Recent patents on anti-cancer drug discovery最新文献

{"title":"Differential Expression and Distribution of Slco4a1 and Slco1b2 in an Internal Environment Disorder-induced Hepatocellular Carcinoma Mouse Model.","authors":"Haoxuan Luo, Yang Xie, Shan Huang, Yu Zhang","doi":"10.2174/0115748928351523241204071335","DOIUrl":"10.2174/0115748928351523241204071335","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to enhance the understanding of underlying mechanisms and potential therapies of the solute carrier organic anion (SLCO) transporter family in internal environment disorder (IED)-induced hepatocellular carcinoma (HCC). This could lead to new therapeutic strategies and offer new directions for the creation of new patents for HCC treatment products.</p><p><strong>Methods: </strong>The orthotopic transplantation (OT), IED and IED-based OT (IED-OT) mouse models were established. Expression patterns of Slco4a1 and Slco1b2 were determined using reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blotting (WB) and immunohistochemistry (IHC) in various tissues, including lung, stomach, liver, spleen, kidney, colon, small intestine, HCC tissues and adjacent non-cancerous tissues.</p><p><strong>Results: </strong>Animals exhibited symptoms, including weight loss, lethargy, chills, dyspnea, altered hair texture, and gastrointestinal disturbances, confirming the successful establishment of the IED model. The analysis demonstrated differential expression and tissue-specific distribution of Slco4a1 and Slco1b2, which are associated with IED-induced changes. These alterations potentially disrupt organ transport functions, thereby promoting the development of HCC. Additionally, they suggest a role in rebalancing the tumor microenvironment and mitigating damage resulting from abnormal substance accumulation.</p><p><strong>Discussion: </strong>This study reveals that IED promotes HCC progression by altering the expression and distribution of Slco4a1 and Slco1b2, leading to transport dysfunction in affected organs. Furthermore, IED and OT exhibit synergistic effects in HCC development. These findings enhance the understanding of the underlying mechanisms of IED related HCC. Future studies should establish animal models incorporating both internal and external factors, with cellular experiments needed to further validate the mechanisms.</p><p><strong>Conclusion: </strong>Changes in SLCO expression and distribution induced by IED may play pivotal roles in the development of HCC. These findings contribute insights that could inform novel therapeutic strategies against HCC.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"75-86"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin Promotes the M1-to-M2 Macrophage Phenotypic Switch During Liver Fibrosis Treatment by Modulating the JAK2/STAT3 Signaling Pathway.","authors":"Dongqi Sun, Xiaoling Zhou, Teng Wu, Zepeng Li, Shigao Huang, Zheng Peng","doi":"10.2174/0115748928318948240920044716","DOIUrl":"10.2174/0115748928318948240920044716","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the underlying mechanism by which quercetin (Que) regulates macrophage polarization and its subsequent therapeutic effect on liver fibrosis, an important pathological precondition for hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>In vitro experiments were performed on the RAW264.7 mouse macrophage line. After the induction of M1-type macrophages with LPS, the effects of Que on cell morphology, M1/M2 surface marker expression, cytokine expression, and JAK2/STAT3 expression were analyzed. In vivo, male SD rats were used as a model of CCL4-induced hepatic fibrosis, and the effects of Que on serum aminotransferase levels, the histopathological structure of liver tissues, and macrophage-associated protein expression in liver tissues were analyzed.</p><p><strong>Results: </strong><i>In vitro</i> experiments revealed that Que can suppress the activation of the JAK2/STAT3 signaling pathway, leading to decreases in the expression of M1 macrophage surface markers and cytokines. Additionally, Que was found to increase the expression of M2 macrophage surface markers and cytokines. In vivo, assays demonstrated that Que significantly ameliorated the development of inflammation and fibrosis in a rat liver fibrosis model.</p><p><strong>Discussion: </strong>These findings identify quercetin as an orally bioavailable small-molecule modulator of macrophage fate and provide preclinical proof-of-concept for targeting JAK2/STAT3 to reverse inflammation-driven fibrosis in chronic liver disease.</p><p><strong>Conclusion: </strong>Que can inhibit hepatic fibrosis by promoting M1 to M2 macrophage polarization, which could be associated with its ability to suppress the JAK2/STAT3 signaling pathway in macrophages.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"31-46"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142368106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Metronomic Chemotherapy in Nasopharyngeal Carcinoma with Radiotherapy Interruptions: A Lesson Learned from the Lockdown Due to COVID-19.","authors":"Yuan Zhou, Rui Zhou, Yi-Feng Yu, Zheng-Jie Huang, San-Gang Wu","doi":"10.2174/0115748928378983250604171225","DOIUrl":"10.2174/0115748928378983250604171225","url":null,"abstract":"<p><strong>Purpose: </strong>Metronomic chemotherapy (MC) represents a therapeutic approach characterized by the long-term administration of chemotherapeutic agents at relatively low doses, with minimal or no drug-free intervals (US20150283237, CN111110681A). This study aimed to evaluate the treatment characteristics, prognosis, and efficacy of S-1 MC as a compensatory strategy for nasopharyngeal carcinoma (NPC) patients who experienced radiotherapy interruption (RI) during the COVID-19 pandemic.</p><p><strong>Methods: </strong>This study included NPC patients who experienced RI due to the COVID-19 pandemic. Patient characteristics, details of treatment after RI, compensatory treatment, and survival outcomes were analyzed.</p><p><strong>Results: </strong>A total of 8 patients were identified, with a median RI duration of 19 days. All patients received an additional fraction of radiotherapy due to the interruption. Following RI, all patients completed the recommended radiotherapy regimen and underwent comprehensive locoregional and systemic assessment three months post-treatment. Complete remission of the nasopharyngeal tumor and cervical lymph nodes was achieved in 7 (87.5%) patients. These patients were administered oral tegafur, gimeracil, and oteracil potassium (S-1) MC. All patients completed one year of MC without experiencing grade 3-4 adverse reactions. With a median follow-up of 34.4 months, no instances of disease recurrence were observed. The 2-year disease-free survival and overall survival were both 100%.</p><p><strong>Conclusion: </strong>MC may serve as an effective compensatory treatment strategy for NPC patients experiencing RI. These findings offer valuable insights for future clinical trials involving NPC patients with RI due to various reasons.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"201-210"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13312380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144319079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"B-9-8, a Novel Harman Dimer, Reverses ABCG2-mediated Chemotherapeutic Drug Resistance.","authors":"Rui-Qiang Zhao, Yan Wen, Chao-Yun Cai, Jing-Quan Wang, Pranav Gupta, Zi-Ning Lei, Dong-Hua Yang, Ri-Hui Cao, Zhe-Sheng Chen","doi":"10.2174/0115748928357067250512112852","DOIUrl":"10.2174/0115748928357067250512112852","url":null,"abstract":"<p><strong>Background: </strong>Multidrug resistance (MDR) in cancer is a major obstacle to achieving success in clinical chemotherapy. It has been observed that overexpression of ATP-Binding Cassette (ABC) transporters plays a crucial role in MDR.</p><p><strong>Objective: </strong>This study aimed to find an effective resistance-reversed agent of ABC transporter. A series of new β-carboline derivatives have been synthesized and are being applied in various invention patents. One of these is B-9-8, a novel harman dimer, which was synthesized to conduct a series of experiments.</p><p><strong>Methods: </strong>In this study, we investigated whether B-9-8 could reverse ABCG2-mediated drug resistance by using MTT assay, [³H]-mitoxantrone accumulation/efflux assay, western blot analysis, immunofluorescence analysis, ATPase assay, and molecular modeling assay.</p><p><strong>Results: </strong>The results showed that B-9-8 could significantly increase the sensitivity to mitoxantrone, SN-38, and topotecan and effectively overcame drug resistance at non-toxic concentrations in ABCG2-overexpressing cells. Further studies showed that B-9-8 increased the intracellular accumulation of [³H]-mitoxantrone by suppressing the efflux function of ABCG2 in ABCG2- overexpressing cells. B-9-8 could down-regulate the ABCG2 protein expression but did not change the subcellular localization of ABCG2. ATPase analysis indicated that B-9-8 inhibited the ATPase activity of ABCG2 in a concentration-dependent manner. In the molecular docking analysis, B-9-8 demonstrated a strong interaction with the human ABCG2 transporter protein.</p><p><strong>Discussion: </strong>B-9-8, as a novel harman dimer, exhibits its reversal activity against ABCG2- mediated multidrug resistance without obvious cytotoxicity. Its actions of inhibiting ABCG2 efflux function and down-regulating the protein expression of ABCG2 are crucial for overcoming drug resistance. This makes B-9-8 a possible candidate drug for combined chemotherapy. Its inhibitory effect of ATPase activity and the strong affinity to ABCG2 further demonstrate the potential of B-9-8 as a targeted modulator for drug resistance.</p><p><strong>Conclusion: </strong>Our findings indicated that B-9-8 could reverse ABCG2-mediated MDR as a potential and reversible modulator in combination with conventional chemotherapeutic drugs.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"173-187"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Covalent Inhibitor Screening for Targeting LOXL2: Studied by Virtual Screening and Experimental Validation.","authors":"Lirui Lin, Kai Lin, Lichun Chen, Yiwen Wang, Li-Yan Xu, En-Min Li, Qingping Liu, Haiying Zou, Geng Dong","doi":"10.2174/0115748928356643241216132041","DOIUrl":"10.2174/0115748928356643241216132041","url":null,"abstract":"<p><strong>Background: </strong>Lysyl oxidase-like 2 (LOXL2) is a metalloenzyme that catalyzes oxidative deamination ε-amino group of lysine. It has been found that LOXL2 is a promotor for the metastasis and invasion in kinds of tumors. Previous studies show that disulfide bonds are important components in LOXL2, and their bioactivity can be regulated by those bonds. In this way, a small molecule covalently binds to the thiol group of cysteine residue could be an effective way to change the function of LOXL2 by blocking the formation of the disulfide bond.</p><p><strong>Objective: </strong>This investigation is aiming to screen covalent inhibitor for LOXL2.</p><p><strong>Methods: </strong>Covalent molecule libraries of Life Chemical and Enamine were used. The structures of those molecules were optimized by using LigPrep module of Schrödinger. Then optimized by using the LigPrep module of Schrödinger to generate optimal conformations. For covalent docking, CovDock in Glide module was used for the virtual screening. Finally, wound-healing assays were performed to examine the effects of the potential inhibitors.</p><p><strong>Results: </strong>Eight potential small molecules were selected by covalent docking from the databases (in total 7,908 candidates). ADMET evaluation indicated that all those eight small molecules satisfy the general standard. Furthermore, wound healing experiments showed that the compound (F50972176) significantly inhibits the migration of cancer cells.</p><p><strong>Discussion: </strong>Through advanced methodologies, namely binding affinity calculations and ADMET prediction, this strategy enables a decrease in time consumption and improves operational efficacy in the rapid screening of LOXL2 covalent inhibitors, which constitutes a crucial research area.</p><p><strong>Conclusion: </strong>Virtual screening and experimental verification methods were used to screen covalent inhibitors of LOXL2 by targeting functional disulfide bonds. The compound (F50972176) effectively inhibited the migration of esophageal squamous cell carcinoma cells.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"87-101"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nano-carriers based Approaches Loaded with Herbal Bioactive Compounds for the Treatment of Cancer: Recent Updates and Future Prospects.","authors":"Ameeduzzafar Zafar, Omar Awad Alsaidan, Md Ali Mujtaba","doi":"10.2174/0115748928377734250731191700","DOIUrl":"10.2174/0115748928377734250731191700","url":null,"abstract":"<p><strong>Introduction: </strong>Traditional cancer therapies like chemotherapy and radiotherapy frequently face challenges, such as systemic toxicity, the development of resistance, and poor tolerance among patients. Recently, there has been a growing interest in herbal bioactive compounds because of their wide-ranging anticancer properties and natural sources. Nonetheless, the clinical use of these compounds is restricted by their low solubility in water, limited bioavailability, and rapid metabolic clearance.</p><p><strong>Methods: </strong>This review comprehensively assesses studies from 2010 to 2023 that investigate nanoformulation strategies aimed at enhancing the delivery of herbal bioactive agents in cancer treatment. The selection of studies was based on their examination of important nanocarrier systems, such as polymeric nanoparticles, liposomes, and lipid-based delivery platforms. The focus was on advancements in pharmacokinetics, drug targeting, and therapeutic outcomes.</p><p><strong>Results: </strong>Research shows that nanoformulated herbal compounds show improved stability, solubility, and controlled release characteristics. Polymeric and lipid-based nanocarriers significantly enhance drug accumulation in tumor tissues, thereby improving antitumor effectiveness and reducing systemic side effects. Numerous studies also demonstrate increased cellular uptake and extended circulation times with nano-encapsulated phytochemicals.</p><p><strong>Discussion: </strong>Nanoformulation technologies have effectively tackled numerous pharmacological challenges linked to herbal therapeutics. However, while laboratory and preclinical outcomes are promising, obstacles like obtaining regulatory approval, scaling up production, and ensuring consistent quality control impede clinical application. Additionally, the variability in plantderived compounds requires standardization to ensure reproducibility and safety.</p><p><strong>Conclusion: </strong>Nanoformulations of herbal bioactive compounds mark a significant advance in cancer treatment, providing enhanced solubility, targeted delivery, and lower toxicity. Despite the progress made, additional research is required to refine these formulations, address manufacturing and regulatory challenges, and incorporate these strategies into personalized cancer therapy models.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"245-272"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How Oncovirus Affects Drug Resistance in Cancer Cells.","authors":"Yuping Yang, Yuwen Wang, Zhengdong Zhou, Junlong Zhuang, Wei Zhao","doi":"10.2174/0115748928324072250317050917","DOIUrl":"10.2174/0115748928324072250317050917","url":null,"abstract":"<p><p>Cancer drug resistance has emerged as a formidable challenge in the field of clinical oncology, significantly hampering the success of treatment strategies and leading to suboptimal outcomes for patients. In a broad array of therapeutic settings, the emergence of resistance has become a primary source of concern, ranging from conventional chemotherapy to modern immunotherapy and targeted therapies. The complexity of cancer drug resistance is further exacerbated by the involvement of oncoviruses, such as human papillomavirus (HPV), Epstein-Barr virus (EBV), and hepatitis B virus (HBV), which play pivotal roles in the initiation, progression, and response to treatment of various cancers. The intricate interactions between these oncoviruses and cancer cells have been found to significantly influence drug efficacy. These viruses can alter critical cellular pathways, including drug metabolism, DNA repair mechanisms, and the tumor microenvironment, thus promoting drug resistance. A profound understanding of these virus-cancer-drug interactions is crucial for the development of novel treatment approaches that can effectively overcome drug resistance. This review aimed to contribute to a broader awareness of the multifaceted nature of cancer drug resistance, particularly in the context of oncovirus involvement. By highlighting the critical role of oncoviruses in cancer development and treatment response, this review hopes to stimulate further research and the development of novel treatment strategies that can effectively overcome drug resistance and ultimately improve patient outcomes. As we advance toward precision oncology, a more holistic understanding of the complex interplay among cancer, its associated viruses, and therapeutic drugs is crucial for achieving optimal therapeutic responses.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"113-125"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dahuang Zhechong Pill Combined with TNS4 Silencing Inhibits the NF-Κb/VEGF Pathway To Slow Down The Progression Of Pancreatic Cancer.","authors":"Dawei Yan, Yayi Jiang, Youpeng Hu, Zhipeng Hu, Haoyue Feng, Rensong Yue","doi":"10.2174/0115748928379439250621171215","DOIUrl":"10.2174/0115748928379439250621171215","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Pancreatic cancer (PC) is a highly aggressive malignancy with limited treatment options and poor prognosis. Dahuang Zhechong Pill, a traditional Chinese medicine, has shown promise in inhibiting inflammation. This study investigates the effects of combining Dahuang Zhechong Pill with TNS4 silencing on PC, focusing on their combined role in suppressing PC progression and exploring potential therapeutic applications. Intellectual property implications related to this combination are also explored.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Bioinformatic analysis was used to identify the key role of TNS4 in PC. CFPAC-1 PC cells were cultured and genetically modified using lentiviral transfection to stably knock down TNS4 expression. Cell proliferation was assessed using the CCK-8 assay, while cell migration and invasion capabilities were evaluated through Transwell assays. Colony formation and flow cytometry were performed to analyze clonogenic potential and cell cycle distribution, respectively. Apoptosis was assessed using tunel staining. Subcutaneous and orthotopic tumor models were established in nude mice to investigate the in vivo effects. Mice were treated with Dahuang Zhechong Pill by oral gavage. Immunohistochemistry and immunofluorescence were employed to detect the expression of key proteins involved in the NF-κB/VEGF pathway, including E-cadherin and Vimentin. ELISA was used to measure circulating IL-17 and amylase levels in mouse serum to test inflammation response.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;TNS4 was upregulated in PC and positively associated with PC progression. TNS4 silencing significantly reduced CFPAC-1 cell proliferation, migration, and invasion in vitro. Flow cytometry demonstrated an increase in G0/G1 phase arrest and apoptosis in the TNS4 silencing group. Subcutaneous models showed the anti-tumor effect of TNS4 silencing. Furthermore, Dahuang Zhechong Pill treatment, when combined with TNS4 knockdown, resulted in a marked decrease in tumor size in orthotopic models. Immunohistochemical analysis revealed reduced expression of NF-κB and VEGF in tumor tissues from the combination treatment group. ELISA results indicated lower levels of serum IL-17, and amylase and higher levels of insulin in combination-treated mice.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;We proposed an innovative therapeutic patent combining traditional Chinese medicine with targeted gene silencing to inhibit PC progression. By investigating the synergistic effects of TNS4 silencing and Dahuang Zhechong Pill in suppressing the NF-κB/VEGF signaling pathway, our findings highlighted a promising strategy that targets tumor proliferation and modulates the inflammatory microenvironment in PC.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Dahuang Zhechong Pill, in combination with TNS4 silencing, effectively inhibits the NF-κB/VEGF pathway and inflammation response, leading to reduced PC progression. These findings suggest a potential therapeutic approach","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"211-223"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144577482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ER Stress-related Gene Prognostic Signature for Predicting Chemosensitivity and Prognosis in AML.","authors":"Jie Guo, Hongwei Peng, Luyao Long, Li Sun, Lin Yang, Simei Ren","doi":"10.2174/0115748928349165250202172440","DOIUrl":"10.2174/0115748928349165250202172440","url":null,"abstract":"<p><strong>Introduction: </strong>Acute myeloid leukemia is characterized by high heterogeneity, and the current European Leukemia Net (ELN) risk stratification system is not universally applicable to all AML patients, requiring approximately three weeks for testing.</p><p><strong>Aim: </strong>This study aimed to develop an applicable prognostic tool capable of addressing the limitations of current methods. We selected AML patients from the clinic and TCGA database to explore the role of ER stress in response to chemotherapy.</p><p><strong>Methods: </strong>Patients from the TCGA database were employed as the training cohort, and two GEO datasets were used as external validation cohorts. Univariate/multivariate COX and LASSO regression were exemplified to establish the prognostic model. Kaplan-Meier and timedependent ROC were used to assess and compare the efficiency of the model with ELN stratification and other models. In the training cohort, we selected 5 ER stress-related genes to predict chemosensitivity and establish the ERS-5 prognostic model.</p><p><strong>Results and discussion: </strong>The model successfully predicted the overall survival of patients (p < 0.0001, HR = 4.86 (2.79-8.44); AUC = 0.83). It was verified in validation cohorts and could further stratify the risk of various AML subgroups. It also enhanced the ability of ELN to predict the response of patients with AML to main chemotherapeutic drugs. Finally, an \"ERS-5\" risk score was constructed by the nomogram based on the ERS-5 model and age.</p><p><strong>Conclusion: </strong>Consequently, in this study, the ERS-5 model was constructed, which allowed more rapid (about 3 hours) and accurate risk stratification and complemented the ability of ELN to assess chemosensitivity.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"62-74"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Therapeutic Potential and Molecular Mechanisms of Daphnetin: A Comprehensive Review.","authors":"Linyue Zhang, Jingwu Wu, Jinzhenwan Xue, Zhihong Jia, Xiaoni Zhou, Gang Hu","doi":"10.2174/0115748928371118250327084127","DOIUrl":"10.2174/0115748928371118250327084127","url":null,"abstract":"<p><p>Coumarins, a ubiquitous class of aromatic compounds present in a broad spectrum of organisms, including bacteria, fungi, and over 150 plant species, have been extensively studied over the years. Researchers have isolated and characterized more than 1,300 natural coumarins, many of which exhibit promising biomedical properties. Among these, daphnetin has emerged as a distinctive coumarin derivative that is characterized by its unique structural features to impart special physicochemical attributes. Daphnetin is renowned for its diverse range of biological activities, encompassing anticancer, anti-inflammatory, and antiallergic effects. These activities can be attributed to its ability to regulate specific molecular pathways within the body, making it a highly attractive compound for pharmacological research. Consequently, daphnetin has garnered considerable attention within the scientific community, specifically prompting an extensive investigation into its therapeutic potential across diverse clinical conditions. In this comprehensive review, we delved into the structure and sources of daphnetin, with a focus on its unique characteristics that underscore its potential as a therapeutic agent. We further explored the therapeutic potential of daphnetin, highlighting its multifaceted biological activities and the underlying molecular mechanisms. In addition, we scrutinized the potentially toxic effects of daphnetin in light of the current research status and prospects in this direction. By emphasizing the clinical significance of daphnetin, we aim to contribute to the ongoing endeavors toward the development of innovative and efficacious therapeutic strategies for an array of diseases.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"309-322"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}