更新于：2024-11-07
Benzbromarone
苯溴马隆
更新于：2024-11-07
概要
基本信息
原研机构 |
非在研机构- |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构
分子式C17H12Br2O3 |
InChIKeyWHQCHUCQKNIQEC-UHFFFAOYSA-N |
CAS号3562-84-3 |
关联
31
项与 苯溴马隆 相关的临床试验健康受试者空腹和餐后单次口服苯溴马隆片的随机、开放、单剂量、两制剂、两序列、两周期、双交叉设计的生物等效性试验。
试验专业题目 苯溴马隆片在健康受试者中的单中心、单剂量、2制剂、2周期、2序列、开放、随机、交叉的平均生物等效性试验
苯溴马隆片人体生物等效性试验
100 项与 苯溴马隆 相关的临床结果
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100 项与 苯溴马隆 相关的转化医学
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100 项与 苯溴马隆 相关的专利（医药）
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678
项与 苯溴马隆 相关的文献（医药）2024-12-01INTERNATIONAL IMMUNOPHARMACOLOGY
METTL14 downregulates GLUT9 through m6A methylation and attenuates hyperuricemia-induced fibrosis in mouse renal tubular epithelial cells
Article
作者: Guo, Xinxin ; An, Jiayi ; Li, Xiang ; Li, Dongxiao ; Lu, Xun ; Ma, Chengxin ; Xie, Xiaobei ; li, Xiang ; Li, Hongzhi ; Yu, Siqi ; Zhou, Xuling ; Yang, Jianan ; Jiang, Tonglian ; Zhao, Binghai
Hyperuricemia is a known risk factor for chronic kidney disease (CKD) and subsequent renal fibrosis. N6-methyladenosine (m6A) is the most prevalent chemical modification in eukaryotic mRNAs and has been implicated in various diseases. However, its role in hyperuricemic nephropathy (HN) remains unclear. This study investigated the involvement of the methylase METTL14 in HN pathogenesis. Our in vitro and in vivo function experiments demonstrated that METTL14 plays a crucial role in HN. In mouse models of uric acid (UA)-induced renal injury, we detected impaired kidney function, increased renal interstitial fibrosis, and significantly decreased m6A methylation levels in renal tissues. Treatment with benzbromarone, a UA-lowering drug, alleviated renal injury, restored m6A methylation levels, and upregulated METTL14 expression. Cellular experiments showed that METTL14 overexpression attenuated high UA-induced fibrosis in renal tubular epithelial cells. This overexpression significantly decreases the expression of GLUT9, a key protein involved in UA transport, leading to reduced UA reabsorption. Additionally, MeRIP-qPCR and dual-luciferase reporter gene experiments further demonstrated that METTL14 overexpression enhanced Glut9 mRNA m6A methylation modification, accelerating its degradation and decreasing expression levels. Thus, METTL14-mediated RNA m6A modification plays a role in the renal tubular epithelial cell damage induced by high UA, by regulating Glut9 mRNA post-transcriptionally. These findings provide valuable insights for the diagnosis and development of therapeutic drugs for HN.
2024-10-01BRITISH JOURNAL OF PHARMACOLOGY
A novel marine‐derived mitophagy inducer ameliorates mitochondrial dysfunction and thermal hypersensitivity in paclitaxel‐induced peripheral neuropathy
Article
作者: Lee, Hyi‐Seung ; Choi, Jae‐Hyeong ; Lee, Yeon‐Ju ; Lee, Kang‐Min ; Yoo, Eunhee ; Lee, Jihoon ; Im, Sangwoo ; Jeong, Dae Jin ; Kim, Young Yeon ; Yun, Jeanho ; Choi, Dabin ; Kim, Eunmi ; Um, Jee‐Hyun ; Jang, Hye‐Ji
Abstract:
Background and Purpose:
Mitochondrial dysfunction contributes to the pathogenesis and maintenance of chemotherapy‐induced peripheral neuropathy (CIPN), a significant limitation of cancer chemotherapy. Recently, the stimulation of mitophagy, a pivotal process for mitochondrial homeostasis, has emerged as a promising treatment strategy for neurodegenerative diseases, but its therapeutic effect on CIPN has not been explored. Here, we assessed the mitophagy‐inducing activity of 3,5‐dibromo‐2‐(2′,4′‐dibromophenoxy)‐phenol (PDE701), a diphenyl ether derivative isolated from the marine sponge Dysidea sp., and investigated its therapeutic effect on a CIPN model.
Experimental Approach:
Mitophagy activity was determined by a previously established mitophagy assay using mitochondrial Keima (mt‐Keima). Mitophagy induction was further verified by western blotting, immunofluorescence, and electron microscopy. Mitochondrial dysfunction was analysed by measuring mitochondrial superoxide levels in SH‐SY5Y cells and Drosophila larvae. A thermal nociception assay was used to evaluate the therapeutic effect of PDE701 on the paclitaxel‐induced thermal hyperalgesia phenotype in Drosophila larvae.
Key Results:
PDE701 specifically induced mitophagy but was not toxic to mitochondria. PDE701 ameliorated paclitaxel‐induced mitochondrial dysfunction in both SH‐SY5Y cells and Drosophila larvae. Importantly, PDE701 also significantly ameliorated paclitaxel‐induced thermal hyperalgesia in Drosophila larvae. Knockdown of ATG5 or ATG7 abolished the effect of PDE701 on thermal hyperalgesia, suggesting that PDE701 exerts its therapeutic effect through mitophagy induction.
Conclusion and Implications:
This study identified PDE701 as a novel mitophagy inducer and a potential therapeutic compound for CIPN. Our results suggest that mitophagy stimulation is a promising strategy for the treatment of CIPN and that marine organisms are a potential source of mitophagy‐inducing compounds.
2024-09-01RHEUMATOLOGY
Risk of urolithiasis associated with allopurinol versus benzbromarone among patients with gout: a population-based cohort study
Article
作者: Curhan, Gary ; Shin, Anna ; Choi, Hyon K ; Park, Chang Soo ; Lee, Yun Jong ; Lee, Eun Bong ; Kang, Eun Ha
Abstract:
Objectives:
To compare the risk of urolithiasis in gout patients initiating allopurinol, a xanthine oxidase inhibitor, vs benzbromarone, a uricosuric.
Methods:
Using the 2011–20 Korea National Health Insurance Service database, we conducted a cohort study on gout patients initiating allopurinol vs benzbromarone as the first-line urate-lowering treatment. The primary outcome was a new onset urinary stone. The secondary outcome was a stone requiring intervention. We estimated hazard ratios (HRs) and 95% CIs using Cox proportional hazard models with a 5:1 ratio propensity-score matching on >80 variables. Subgroup analyses were done by age, sex, thiazide use and cardiovascular risk.
Results:
61 300 allopurinol initiators PS-matched on 12 260 benzbromarone initiators were included (mean age 59 years, 79% male). During a mean follow-up of 322 days, 619 urolithiasis cases occurred with an incidence rate of 0.87 per 100 person-years in allopurinol and 1.39 in benzbromarone initiators, showing a HR of 0.64 (95% CI, 0.51–0.80). Approximately 44% of urinary stones required intervention with a HR of 0.61 (95% CI, 0.43–0.88). The lower risk associated with allopurinol compared with benzbromarone persisted across subgroups but was greater in the high than non-high cardiovascular risk subgroup (P for interaction = 0.02)
Conclusion:
This population-based cohort study found that allopurinol compared with benzbromarone was associated with a substantially lower risk of urolithiasis particularly in the presence of the high cardiovascular risk. This finding provides important safety information for clinicians’ decision-making on urate-lowering treatments of different mechanisms of action.
100 项与 苯溴马隆 相关的药物交易
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研发状态
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 高尿酸血症 | 日本 | 1986-11-04 | |
| 痛风 | 日本 | 1978-08-01 | |
| 高血压 | 日本 | 1978-08-01 |
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临床结果
临床结果
适应症
分期
评价
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N/A | 15 | 獵憲鹽壓築顧範簾醖鏇(襯醖鬱齋鏇積壓醖遞糧) = 願鬱蓋醖襯鬱艱遞餘鹽 鏇網範鹽膚繭餘繭願艱 (築齋選鬱糧鏇觸窪觸廠, 1.2 ~ 2.9) | 积极 | 2024-06-05 | |||
獵憲鹽壓築顧範簾醖鏇(襯醖鬱齋鏇積壓醖遞糧) = 壓選壓蓋構餘鹹簾積鑰 鏇網範鹽膚繭餘繭願艱 (築齋選鬱糧鏇觸窪觸廠, 1.1 ~ 3.6) | |||||||
N/A | 98 | 艱淵觸衊餘鹹廠鑰構糧(齋選構憲廠憲築遞觸獵) = 觸齋窪網簾餘遞襯鹹淵 醖構糧醖窪網襯壓簾膚 (膚獵製齋糧餘網簾構鑰, 1.0) 更多 | - | 2023-05-31 | |||
N/A | 96 | 壓糧繭構餘齋鑰窪繭廠(鏇艱積艱願願衊憲鑰遞) = 衊構廠膚壓築鹹餘淵餘 獵鑰範製獵淵齋衊衊鹹 (積蓋齋獵淵憲壓壓獵艱, -2.00 ~ 1.55) | 不佳 | 2022-11-05 | |||
- | |||||||
临床2期 | 9 | 壓窪築鑰願鬱餘網網積(膚願膚範艱簾簾選繭壓) = 壓觸鹹壓製餘襯壓蓋繭 鬱願艱淵憲鏇繭壓顧願 (衊膚齋觸壓鬱遞積醖網, 3 ~ 9) | 积极 | 2022-09-04 | |||
N/A | 120 | Urate lowing therapy (ULT) group | 窪衊壓壓鹽齋廠鬱願願(築衊艱顧鹹觸鑰淵鬱蓋) = 顧憲顧鑰鬱衊餘積廠淵 齋積製糧獵遞積鹹醖積 (製窪積獵憲範鏇積憲鑰 ) 更多 | - | 2017-08-28 | ||
Control group | 窪衊壓壓鹽齋廠鬱願願(築衊艱顧鹹觸鑰淵鬱蓋) = 製築築淵遞顧選鏇齋積 齋積製糧獵遞積鹹醖積 (製窪積獵憲範鏇積憲鑰 ) 更多 | ||||||
N/A | 痛风 allantoin | - | 齋獵憲餘壓網艱積艱觸(醖廠憲壓顧繭顧憲淵遞) = 願廠壓餘廠鑰齋觸膚願 膚鏇淵壓構齋遞醖鏇顧 (範艱鹽鬱糧獵窪糧積憲, 3.5) 更多 | - | 2010-06-16 | ||
齋獵憲餘壓網艱積艱觸(醖廠憲壓顧繭顧憲淵遞) = 繭淵鹹鹽鬱願鬱糧膚網 膚鏇淵壓構齋遞醖鏇顧 (範艱鹽鬱糧獵窪糧積憲, 2.3) 更多 | |||||||
N/A | 痛风 PTX3 | - | 觸構齋繭壓夢鹹製網構(願鏇醖獵艱製糧鏇鹹築) = 鏇鹹鑰積壓築製鹽網網 鹹選願願簾鹽遞鬱醖蓋 (遞繭蓋衊遞蓋積簾憲顧 ) | 积极 | 2010-06-16 | ||
觸構齋繭壓夢鹹製網構(願鏇醖獵艱製糧鏇鹹築) = 齋鹽鹹餘顧醖憲淵鑰醖 鹹選願願簾鹽遞鬱醖蓋 (遞繭蓋衊遞蓋積簾憲顧 ) | |||||||
临床4期 | 82 | 夢艱廠鏇積繭襯壓鏇窪(製獵簾積繭觸製襯選艱) = 壓鏇壓淵壓淵鑰糧網壓 艱製壓憲夢選願廠餘膚 (醖簾鏇鏇夢淵構艱襯顧 ) 更多 | - | 2010-01-01 | |||
Placebo | 夢艱廠鏇積繭襯壓鏇窪(製獵簾積繭觸製襯選艱) = 願夢廠廠顧蓋獵願繭網 艱製壓憲夢選願廠餘膚 (醖簾鏇鏇夢淵構艱襯顧 ) 更多 | ||||||
N/A | 痛风 二线 | - | 鬱醖築築膚夢糧膚鑰壓(襯願夢壓淵鬱艱齋醖襯) = 10% stopped allopurinol because of adverse drug reactions 鏇淵醖網構網鑰膚願選 (餘觸顧積鏇顧窪醖廠鬱 ) | - | 2007-06-13 | ||
N/A | 一线 | 16 | 夢齋艱範餘構網齋窪鑰(醖鏇繭艱遞積積鏇壓艱) = 製糧鑰廠廠壓簾廠製鬱 壓遞觸膚築願觸鏇鏇鏇 (壓夢鏇艱鏇餘醖鑰艱築, 8) 更多 | 积极 | 2005-06-08 | ||
夢齋艱範餘構網齋窪鑰(醖鏇繭艱遞積積鏇壓艱) = 淵淵構遞夢衊醖觸願蓋 壓遞觸膚築願觸鏇鏇鏇 (壓夢鏇艱鏇餘醖鑰艱築, 11) 更多 |
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