Biochemical pharmacology最新文献

{"title":"Implication of Let7b/AhR/ARNT/HMGB1/RAGE cascade in neuroplasticity disturbances induced by glucocorticoids and the promising reversible effect of 3,3 diindolymethane: Bidirectional crosstalk of Aryl hydrocarbon receptors","authors":"Mai A. Abd-Elmawla ,&nbsp;Asmaa A. ElMonier ,&nbsp;Enas S. Gad ,&nbsp;Haneen Y. Khidr ,&nbsp;May A. Azzam","doi":"10.1016/j.bcp.2024.116692","DOIUrl":"10.1016/j.bcp.2024.116692","url":null,"abstract":"<div><div>Prolonged exposure to glucocorticoids (GC) disrupts neuronal architecture, hinders neuroplasticity, and triggers neuroinflammation. However, the precise underlying mechanisms have not been studied yet. The current study aimed to investigate the mechanisms of GC-induced neuroinflammatory effects by stimulating the miRNA let7b, aryl hydrocarbon receptor (AhR)/ARNT, HMGB1/RAGE, and other downstream targets. Rats were divided into 4 groups; control, GC (20 mg/kg, S.C.), 3,3′-diindolylmethane (DIM) 50 mg/kg/day, and donepezil (DNZ) 4 mg/kg/day for 21 days. Behavioral tests and histopathological investigations of cerebral cortex were done. Let7b, AhR, ARNT, and cytochrome A1A were estimated using qRT-PCR. HMGB1, RAGE, NQO1and NRF2 were estimated using ELISA, whereas GFAP and TNF-α by immunohistochemical analysis. Keap1 was estimated using Western technique. GSH and TBARS were assessed by colorimetric assay. In the current study, GC elevates the gene expressions of let7b, AhR, ARNT, and cytochrome A1A, along with the protein contents of HMGB1, RAGE, NQO1and NRF2. In addition, GC showed increased GFAP, TNF-α, and TBARS, together with decreased Keap1 and GSH. On the other side, DIM and DNZ reversed all the above-mentioned findings. Collectively, the study documents for the first time the effect of GC in upregulating let7b and activating the AhR/ARNT loop which subsequently stimulates RAGE/HMGB1 and NRF2/Keap1 cascade leading to stimulating further inflammatory and oxidative signaling pathways. Certainly, these effects are responsible for the behavioral fluctuations, the brain’s histological disruption, altered neuroplasticity, and neuroinflammation induced by GC. Moreover, DIM conquers GC-induced neuroinflammation due to its characteristic role in modulating AhR and its downstream targets.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116692"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142783690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT-2 inhibition by AK-7 orchestrates fibrotic cascades in airways through neuroimmune interaction via TRPA1, TRPM8 and TGF-β signalling","authors":"Vandana Yadav ,&nbsp;Vinita Pandey ,&nbsp;Pratikkumar Gaglani ,&nbsp;Atul Srivastava ,&nbsp;Soni ,&nbsp;Subhashini","doi":"10.1016/j.bcp.2024.116689","DOIUrl":"10.1016/j.bcp.2024.116689","url":null,"abstract":"<div><div>Chronic obstructive pulmonary diseases (COPD) is characterized by airflow limitation, chronic inflammation and airway remodeling (AR) in airways and lung parenchyma. AR, a lung response, involves mucus production, airflow issues, and structural changes. It is exacerbated by neurogenic inflammation from activated sensory nerves, highlighting the interplay between neuronal and immune regulation in COPD. Sirtuins play a crucial role in lung remodeling, with SIRT-2 being the least studied. Present study explores how SIRT-2 regulates neurogenic inflammation and fibrosis in experimental BALB/c mice with cigarette smoke-induced COPD. Mice from each group, except the control, were exposed to CS for 60 days and AK-7 (100ug/kg and 200ug/kg) was administered intranasally. The study evaluated lung injury and inflammation marked by increased Cortisol, ACTH, COX-2 and LDH in COPD group with its attenuation by SIRT-2 inhibition. Additionally, CS exposure exhibited neurogenic inflammation represented by activated TPRV1 and TRPM8, elevated neuromediators levels (dopamine, acetylcholine, substance P, serotonin) and their respective receptors which were mitigated by AK-7. CS exposure enhanced fibrosis by targeting the fibrotic cascade, enhancing MMP-9, total collagen, hydroxyproline, and upregulating αSMA, MUC5AC, TGF-β, PKA, GATA-3, FOXO3, and STAT-6. SIRT-2 inhibition effectively reversed all these factors suppressing fibrosis further supported by downregulated SIRT-2 expression and histopathological studies where collagen deposition and mucus production were also attenuated by AK-7. Molecular docking revealed strong binding affinity of certain protein such as COX-2, D5DR and 5HT with AK-7. Overall, targeting SIRT-2 to modulate neuro-immune interplay presents a promising therapeutic approach for addressing AR in COPD.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116689"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel-designed antimicrobial peptides with dual antimicrobial and anti-inflammatory actions against Cutibacterium acnes for acne vulgaris therapy","authors":"Hyun Kim ,&nbsp;Ju Hye Jang ,&nbsp;Ha Rang Kim ,&nbsp;Ju Hyun Cho","doi":"10.1016/j.bcp.2024.116708","DOIUrl":"10.1016/j.bcp.2024.116708","url":null,"abstract":"<div><div>Acne vulgaris is a prevalent skin condition among adolescents, primarily instigated by over-colonization and subsequent inflammation triggered by <em>Cutibacterium acnes</em>. Although topical and oral antibiotics are standard treatments, they often lead to the proliferation of antibiotic-resistant bacteria and are associated with undesirable side effects. Antimicrobial peptides (AMPs) are considered a promising solution to these challenges. In this study, we aimed to develop novel short AMPs to combat <em>C. acnes</em>. By comparing sequences and abstracting the distribution of residue types of established AMPs, we derived a sequence template. Using this template, we crafted novel anti-<em>C. acnes</em> peptides comprising 13 amino acid residues. To enhance their potential therapeutic application, we designed a series of peptides by varying the number and position of the tryptophan residues. Among these peptides, DAP-7 and DAP-10 demonstrated potent antimicrobial activity against both antibiotic-susceptible and -resistant strains of <em>C. acnes</em>, with minimal cytotoxicity. The antimicrobial action of these peptides was attributed to their ability to target the bacterial membrane, resulting in permeabilization and rupture. Moreover, DAP-7 and DAP-10 effectively reduced the expression of pro-inflammatory cytokines induced by <em>C. acnes</em> and remained stable for up to 12 h after exposure to proteases found in acne lesions. Notably, DAP-7 decreased the <em>C. acnes</em> colonies on the ears and significantly alleviated <em>C. acnes</em>-induced ear swelling in a mouse model. Our findings suggest that the DAP-7 and DAP-10 peptides hold promise as candidates for developing a new acne vulgaris treatment.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116708"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep deprivation alters hepatic UGT1A9 and propofol metabolism in mice","authors":"Zhiqian Yan ,&nbsp;Linna Ha ,&nbsp;Hui Chen ,&nbsp;YiFei Xiao ,&nbsp;Min Chen ,&nbsp;Baojian Wu ,&nbsp;Haiman Xu ,&nbsp;Dong Dong","doi":"10.1016/j.bcp.2024.116713","DOIUrl":"10.1016/j.bcp.2024.116713","url":null,"abstract":"<div><div>Sleep deprivation (SD) causes circadian misalignment, and circadian clock disruption is associated with metabolic diseases such as obesity, insulin resistance, and diabetes. However, the underlying mechanism for SD-induced circadian clock disruption as well as metabolic enzyme changes is still lacking. Here, we developed SD sensitizes mice with disrupted circadian rhythms to demonstrate the regulation role and mechanism of SD in UDP-glucuronosyltransferases (UGTs) expression and the metabolism of corresponding substrates. We found that UGT Family 1 Member A9 (UGT1A9) expression was significantly decreased in the liver of SD mice, which led to an elevation exposure and prolonged anesthesia effect of propofol, which was attributed to the decreased metabolism. Meanwhile, SD down-regulated basic helix-loop-helix ARNT like 1 (BMAL1) and its target clock genes period circadian clock (<em>Per</em>), cryptochrome circadian regulator (<em>Cry</em>), and nuclear receptor subfamily 1 group D member 1 (<em>Rev-erb</em>) expression in mice. Furthermore, the positive regulation of UGTIA9 mRNA and protein levels by <em>Bmal1</em> was confirmed in hepatocyte-specific <em>Bmal1</em>-knockout mice (<em>Bmal1</em>-hkO) and <em>Bmal1</em>-overexpressed AML-12 cells. At last, through a combination of promoter analysis, luciferase reporter assay, and chromatin immunoprecipitation (ChIP) assay, it was conducted that <em>Bmal1</em> regulates <em>Ugtla9</em> expression by directly binding the −864 bp E-box in <em>Ugtla9</em> promotor or indirectly acting on the <em>Rev-erbα</em>- differentiated embryo chondrocyte 2 (<em>Dec2</em>) axis. In conclusion, our findings suggested that SD can lead to altered drug disposition and effects in <em>vivo</em>, and <em>Bmal1</em> plays a crucial role in the crosstalk between SD-induced circadian clock disruption and drug metabolism. It initiates a new direction for the understanding of drug efficacy and toxicity changes in SD conditions and provides a scientific basis for improving the rationality of drug use.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116713"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic data integration and analysis revealing potential mechanisms of doxorubicin resistance in chondrosarcoma cells","authors":"Jui-Chieh Chen ,&nbsp;Ming-Shan Chen ,&nbsp;Shin-Kuang Jiang ,&nbsp;Chi-Yang Eaw ,&nbsp;Yu-Jiao Han ,&nbsp;Chih-Hsin Tang","doi":"10.1016/j.bcp.2024.116733","DOIUrl":"10.1016/j.bcp.2024.116733","url":null,"abstract":"<div><div>Chondrosarcoma is a type of bone cancer that originates from cartilage cells. In clinical practice, surgical resection is the primary treatment for chondrosarcoma, but chemotherapy becomes essential for patients with metastasis or tumors in surgically inaccessible sites. However, drug resistance often leads to treatment failure. Tumor microenvironment proteins modulate intercellular communication, contributing to drug resistance. Doxorubicin (Dox) is a common chemotherapeutic agent.</div><div>The present study aimed to establish Dox-resistant chondrosarcoma cells and compare their secretome with parental cells using antibody arrays. Results showed significantly heightened secretion of hepatocyte growth factor (HGF). Knockdown of both HGF and its receptor MET increased Dox sensitivity in chondrosarcoma cells. Treatment of chondrosarcoma cells with conditioned media (CM) from cells secreting high levels of HGF resulted in MET activation. Additionally, the expression levels of HGF and MET were significantly elevated in chondrosarcoma tissues compared to normal cartilage tissues, as confirmed by analysis of GEO database. RNA sequencing and Gene Set Enrichment Analysis (GSEA) elucidated the mechanism involving HGF. Additionally, genes with log fold change &gt; 1 underwent bioinformatics analysis using the ShinyGO web server. The results from both GSEA and ShinyGO analyses corroborate each other, indicating the significance of HGF in cellular signal transduction, regulation of cell motility, developmental processes, immune-inflammatory responses, and functions related to blood and neural systems.</div><div>In summary, highly secreted HGF can activate signaling pathways through its receptor MET, particularly Ras and Akt activation, enhancing drug resistance in chondrosarcoma cells. The present study may guide the development of novel therapeutic strategies targeting HGF, ultimately improving treatment outcomes and prognosis for malignant chondrosarcoma patients.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116733"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements in understanding the role and mechanism of sirtuin family (SIRT1-7) in breast cancer management","authors":"Deepak Sharma ,&nbsp;Muthukumaran Panchaksaram ,&nbsp;Rajiniraja Muniyan","doi":"10.1016/j.bcp.2025.116743","DOIUrl":"10.1016/j.bcp.2025.116743","url":null,"abstract":"<div><div>Breast cancer (BC) is the most prevalent type of cancer in women worldwide and it is classified into a few distinct molecular subtypes based on the expression of growth factor and hormone receptors. Though significant progress has been achieved in the search for novel medications through traditional and advanced approaches, still we need more efficacious and reliable treatment options to treat different types and stages of BC. Sirtuins (SIRT1-7) a class III histone deacetylase play a major role in combating various cancers including BC. Studies reveal that<!--> <!-->each sirtuin has a unique and well-balanced biology, indicating that it regulates a variety of biological processes that result in the initiation, progression,<!--> <!-->and metastasis of BC. SIRT also plays a major role in numerous vital biological functions, including apoptosis, axonal protection, transcriptional silencing, DNA recombination and repair, fat mobilization, and aging. As per the current demand, we wish to outline the structural insights into sirtuin’s catalytic site, substantial variations among all SIRT types, and their mechanism in BC management. Additionally, this review will focus on the application of SIRT modulators along with their clinical significance, hurdles, and future perspective to develop successful SIRT-based drug candidates to conquer the BC problem.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116743"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142962138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanoengineered immune check point inhibitors delivery for targeted brain cancer treatment: Current status and future perspectives","authors":"Juan Liu ,&nbsp;Yichao Wang ,&nbsp;Zhidu Song ,&nbsp;Yukai Zhang","doi":"10.1016/j.bcp.2025.116789","DOIUrl":"10.1016/j.bcp.2025.116789","url":null,"abstract":"<div><div>Brain tumors create special difficulties because of their position and the protective covering of blood brain barrier (BBB) that restricts efficient medication access. Treatment alternatives such as surgery and chemotherapy demonstrate poor performance against severe brain tumors. The use of immune checkpoint inhibitors (ICIs) hints at effective cancer therapy; however, their application to brain cancer faces challenges due to inefficient delivery through the BBB and the tumor’s suppressive environment. Nanoengineering can increase the transport of ICIs to brain tumors. Numerous nano-delivery systems such as liposomes and micelles have explored ways to avoid the BBB via transcytosis and the EPR mechanism. Functionalization of nanocarriers enhances targeting tumor cells and improves treatment accuracy. New developments involve delivering ICIs together with adjuvants to change the TME and focusing on immune cells such as TAMs and Tregs to boost immunity against tumors. Nanoengineered ICIs have shown effective improvement in animal models by reducing toxicity and enhancing efficacy. Converting these successes into real clinical trials is not easy as they face regulatory concerns and safety challenges. Clinical trials currently examine the use of nanocarriers for treating brain cancer; however, scalability’ and ’long-term safety’ continue to pose challenges. Future approaches will focus on combining customized medicine with advanced nanotechnology and AI to refine treatment methods. Despite obstacles ahead, nanotechnology-based ICIs offer a hopeful approach to enhance brain cancer efficacy and address existing therapeutic constraints.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"233 ","pages":"Article 116789"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143121963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gambogic acid induces GSDME dependent pyroptotic signaling pathway via ROS/P53/Mitochondria/Caspase-3 in ovarian cancer cells","authors":"Danya Zhang ,&nbsp;Yuxin Chen ,&nbsp;Yue Sun ,&nbsp;Hanjie Xu ,&nbsp;Rui Wei ,&nbsp;Ying Zhou ,&nbsp;Fei Li ,&nbsp;Jie Li ,&nbsp;Jing Wang ,&nbsp;Pingbo Chen ,&nbsp;Ling Xi","doi":"10.1016/j.bcp.2024.116695","DOIUrl":"10.1016/j.bcp.2024.116695","url":null,"abstract":"<div><div>Gambogic acid (GA) is a naturally active compound extracted from the Garcinia hanburyi with various anticancer activities. However, whether GA induces pyroptosis (a newly discovered inflammation-mediated programmed cell death mechanism) in ovarian cancer (OC) has not yet been reported. This study revealed that GA treatment reduced cell viability by inducing pyroptosis in OC cell lines. Typical pyroptosis morphological manifestations such as cell swelling with large bubbles and loss of cell membrane integrity, were observed. Cleaved caspase-3 and GSDME-N levels increased after GA treatment, and knocking out GSDME or using a caspase-3 inhibitor could switch GA-induced cell death from pyroptosis to apoptosis, indicating GA induced caspase-3/GSDME-dependent pyroptosis. Furthermore, this research indicated that GA significantly increased reactive oxygen species (ROS) and p53 phosphorylation. OC cells pretreated with ROS inhibitor N-Acetylcysteine (NAC) and the specific p53 inhibitor pifithrin-μ could completely reverse the pyroptosis post-treatment. Elevated p53 and phosphorylated p53 reduced mitochondrial membrane potential (MMP) and Bcl-2, increase the expression of Bax, and damage mitochondria by releasing cytochrome <em>c</em> to activate the downstream pyroptosis pathway. Different doses of GA inhibited tumor growth in ID8 tumor-bearing mice, and high-dose GA increased in tumor-infiltrating lymphocytes CD3, CD4, and CD8 were detected in tumor tissues. Notably, the expressions of GSDME-N, cleaved caspase-3 and other proteins were increased in tumor tissues with high-dose GA groups. These findings demonstrate that GA-treated OC cells could induce GSDME-mediated pyroptosis through the ROS/p53/mitochondria signaling pathway and caspase-3/-9 activation. Thus, GA is a promising therapeutic agent for OC treatment.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116695"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142790960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peptide-based CAR-NK cells: A novel strategy for the treatment of solid tumors","authors":"Qianqian Wang ,&nbsp;Xin Yuan ,&nbsp;Cuijuan Liu ,&nbsp;Ying Huang ,&nbsp;Lin Li ,&nbsp;Yimin Zhu","doi":"10.1016/j.bcp.2025.116741","DOIUrl":"10.1016/j.bcp.2025.116741","url":null,"abstract":"<div><div>CAR-T cell therapy has been proven to be effective on hematological tumors, although graft-versus-host disease and cytokine release syndrome(CRS) limit its application to a certain extent. However, CAR-T therapy for solid tumors met challenges, among which the lack of tumor-specific antigens (TSA) and immunosuppressive tumor microenvironment (TME) are the most important factors. CAR-NK could be a good alternative to CAR-T in some ways since they can induce mild CRS and are independent of HLA-matching, but the efficacy of CAR-NKs remains limited in solid tumors. CAR cells armed with multiple tumor targeting molecules may obtain higher therapeutic efficacy against solid tumors. Due to large molecular weight, multivalent scFvs cannot be displayed efficiently on T cells and the high affinity of scFv to the target makes it easy to cause on-target, off-tumor(OTOT) toxicity. Peptides with low molecular weight and slightly lower affinity than scFvs allow immune cells to display multiple peptides to increase killing ability and reduce OTOT toxicity. In our study, peptide-based CAR-NK cells were designed to solve the dilemma of CAR-T in solid tumors. Firstly, the peptide-based CAR-NK92MI cells with A1 peptide were constructed and their inhibitory effects on the growth of A549 tumor cells were identified. Secondly, the tri-specific CAR-NK92MI cells with peptides that simultaneously targeted PD-L1, EGFR and VEGFR2 were developed for the combinatory therapy. Tri-specific CAR-NK92MI exhibited comparable killing activities to scFv-based CAR-NK92MI. Moreover, peptide-based CAR NK92MI mitigated OTOT toxicity. Our study implied that peptide-based CAR-NKs could behave as promising tools in solid tumor.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116741"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142962163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “Activating transcriptional coactivator with PDZ-binding motif by (R)-PFI-2 attenuates osteoclastogenesis and prevents ovariectomized-induced osteoporosis” [Biochem. Pharmacol. 219 (2024) 115964]","authors":"Rongjian Xu ,&nbsp;Xuewen Liu ,&nbsp;Yufeng Zhang ,&nbsp;Kelei Wang ,&nbsp;Zhuolin Chen ,&nbsp;Jiewen Zheng ,&nbsp;Tan Zhang ,&nbsp;Peijian Tong ,&nbsp;Yu Qian ,&nbsp;Wanlei Yang","doi":"10.1016/j.bcp.2024.116687","DOIUrl":"10.1016/j.bcp.2024.116687","url":null,"abstract":"","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"Article 116687"},"PeriodicalIF":5.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142783895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}