Folia Pharmacologica Japonica最新文献

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[Pharmacological and clinical profiles of belumosudil mesylate (REZUROCK® Tablets), a selective inhibitor of ROCK2]. [选择性ROCK2抑制剂甲磺酸白莫地尔(REZUROCK®片)的药理学和临床研究概况]。
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24091
Yuya Nishimura, Toshiyuki Tsuchiya, Koji Kijima, Takashi Matsuhira
{"title":"[Pharmacological and clinical profiles of belumosudil mesylate (REZUROCK<sub>®</sub> Tablets), a selective inhibitor of ROCK2].","authors":"Yuya Nishimura, Toshiyuki Tsuchiya, Koji Kijima, Takashi Matsuhira","doi":"10.1254/fpj.24091","DOIUrl":"10.1254/fpj.24091","url":null,"abstract":"<p><p>Belumosudil mesylate (REZUROCK<sub>®</sub> Tablets hereafter belumosudil) is a novel selective rho-associated, coiled-coil containing protein kinase 2 (ROCK2) inhibitor. ROCK2 is a kinase involved in immune cell differentiation and tissue fibrosis. Belumosudil exerts its effect by decreasing the inflammation and fibrosis in various organs which are the two key features of cGVHD. In the phase III clinical study in Japan, the primary endpoint was met, best overall response rate (best ORR), defined as the percentage of patients who achieved complete response (CR) or partial response (PR), was 85.7%. Belumosudil received manufacturing and marketing approval for the treatment of chronic graft-versus-host disease (cGVHD) in patients who have insufficient response to steroid therapy in March 2024 and launched in May 2024. The Japanese MHLW has also granted orphan drug designation in May 2023 for the treatment of cGVHD.</p>","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 2","pages":"141-151"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536999","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}
引用次数: 0
[Efforts to develop therapeutic agents for bacterial infections to fight against AMR (antimicrobial resistance)]. [开发细菌感染治疗剂以对抗抗生素耐药性的努力]。
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24082
Miki Takemura
{"title":"[Efforts to develop therapeutic agents for bacterial infections to fight against AMR (antimicrobial resistance)].","authors":"Miki Takemura","doi":"10.1254/fpj.24082","DOIUrl":"https://doi.org/10.1254/fpj.24082","url":null,"abstract":"<p><p>The global spread of antimicrobial resistance (AMR) is a threat to the international community, but few new antimicrobials are in the development stage and there are few options to treat AMR infections. In light of this situation, AMR has been continuously featured on the G7 agenda since 2015, and the 2023 G7 Hiroshima Leaders' Communiqué also states that in recognition of the global and rapid spread of AMR, push and pull incentives will be explored and implemented. In addition, the World Health Assembly adopted the Global Action Plan on AMR in 2015, and Japan developed its first AMR action plan in 2016. An updated version has been released in 2023. It is hoped that the attractiveness of the antibiotic market will be improved, and the new antibiotic development will be revitalized by further expansion and enhancement of the pull incentive systems. Cefiderocol, a novel siderophore cephalosporin, demonstrates potent antibacterial activity against carbapenem-resistant Gram-negative bacteria, which are considered to be particularly high-priority pathogens by the World Health Organization (WHO) and other organizations. A partnership between the SHIONOGI, the Global Antibiotic Research and Development Partnership (GARDP) and the Clinton Health Access Initiative (CHAI) formed to improve access to cefiderocol in countries around the world, including low- and middle-income countries. In order to bring these efforts to fruition in the fight against AMR, it is important to have further understanding and cooperation from people around the world, regardless of country or field.</p>","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 3","pages":"184-190"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001226","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}
引用次数: 0
[Development of drug discovery support system using chemoinformatics and generative AI technology]. [利用化学信息学和生成式人工智能技术开发药物发现支持系统]。
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24094
Atsushi Yoshimori
{"title":"[Development of drug discovery support system using chemoinformatics and generative AI technology].","authors":"Atsushi Yoshimori","doi":"10.1254/fpj.24094","DOIUrl":"10.1254/fpj.24094","url":null,"abstract":"<p><p>In recent years, the rapid development of generative AI has given rise to a variety of services such as machine translation, sentence summarization, and programming code generation. In drug discovery, generative AI and chemoinformatics have been used for seed/lead compound generation and optimization, and several successful cases were reported. The use of AI technology in drug discovery is expected to solve previously difficult problems and dramatically improve success rate in drug discovery. ITM, Inc. is a venture company established in 2004 to support drug discovery in silico using original chemoinformatics technology. Currently, ITM is developing a drug discovery support system that combines state-of-the-art AI technology and chemoinformatics technology. This paper introduces ITM's technology with a focus on the use of generative AI.</p>","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 2","pages":"120-126"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536989","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}
引用次数: 0
[Recent findings on the heterogeneity of astrocytes]. [星形胶质细胞异质性的最新发现]。
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.25024
Yuta Kohro
{"title":"[Recent findings on the heterogeneity of astrocytes].","authors":"Yuta Kohro","doi":"10.1254/fpj.25024","DOIUrl":"https://doi.org/10.1254/fpj.25024","url":null,"abstract":"","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 4","pages":"306"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552782","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}
引用次数: 0
[Clinical features of JAK1 gain-of-function variants and perspectives on ‍monogenic disorders in allergic diseases]. [JAK1功能获得性变异的临床特征及对过敏性疾病‍单基因疾病的看法]。
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.25011
Kenji Toyokuni, Satoshi Fujita, Hideaki Morita
{"title":"[Clinical features of JAK1 gain-of-function variants and perspectives on ‍monogenic disorders in allergic diseases].","authors":"Kenji Toyokuni, Satoshi Fujita, Hideaki Morita","doi":"10.1254/fpj.25011","DOIUrl":"10.1254/fpj.25011","url":null,"abstract":"<p><p>The prevalence of allergic diseases is increasing worldwide, with approximately one in two individuals in Japan affected by some form of allergic condition, making it a common disease. While most allergic diseases are multifactorial, involving a complex interplay between genetic predispositions and environmental factors, a subset of cases is attributed to monogenic disorders, which have been increasingly reported in recent years. This article focuses on JAK1 gain-of-function (GOF) variants, highlighting their clinical features, therapeutic potential, and the future prospects of research on monogenic disorders in allergic diseases. JAK1-GOF variants are characterized by early onset and severe atopic dermatitis that does not respond to conventional therapies. They are also frequently associated with other allergic diseases, such as food allergies and asthma, as well as autoimmune diseases and growth impairments. JAK inhibitors represent a promising therapeutic option for JAK1-GOF mutations, with previous reports suggesting their efficacy. Predicting drug efficacy through in vitro studies could enable the selection of tailored treatments for individual patients, potentially leading to significant clinical improvements. It is hypothesized that undiagnosed patients with such monogenic disorders may exist. Accurate diagnosis of these patients could facilitate effective treatments. Moreover, research on monogenic disorders has the potential to lead to the development of novel molecular-targeted therapies through the elucidation of disease pathophysiology, benefiting not only patients with rare genetic disorders but ultimately a broader population.</p>","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 4","pages":"239-243"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552752","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}
引用次数: 0
[Cardiotoxicity risk assessment of anticancer drugs by focusing on mitochondrial quality of human iPS cell-derived cardiomyocytes]. [通过关注人类iPS细胞衍生心肌细胞的线粒体质量来评估抗癌药物的心脏毒性风险]。
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24056
Yuri Kato, Yuya Nakamura, Moe Kondo, Yasunari Kanda, Motohiro Nishida
{"title":"[Cardiotoxicity risk assessment of anticancer drugs by focusing on mitochondrial quality of human iPS cell-derived cardiomyocytes].","authors":"Yuri Kato, Yuya Nakamura, Moe Kondo, Yasunari Kanda, Motohiro Nishida","doi":"10.1254/fpj.24056","DOIUrl":"https://doi.org/10.1254/fpj.24056","url":null,"abstract":"<p><p>Currently, a variety of anticancer agents are used in the treatment of cancer. Since anticancer agents are used continuously over a long time, they carry the risk of side effects. One of the major side effects is cardiac dysfunction. For example, doxorubicin, an anthracycline-type anticancer agent, is clinically restricted because of its dose-dependent cardiotoxicity. Cardiotoxicity includes decreased ejection fraction, arrhythmias, and congestive heart failure, all of which are associated with high mortality rates. Therefore, it is important to assess the risk of cardiotoxicity of anticancer agents in advance. Cardiomyocytes require energy to beat and retain an abundance of mitochondria. We established quantitative measurements of mitochondrial length and respiratory activities using cardiomyocytes. We found that exposure of human iPS cell-derived cardiomyocytes (hiPSC-CMs) to anticancer agents with reported cardiotoxicity enhanced mitochondrial hyperfission and the oxygen consumption rate was significantly reduced. Knockdown of dynamin-related protein 1 (Drp1), mitochondrial fission-accelerating GTP-binding protein, suppressed mitochondrial hyperfission in hiPSC-CMs. This indicates that visualizing mitochondrial functions in hiPSC-CMs will be helpful in assessing the risk of cardiotoxicity caused by anticancer agents and that maintaining mitochondrial quality will become a new strategy to reduce anticancer agents-induced cardiotoxicity. In this review, we present the evaluation of cardiotoxicity targeting mitochondrial quality in anticancer agents, using osimertinib, a non-small cell lung cancer drug, as an example.</p>","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 1","pages":"9-12"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931035","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}
引用次数: 0
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24105
Takahiro Iwamoto, Takayuki Nemoto
{"title":"","authors":"Takahiro Iwamoto, Takayuki Nemoto","doi":"10.1254/fpj.24105","DOIUrl":"https://doi.org/10.1254/fpj.24105","url":null,"abstract":"","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 2","pages":"152"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536958","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}
引用次数: 0
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24107
Junichi Kurihara
{"title":"","authors":"Junichi Kurihara","doi":"10.1254/fpj.24107","DOIUrl":"https://doi.org/10.1254/fpj.24107","url":null,"abstract":"","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 2","pages":"63-64"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536960","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}
引用次数: 0
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24101
Minoru Narita, Naoko Kuzumaki
{"title":"","authors":"Minoru Narita, Naoko Kuzumaki","doi":"10.1254/fpj.24101","DOIUrl":"https://doi.org/10.1254/fpj.24101","url":null,"abstract":"","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 1","pages":"61"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931011","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}
引用次数: 0
[Elucidation of the pathogenesis of optic nerve diseases and new therapeutic strategies to protect visual function]. [阐明视神经疾病的发病机制和保护视力功能的新治疗策略]。
Folia Pharmacologica Japonica Pub Date : 2025-01-01 DOI: 10.1254/fpj.24049
Chikako Harada, Kazuhiko Namekata, Xiaoli Guo, Takayuki Harada
{"title":"[Elucidation of the pathogenesis of optic nerve diseases and new therapeutic strategies to protect visual function].","authors":"Chikako Harada, Kazuhiko Namekata, Xiaoli Guo, Takayuki Harada","doi":"10.1254/fpj.24049","DOIUrl":"10.1254/fpj.24049","url":null,"abstract":"<p><p>Approximately 80% of all the information we receive about the world comes through the visual pathways and visual function deterioration causes severe decline in QOL. Glaucoma is the leading cause of blindness in the world, in which visual field deficit deteriorates as the optic nerve degeneration progresses. Hence, the development of fundamental cure is needed. Our research focuses on the signaling of brain-derived neurotrophic factor (BDNF), one neurotrophic factor reduced with aging and glaucoma patients. We generated modified tropomyosin receptor kinase B (TrkB) which can be constitutively activated in the absence of its ligand BDNF. The active site of TrkB is localized to the plasma membrane, allowing for constitutive activation of intracellular signaling. Gene therapy with the modified TrkB in a mouse model of glaucoma was proven to be protective. In addition, our group reported that apoptosis signal-regulating kinase 1 (ASK1), one of the stress response factors, is related to the severity of optic neuritis and myelitis in model mice of multiple sclerosis. We generated four lines of cell type specific ASK1 conditional knockout mice and found that ASK1 in glial cells increased the severity of neuroinflammation while ASK1 deficiency in immune cells had no significant effects. Further, we found that ASK1 is required in microglia and astrocytes to cause and maintain neuroinflammation by a feedback loop between these two cell types. Our results suggest that ASK1 might be a promising therapeutic target for reducing neuroinflammation including optic neuritis.</p>","PeriodicalId":12208,"journal":{"name":"Folia Pharmacologica Japonica","volume":"160 2","pages":"68-72"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536992","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}
引用次数: 0
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