Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie最新文献

{"title":"Targeting acute myeloid leukemia resistance with two novel combinations demonstrate superior efficacy in TP53, HLA-B, MUC4 and FLT3 mutations.","authors":"Elham Gholizadeh, Ehsan Zangene, Alun Parsons, Mika Kontro, Caroline A Heckman, Mohieddin Jafari","doi":"10.1016/j.biopha.2025.118647","DOIUrl":"https://doi.org/10.1016/j.biopha.2025.118647","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a genetically heterogeneous malignancy characterized by the clonal expansion of myeloid precursor cells. Despite the advent of venetoclax-based regimens, resistance mechanisms remain a major clinical challenge, particularly in patients with high-risk mutations such as TP53, MUC4, HLA-B and FLT3. Here, we evaluate two rational combination therapies, LY3009120 (pan-RAF) plus sapanisertib (mTOR) (LS), and ruxolitinib (JAK1/2) plus ulixertinib (ERK) (RU), across ten AML cell lines and a zebrafish embryo xenograft model. The study integrates real-time cell viability assays, xenograft imaging, and genetic analyses and relates responses to mutational profiles and benchmarks against first line treatment (venetoclax based combinations), the current standard for older and unfit AML. Both combinations outperformed or matched venetoclax-based comparators, with LS markedly reducing viability and RU showing robust efficacy in AML cell lines. In zebrafish, LS and RU suppressed leukemic burden with zero mortality and with modest effects on embryo length, indicating supportive but preliminary tolerability under the conditions tested. Mutation response analyses and clustering highlighted TP53, MUC4, HLA-B and FLT3 as correlates of LS and RU sensitivity, supporting mutation-informed prioritization. Collectively, our results nominate LS and RU as promising candidates, particularly in AML with TP53, FLT3, HLA-B or MUC4 alterations, and motivate prospective validation in stratified AML cohorts.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"192 ","pages":"118647"},"PeriodicalIF":7.5,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294563","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":"Bee venom in pharmacology: Mechanistic insights from pro-inflammatory trigger to anti-inflammatory therapeutic agent.","authors":"Sriwidodo Sriwidodo, Cecep Suhandi, Gofarana Wilar, Nasrul Wathoni","doi":"10.1016/j.biopha.2025.118636","DOIUrl":"https://doi.org/10.1016/j.biopha.2025.118636","url":null,"abstract":"<p><p>Bee venom (BV) is inherently toxic, traditionally recognized for provoking pain, edema, and hypersensitivity via components such as melittin and bee venom-derived phospholipase A₂ (bvPLA₂). Paradoxically, these same peptides exhibit potent anti-inflammatory and immunomodulatory activities when administered in carefully controlled doses or optimized formulations. Preclinical studies, as summarized across multiple disease models, consistently demonstrate suppression of pro-inflammatory cytokines, inhibition of NF-κB signaling, modulation of T-cell and macrophage responses, and enhancement of antioxidant defenses. Early clinical evidence further suggests potential benefits in rheumatoid arthritis, multiple sclerosis, and inflammatory skin disorders. Nonetheless, BV's allergenic and cytotoxic properties highlight the urgent need for standardized preparations and advanced delivery strategies, such as nanocarriers and microneedle systems, to improve stability, safety, and therapeutic precision. Together, these findings underscore the dual-edged nature of BV, positioning it not merely as a pro-inflammatory toxin but as a candidate anti-inflammatory and immunomodulatory therapy with translational potential.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"192 ","pages":"118636"},"PeriodicalIF":7.5,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294733","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":"Effects of JNJ-46356479 and clozapine on VGLUT1 and GAD65/67 brain levels and expression of genes related to glutamate and GABA in mice postnatally exposed to ketamine.","authors":"Albert Martínez-Pinteño, David Olivares-Berjaga, Natalia Rodríguez, Juan-Ignacio Mena, Lucia Prohens, Sergi Mas, Constanza Morén, Eduard Parellada, Patricia Gassó","doi":"10.1016/j.biopha.2025.118639","DOIUrl":"https://doi.org/10.1016/j.biopha.2025.118639","url":null,"abstract":"<p><p>Schizophrenia (SZ) is a complex mental disorder influenced by genetic, environmental, and neurobiological factors, with current treatments ineffective for negative symptoms and cognitive deficits. The glutamatergic hypothesis of SZ highlights the N-methyl-D-aspartic acid (NMDA) receptor dysfunction as a key factor, causing excitatory-inhibitory imbalance and synaptic inefficiency. Positive allosteric modulators (PAMs) of the metabotropic glutamate receptor 2 (mGluR2), such as JNJ-46356479 (JNJ), could be useful in treating these symptoms, especially when used in early stages of the disease. Previous results have shown that JNJ can reverse certain SZ-related behavioral and neuropathological deficits. This study evaluates, for the first time, the effects of early treatment with JNJ or clozapine (CLZ) in reversing molecular deficits related to glutamatergic and GABAergic pathways in mice postnataly exposed to ketamine (KET) on postnatal days (PND) 7, 9, and 11. Animals received JNJ or CLZ daily in the adolescent period (PND 35-60). Specifically, we investigated alterations in brain protein levels of VGLUT1, as a marker of glutamatergic synapses, and GAD65/67, as markers of GABAergic synapses. Changes in brain expression of 240 selected genes involved in glutamate and GABA pathways were also evaluated. Results demonstrated that postnatal KET exposure increased hippocampal VGLUT1 levels which were partially normalized after both pharmacological treatments, especially with JNJ. Additionally, we identified some genes that showed altered brain expression after drug treatment in our mouse model. In conclusion, this study provides evidence of SZ-related glutamate signaling alterations in adult mice postnatally exposed to KET, as well as of the effectiveness of JNJ in improving these alterations when administered during the early stages of the disease.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"192 ","pages":"118639"},"PeriodicalIF":7.5,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145282164","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":"Corrigendum to \"Total flavonoids of rhizoma drynariae ameliorates bone formation and mineralization in BMP-Smad signaling pathway induced large tibial defect rats\" [Biomed. Pharmacother., vol. 138 (2021) 111480].","authors":"Weipeng Sun, Minying Li, Yan Zhang, Yingjie Huang, Qunzhang Zhan, Yueyi Ren, Hang Dong, Jiena Chen, Zige Li, Chun Fan, Feng Huang, Zhen Shen, Ziwei Jiang","doi":"10.1016/j.biopha.2025.118580","DOIUrl":"https://doi.org/10.1016/j.biopha.2025.118580","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"118580"},"PeriodicalIF":7.5,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276926","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":"Corrigendum to \"A new peptide originated from amphibian skin alleviates the ultraviolet B-induced skin photodamage\" [Biomed. Pharma., 150 (2022) 112987].","authors":"Siyu Wang, Meifeng Yang, Saige Yin, Yingxuan Zhang, Yue Zhang, Huiling Sun, Longjun Shu, Yixiang Liu, Zijian Kang, Naixin Liu, Jiayi Li, Ying Wang, Li He, Mingying Luo, Xinwang Yang","doi":"10.1016/j.biopha.2025.118646","DOIUrl":"https://doi.org/10.1016/j.biopha.2025.118646","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"118646"},"PeriodicalIF":7.5,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276979","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":"Corrigendum to \"Exosomes in Alzheimer's disease: From pathogenesis to therapeutics - A comprehensive review of diagnostic and drug delivery applications\" [Biomed. Pharmacother. 192 (2025) 118548].","authors":"Mona Shahlaei, Hamed Afkhami, Amirhossein Ahmadieh-Yazdi, Seyed Hashem Mirmazloumi, Seyedeh Saeideh Sahraei, Mohammad Akbari, Piao Yang, Hamed Manoochehri, Hamid Tanzadehpanah, Hanie Mahaki, Aravind Sundararaman, Sreedivya Mohan, Mohsen Sheykhhasan, Sharafaldin Al-Musawi, Paola Dama","doi":"10.1016/j.biopha.2025.118632","DOIUrl":"https://doi.org/10.1016/j.biopha.2025.118632","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"118632"},"PeriodicalIF":7.5,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260025","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":"Expression of concern \"Ex vivo, in vitro, and in silico approaches to unveil the mechanisms underlying vasorelaxation effect of Mentha Longifolia (L.) in porcine coronary artery\" [Biomed. Pharmacother. 153 (2022) 113298].","authors":"","doi":"10.1016/j.biopha.2025.118484","DOIUrl":"https://doi.org/10.1016/j.biopha.2025.118484","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"191 ","pages":"118484"},"PeriodicalIF":7.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145133075","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":"Retraction notice to \"CircPIP5K1A activates KRT80 and PI3K/AKT pathway to promote gastric cancer development through sponging miR-671-5p\" [Biomed. Pharmacother. 126 (2020) 109941].","authors":"Hu Song, Yixin Xu, Teng Xu, Ruizhi Fan, Tao Jiang, Meng Cao, Linseng Shi, Jun Song","doi":"10.1016/j.biopha.2025.118382","DOIUrl":"10.1016/j.biopha.2025.118382","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"118382"},"PeriodicalIF":7.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862698","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":"Corrigendum to \"Liraglutide, a glucagon-like peptide-1 receptor agonist, suppresses osteoclastogenesis through the inhibition of NF-κB and MAPK pathways via GLP-1R\" [Biomed. Pharmacother. 130 (2020) 110523].","authors":"Ziyi Li, Shilun Li, Na Wang, Peng Xue, Yukun Li","doi":"10.1016/j.biopha.2025.118545","DOIUrl":"10.1016/j.biopha.2025.118545","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"118545"},"PeriodicalIF":7.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042797","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":"Retraction notice to \"LncRNA LINC00689 promotes the growth, metastasis and glycolysis of glioma cells by targeting miR-338-3p/PKM2 axis\" [Biomed. Pharmacother. 117 (2019) 109069].","authors":"Xin Liu, Qiaojuan Zhu, Yang Guo, Zunqiang Xiao, Linjun Hu, Qiuran Xu","doi":"10.1016/j.biopha.2025.118547","DOIUrl":"10.1016/j.biopha.2025.118547","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"118547"},"PeriodicalIF":7.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145082674","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}