British Journal of Pharmacology最新文献

{"title":"Characterisation of the novel quinoline RCD405: Relaxant effects on cholinergic and histaminergic tone in human bronchi and small airways.","authors":"Paola Rogliani, Clive Page, Francesco Facciolo, Mia Lundblad, Luigino Calzetta","doi":"10.1111/bph.70073","DOIUrl":"https://doi.org/10.1111/bph.70073","url":null,"abstract":"<p><strong>Background and purpose: </strong>Increased contractility of human airway smooth muscle (hASM) is a hallmark of asthma and chronic obstructive pulmonary disease (COPD). Developing new classes of bronchodilators has proved to be challenging because of efficacy and safety concerns. Quinolines hold potential therapeutic applications for the treatment of respiratory disorders.</p><p><strong>Experimental approach: </strong>Relaxant effects of the novel quinoline RCD405 were investigated on contractile responses of hASM to carbachol, histamine and electrical field stimulation (EFS). The role of the non-adrenergic non-cholinergic (NANC) system was assessed using the inducible NO synthase inhibitor aminoguanidine and the TRPV1 agonist capsaicin.</p><p><strong>Key results: </strong>In medium bronchi, RCD405 elicited a maximum relaxant effect (E_max) of 92 ± 4% with a half-maximal effective concentration (EC₅₀) of 45.71 μM for carbachol, and an E_max of 96 ± 1% with a EC₅₀ of 12 μM for histamine. In small airways, RCD405 demonstrated significant relaxant responses, with an E_max of 54 ± 7% (EC₅₀ 17 μM) for carbachol and 90 ± 6% (EC₅₀ 20 μM) for histamine. RCD405 reduced contractility in response to EFS, with E_max values of 63 ± 10% at 25 Hz and 79 ± 9% at 50 Hz in medium bronchi. The NANC system did not affect the bronchorelaxation induced by RCD405.</p><p><strong>Conclusions and implications: </strong>RCD405 showed significant potential as a novel bronchodilator drug for the treatment of asthma and COPD through its ability to induce relaxation of hASM. These findings suggest that further investigation of RCD405 is warranted as a possible novel treatment of chronic respiratory disorders.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101597","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":"Reporting innovations in pharmacology and drug development, upholding excellence and improving author experience at the British Journal of Pharmacology in 2024.","authors":"Andreas Papapetropoulos, Evan E Santo, Stephen P H Alexander, Miriam M Cortese-Krott, Zsuzsanna Helyes, Kirill A Martemyanov, Claudio Mauro, Reynold A Panettieri, Hemal H Patel, Rainer Schulz, Barbara Stefanska, Gary J Stephens, Nathalie Vergnolle, Xin Wang, Stephen Ward, Péter Ferdinandy","doi":"10.1111/bph.70083","DOIUrl":"https://doi.org/10.1111/bph.70083","url":null,"abstract":"","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092595","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":"Matrix metalloproteinase inhibition protects against junctophilin-2 proteolysis during doxorubicin-induced cardiotoxicity.","authors":"Wesam Bassiouni, Brandon Y H Chan, Andrej Roczkowsky, Joshua W Kranrod, Zabed Mahmud, Joseph O Primeau, Woo Jung Cho, Howard S Young, John M Seubert, Richard Schulz","doi":"10.1111/bph.70047","DOIUrl":"https://doi.org/10.1111/bph.70047","url":null,"abstract":"<p><strong>Background and purpose: </strong>Treatment of cancer patients with anthracyclines is known to cause dose-dependent cardiotoxicity through several mechanisms including enhanced oxidative stress, ultimately resulting in defective excitation-contraction coupling. Loss of junctophilin-2 (JPH-2), which tethers transverse tubules (T-tubules) to the sarcoplasmic reticulum, is a feature of doxorubicin-induced cardiotoxicity, yet the protease involved in unclear. As activation of matrix metalloproteinase-2 (MMP-2) is known to contribute to doxorubicin-induced cardiotoxicity, we investigated here the role of MMP-2 in JPH-2 proteolysis and defective calcium transients in it.</p><p><strong>Experimental approach: </strong>C57BL/6J mice were treated with doxorubicin for 4 weeks with or without the MMP inhibitor (doxycycline), MMP-2 preferring inhibitor (ONO-4817) or vehicle, and cardiac function was assessed using echocardiography. JPH-2 levels in ventricular extracts were measured. Calcium transients and JPH-2 levels were measured in neonatal rat ventricular cardiomyocytes treated with doxorubicin and ONO-4817.</p><p><strong>Key results: </strong>Both MMP inhibitors attenuated doxorubicin-induced cardiac systolic and diastolic dysfunction. Doxorubicin treatment resulted in JPH-2 cleavage in mouse hearts as evidenced by the appearance of lower molecular weight products of 63 and 25 kDa, which was prevented by MMP inhibitors. Loss of JPH-2 and impaired calcium transients were observed in neonatal rat ventricular cardiomyocytes treated with doxorubicin, while ONO-4817 attenuated these changes. In silico analysis predicted cleavage sites between JPH-2 MORN repeats and within its unstructured region.</p><p><strong>Conclusions and implications: </strong>These results reveal that JPH-2 proteolysis is a consequence of MMP-2 activation and highlight the beneficial prophylactic action of two orally available MMP inhibitors in preventing doxorubicin-induced cardiotoxicity.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075658","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":"Correction to \"Ethosuximide: Subunit- and Gβγ-dependent blocker and reporter of allosteric changes in GIRK channels\".","authors":"","doi":"10.1111/bph.70074","DOIUrl":"https://doi.org/10.1111/bph.70074","url":null,"abstract":"","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144074995","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":"A novel synthesised STAT3 inhibitor exerts potent anti-tumour activity by inducing lysosome-dependent cell death.","authors":"Marvin Xuejun Xu, Xinxin Liu, Hai-Liang Zhang, Hongyun Xu, Xiangyu Ma, Yupo Yang, Chaoqun Duan, Shanshun Tang, Yaqing Liu, Cen Li, Mengfu Pei, Junkai Xia, Yali Yang, Yanmin Guo, Yang Wang, Songping Luo, Jianguo Ma, Zhengyan Yang, Xiao-Feng Zhu, Chun-Ping Xu","doi":"10.1111/bph.70071","DOIUrl":"https://doi.org/10.1111/bph.70071","url":null,"abstract":"<p><strong>Background and purpose: </strong>Signal transducer and activator of transcription 3 (STAT3) has emerged as a promising therapeutic target for triple-negative breast cancer (TNBC) and multiple myeloma (MM), yet no STAT3-selective drugs have been approved for clinical use.</p><p><strong>Experimental approach: </strong>Newly synthesized compounds were screened by docking, surface plasmon resonance (SPR) and cellular thermal shift assay (CETSA) to measure the binding activity with STAT3. RNA-Seq, luciferase assays, western blot and immunofluorescence assays were conducted to detect the impact of RDp002 on STAT3 signalling. CCK-8, cell cycle, apoptosis assays and transwell were utilised to evaluate the anti-tumour activity of RDp002 in vitro. Xenograft models were used to assess the effectiveness of RDp002 in vivo. Various inhibitors were utilised to investigate how RDp002 causes tumour cell death. The human ether-à-go-go-related gene (hERG/K_v11.1) assays, blood biochemistry and acute toxicity experiments were conducted to explore the toxicity of RDp002.</p><p><strong>Key results: </strong>RDp002 exhibited had strong affinity for STAT3 and impaired the phosphorylation of STAT3 at tyrosine 705 and serine 727 residues. RDp002 suppressed the proliferation, survival, migration, growth and metastasis of TNBC and MM cells. RDp002 inhibited tumour cell viability primarily via lysosome-dependent cell death, which can be weakened by overexpression of STAT3. The toxicity of RDp002 in vivo was minimal based on results from hERG assays, blood biochemistry analysis and acute toxicity tests.</p><p><strong>Conclusion and implications: </strong>RDp002 is a novel STAT3 inhibitor that exerts potent anti-tumour effects mainly by inducing lysosome-dependent cell death. RDp002 represents a promising therapeutic lead for TNBC and MM.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966993","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":"PPARγ is a potential therapeutic target for radiation enteritis via suppressing ferroptosis, mediated by the GAPDH/glycosylation axis.","authors":"Xi Zeng, Liefeng Zhang, Hong Lu, Xinru Xue, Ling Yang, Xiuling Yang, Zhuohui Liu, Xiaoying Cao, Yue Dai, Zhifeng Wei","doi":"10.1111/bph.70045","DOIUrl":"https://doi.org/10.1111/bph.70045","url":null,"abstract":"<p><strong>Background and purpose: </strong>Radiation enteritis (RE) is a severe complication after radiotherapy with no specific therapeutic agents. Here, we have attempted to identify the key therapeutic targets for RE, to advance drug development.</p><p><strong>Experimental approach: </strong>Therapeutic targets were screened and identified using RE patients' intestinal samples, bioinformatics, and mouse models. RNA sequencing, electron microscopy, metabolomics, glycolytic flux, co-immunoprecipitation, molecular docking, point mutation were used to identify mechanisms.</p><p><strong>Key results: </strong>Analysis of gene changes in response to ionising radiation showed extensive regulation of several differentially expressed genes by PPARγ, as well as its deficiency in activation and expression in RE. Both activation and overexpression of PPARγ significantly antagonised RE in vivo. Mechanistically, PPARγ specifically limited ferroptosis in intestinal epithelial cells exposed to ionising radiation, and its selective activation was more effective than full activation because of the reduced effect on the ferroptosis-driving genes PTEN and SAT1. Furthermore, ionising radiation caused the greatest changes in glucose metabolism. PPARγ targeted GAPDH at Lys107 to shift glycolysis to the hexosamine biosynthesis pathway, thereby enhancing glycosylation. In ionising radiation-induced ferroptosis, O/N-GlcNAcylation initially played antagonistic roles and later mediated the process, and they assisted PPARγ in restraining lysosomal degradation of heavy-chain ferritin (FTH1) and the transferrin receptor TFRC, thus controlling storage and transport of iron, and consequently alleviated ferroptosis.</p><p><strong>Conclusion and implications: </strong>PPARγ is a potential therapeutic target for RE, as it elicits GAPDH-mediated glucose metabolic reprogramming and alleviates ionising radiation-induced ferroptosis, in a glycosylation-dependent manner.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970522","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":"Contributions of synaptic energetic dysfunction by microtubule dynamics and microtubule-based mitochondrial transport disorder to morphine tolerance.","authors":"Zheng Li, Jie Liu, Jie Ju, Xiaoling Peng, Wei Zhao, Jihao Ren, Xiaoqian Jia, Jihong Wang, Ye Tu, Feng Gao","doi":"10.1111/bph.70048","DOIUrl":"https://doi.org/10.1111/bph.70048","url":null,"abstract":"<p><strong>Background and purpose: </strong>Morphine is among the most powerful analgesic, but its long-term use can cause tolerance. Synaptic ATP supply is critical for maintaining synaptic transmission. Microtubule-based mitochondrial transport ensures synaptic energy supply. How synaptic energy changes with morphine and the role of microtubule tracks in synaptic mitochondrial energy supply remain elusive. Chronic morphine treatment can destroy microtubule cytoskeletons. We investigated the effect of the microtubule cytoskeleton on synaptic mitochondrial energy supply and the mechanism of microtubule dynamics after morphine exposure.</p><p><strong>Experimental approach: </strong>Rats were treated with long-term morphine and the effect on thermal pain thresholds was evaluated by the tail-flick latency test. Various antagonists and agonists were used elucidated the role and mechanism of synaptic mitochondrial energy supply and microtubules in morphine tolerance in vivo and in SH-SY5Y cells.</p><p><strong>Key results: </strong>Chronic morphine treatment reduced synaptic mitochondrial ATP production. Improving mitochondrial oxidative phosphorylation (OXPHOS) alleviated the downregulation of synaptic ATP levels. Microtubule-stabilizing agents prevented microtubule disruption and ameliorated synaptic energy deficit via microtubule-based microtubule transport. In SH-SY5Y cells, morphine exposure reduced microtubule expression. And re-opening the synaptic Ca²⁺ channel by agonist alleviated microtubule decrease by calcium/calmodulin-dependent protein kinase 2 (CAMKK2)/AMP-activated protein kinase (AMPK) pathway.</p><p><strong>Conclusion and implications: </strong>This study demonstrates that the microtubule cytoskeleton regulated by the Ca²⁺-CAMKK2-AMPK axis is critical for synaptic mitochondrial transport and ATP production, explaining an interplay between chronic morphine-induced abnormal neuroadaptation and synaptic energetic dysfunction. These findings implicated a potential clinical strategy for prolonging the opioid antinociceptive effect during long-term pain control.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976551","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":"Pharmacological characterisation of JNJ-78911118, a novel, centrally-penetrant, selective GluN2A antagonist.","authors":"Brian Lord, Sirak Simavorian, Ian Fraser, Natalie Welty, Ryan Wyatt, Rory Pritchard, Lauren Fletcher, Henk Van Der Linde, Dominic Bounkhoun, Ondrej Libiger, Michael Maher, Wayne Drevets, François Bischoff, Pascal Bonaventure, Robert A Neff","doi":"10.1111/bph.70069","DOIUrl":"https://doi.org/10.1111/bph.70069","url":null,"abstract":"<p><strong>Background and purpose: </strong>Non-selective NMDA receptor antagonism produces rapid symptom improvement in treatment-resistant depression; however, associated side effects necessitate medical oversight during administration. We hypothesised that selective GluN2A antagonism could provide similar efficacy with an improved side effect profile. Here, we report the pharmacology of JNJ-78911118, a brain-penetrant, GluN2A selective antagonist.</p><p><strong>Experimental approach: </strong>JNJ-78911118 pharmacology and mechanism of action was characterised in vitro using fluorescence, voltage clamp and radioligand binding assays. Target engagement was measured using ex vivo receptor autoradiography, and effects on rat prefrontal cortex monoamine levels were measured using microdialysis. Synaptogenesis assays and patch clamp studies were used to demonstrate effects on synaptic plasticity. Cardiovascular safety and neurotoxicity were assessed in rats.</p><p><strong>Key results: </strong>JNJ-78911118 blocked GluN1/2A receptors with an IC₅₀ of 44 nM and showed selectivity against GluN1/2B, 2C and 2D receptors. Systemic administration produced concentration-dependent receptor occupancy, increased prefrontal cortex monoamine levels in wild type, but not in GluN2A knockout mice, and blocked theta burst induced LTP in the hippocampus. In addition, it produced increases in dendritic complexity and synapse number in vitro, and increased mEPSC frequency in rat cortical neurons in vivo. In rat toxicological studies, no Olney's lesions were observed, but acute increases in heart rate and blood pressure were detected.</p><p><strong>Conclusions and implications: </strong>JNJ-78911118 is a potent and selective GluN2A antagonist that reproduces the effect of known rapidly acting antidepressants (RAADs) on neurotransmitter levels and synaptic plasticity. This molecule is a powerful in vivo tool that will enhance understanding of GluN2A biology.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976656","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":"C-model: A comprehensive enhanced pharmacokinetic/pharmacodynamic simulation environment targeting the complement system.","authors":"Lucía Alfonso-González, M Cristina Vega, Francisco J Fernández","doi":"10.1111/bph.70054","DOIUrl":"https://doi.org/10.1111/bph.70054","url":null,"abstract":"<p><strong>Background and purpose: </strong>Recently, there has been increased research on treatments that modulate the complement system because of its significance in many diseases. However, managing patients with complement-related diseases is challenging owing to the different responses to treatments because of the heterogeneity of the aetiology of the different diseases, which may affect different proteins of the complement activation cascade. This study addresses these challenges using a comprehensive computational model, C-model.</p><p><strong>Experimental approach: </strong>C-model is an enhanced pharmacokinetic/pharmacodynamic simulation environment focused on the complement system, which can computationally model the alternative, classical and lectin activation pathways; the terminal/lytic pathway; and their regulation in fluid phase and on erythrocytes and endothelial cells. It incorporates experimental data on patients and simulated drugs.</p><p><strong>Key results: </strong>Our study demonstrates that C-model is effective in forecasting complement biomarkers across healthy and diseased states, as well as their reaction to treatments. The simulations from this study are freely available for academic use at https://cmodel.pythonanywhere.com.</p><p><strong>Conclusions and implications: </strong>This extensive enhanced pharmacokinetic/pharmacodynamic model supports the development of new therapies and personalised patient management by enabling scenario simulation and adaptation to various complement-related diseases. It advances our understanding of the complement system and its role in disease management.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984024","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":"Pharmacokinetics and pharmacodynamics of intranasal insulin in a rat brain.","authors":"Jelena Osmanovic Barilar, Leonarda Vlahov, Ana Babic Perhoc, Jan Homolak, Davor Virag, Eugenio Barone, Melita Salkovic-Petrisic, Ana Knezović","doi":"10.1111/bph.70057","DOIUrl":"https://doi.org/10.1111/bph.70057","url":null,"abstract":"<p><strong>Background and purpose: </strong>Understanding of the insulin-mediated effects on signalling and metabolism is important not only for fundamental knowledge of insulin's action in the brain but also for elucidating the mechanism of therapeutic potential in neurodegenerative disorders with underlying brain metabolic dysfunction. One of the main goals of this research is to clarify and explore the time-dependent regular insulin distribution and activity in the rat brain following intranasal administration.</p><p><strong>Experimental approach: </strong>Male Wistar rats were given insulin (2 IU) intranasally and were killed 3, 7.5, 15, 30, 60 and 120 min after administration. Control animals were killed without intranasal administration. Insulin, C-peptide and glucose concentrations were measured in plasma and cerebrospinal fluid (CSF), while levels and activity of the insulin signal transduction network were measured in brain and epithelia.</p><p><strong>Key results: </strong>Insulin immediately distributed to all brain regions after intranasal administration and was rapidly utilized and/or metabolized. Intranasal insulin positively influences insulin secretion seen as increment of C-peptide and insulin in the periphery and in distinctive brain regions. Secondary activation of AMP-activated protein kinase and calcium/calmodulin-dependent protein kinase occurred, perhaps due to brain region-dependent negative-feedback mechanisms on the overstimulated insulin signalling pathway.</p><p><strong>Conclusion and implications: </strong>The insulin dose was likely too high and caused its transport back to epithelia through unknown mechanisms (most likely by transporter), which could be of relevance for human dose reduction. Possible beneficial insulin action could be due to overstimulation of the insulin-signalling pathway with subsequent inactivation through insulin receptor substrate phosphorylation at Ser307.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983110","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}