endothelial Growth Factor Receptor-2 Inhibitors With Potent Anticancer Activity.","authors":"Hazem Elkady, Walid E Elgammal, Ibrahim H Eissa, Hazem A Mahdy, Aisha A Alsfouk, Fatma G Amin, Dalal Z Husein, Ahmed M Metwaly, Eslam B Elkaeed","doi":"10.1002/ddr.70297","DOIUrl":"https://doi.org/10.1002/ddr.70297","url":null,"abstract":"<p><p>In this study, a novel series of chromene-based derivatives was rationally designed as potential VEGFR-2 inhibitors based on key structural and pharmacophoric features required for antiangiogenic activity. Accordingly, twelve chromene derivatives (13a-e, 15a-e, and 17a-b) were successfully synthesized and structurally characterized. The synthesized compounds were evaluated in vitro for their cytotoxic activity against human cancer cell lines (MCF-7, HepG-2, and HCT-116), in addition to normal WI-38 and WISH cells. Among the tested compounds, compound 13a demonstrated the most potent and selective antiproliferative activity, exhibiting low micromolar IC₅₀ values and favorable selectivity indices. Enzymatic assays confirmed its VEGFR-2 inhibitory activity (IC₅₀ = 1.666 ± 0.025 µM), comparable to the reference drug sorafenib. Mechanistic investigations revealed that compound 13a effectively inhibited cancer cell migration in a wound healing assay, highlighting its potential antiangiogenic properties. Furthermore, compound 13a induced significant G0/G1 cell cycle arrest in MCF-7 cells and triggered apoptosis, as evidenced by Annexin V/PI staining. To support the experimental findings, Density Functional Theory (DFT) calculations confirmed favorable structural stability and electronic properties. Molecular docking studies demonstrated strong binding interactions within the VEGFR-2 ATP-binding site. These results were further validated by 200 ns molecular dynamics simulations, MM-GBSA binding free energy calculations, Protein-Ligand Interaction Fingerprints (Pro-LIF), Principal Component Analysis of Trajectories (PCA-T), and Free Energy Landscape (FEL) analyses, confirming the dynamic stability and favorable energetics of the VEGFR-2-13a complex. Overall, this integrated experimental and computational study identifies compound 13a as a promising VEGFR-2-targeted anticancer lead warranting further preclinical investigation.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70297"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design, Green Synthesis, and Biological Evaluation of Novel Triaryl-Tethered Acryloyl Derivatives as New Generation β-Tubulin Inhibitors for Hepatocellular Carcinoma Treatment.","authors":"Aamal A Al-Mutairi, Mai A E Mourad, Arwa Sultan Alqahtani, Ayman Abo Elmaaty, Islam Zaki","doi":"10.1002/ddr.70303","DOIUrl":"https://doi.org/10.1002/ddr.70303","url":null,"abstract":"<p><p>Inhibition of β-tubulin polymerization has been set as promising therapeutic strategy for cancer therapy. Accordingly, a new set of triaryl-tethered acetohydrazide-acryloyl derivatives were designed and synthesized. The antiproliferative influence was evaluated against liver Huh-7 cell line using MTT colorimetric method with Doxorubicin as a positive control. Compounds 3b, 4f, 4i, and 4j showed excellent cytotoxic activity against Huh-7 cell line. Among the investigated compounds, 2-(naphthalene-2-yloxy)acetohydrazide having 2-(4-methyl)-3-(3,4,5-trimethoxybenzamido)acryloyl moiety (compound 4i) was the most active one with an IC₅₀ value of 2.46 µM. In addition, all compounds were further evaluated in vitro for their β-tubulin polymerization inhibition activity. Results found that compound 4i showed high activity against β-tubulin polymerization with an IC₅₀ value of 2.29 µM, surpassing the activity of the reference Podophyllotoxin (IC₅₀ = 4.45 µM). Further studies revealed the ability of the promising compound 4i to induce apoptosis and halt the cellular cycle at G2/M phase. Furthermore, the apoptosis-inducing activity of naphthalene-tethered acryloyl moiety 4i was correlated to the downregulation of Bcl-2 as well as elevation of both Bax and caspase 9 as concluded from RT-PCR immunoassay measurements. Finally, molecular docking studies were also performed to explain the displayed inhibitory activities.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70303"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Secoisolariciresinol Diglucoside Alleviates LPS-Induced Acute Lung Injury by Inhibiting the NF-κB/NLRP3 Signaling Pathway.","authors":"Yuanyuan Zhong, Yang Zou, Zhen Qu, Kai Zhou, Huijuan Liu, Jiali Yang, Chengzhong Tang, Yuqiang Xu, Zhen Wang","doi":"10.1002/ddr.70285","DOIUrl":"https://doi.org/10.1002/ddr.70285","url":null,"abstract":"<p><p>Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), are life-threatening pulmonary disorders with high mortality rates, and effective treatments are currently lacking. Secoisolariciresinol diglucoside (SDG), a plant lignan derived from flaxseed, possesses anti-inflammatory and antioxidative activities. However, the underlying mechanisms by which SDG ameliorates ALI remain incompletely understood. This study aimed to investigate whether SDG alleviates ALI by modulating the NF-κB/NLRP3 signaling pathway. For the in vivo study, ALI was induced in mice through intranasal administration of LPS. Key indicators included lung histopathological changes, wet/dry weight ratio (W/D), protein concentration in bronchoalveolar lavage fluid (BALF), oxidative stress markers (MDA, SOD, CAT), the expression of inflammatory cytokines and chemokines (IL-1β, IL-18, TNF-α, CCL2), and the level of NF-κB/NLRP3 pathway-related proteins. In vitro experiments using LPS-stimulated RAW264.7 further explored the effects of SDG on the NF-κB/NLRP3 pathway. SDG significantly mitigated LPS-induced lung histopathological damage and nasal mucosal injury, reduced lung W/D ratio and BALF protein, and suppressed oxidative stress. Moreover, SDG downregulated pro-inflammatory cytokines (IL-1β, IL-18, TNF-α) and macrophage infiltration. It also decreased the expression of N-κB/NLRP3 pathway-related proteins. In vitro experiments further confirmed that SDG inhibited the NF-κB/NLRP3 pathway. SDG effectively alleviates LPS-induced ALI through its antioxidant, anti-inflammatory, and NF-κB/NLRP3 pathway-inhibiting properties, providing experimental evidence for its potential as a therapeutic agent for ALI.</p>","PeriodicalId":11291,"journal":{"name":"Drug Development Research","volume":"87 3","pages":"e70285"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765507","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}