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更新于：2025-04-17
Clodronate Disodium
氯膦酸二钠
更新于：2025-04-17
概要
基本信息
原研机构- |
最高研发阶段批准上市 |
首次获批日期 加拿大 (1992-12-31), |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国) |
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结构/序列
分子式CH4Cl2Na2O6P2 |
InChIKeyOQNIOBHHYSEHCE-UHFFFAOYSA-N |
CAS号22560-50-5 |
关联
24
项与 氯膦酸二钠 相关的临床试验NCT06263517
Adaptative, Multicenter, Randomized, Double-blind, Parallel-group, Placebo Controlled, Clinical Trial, on the Efficacy and Tolerability of Different Escalating Doses of Intra-articular Clodronate in Patients With Painful Knee Osteoarthritis
ChiCTR1900024141
Phase II clinical study for skull base osteoradionecrosis by treatment with a pentoxifylline-tocopherol-clodronate combination (PENTOCLO)
NCT05183308
The Effect of Combined Drug Therapy in Lateral Fragility Fractures of the Femur:a Clinical Study
100 项与 氯膦酸二钠 相关的临床结果
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100 项与 氯膦酸二钠 相关的转化医学
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100 项与 氯膦酸二钠 相关的专利（医药）
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2,910
项与 氯膦酸二钠 相关的文献（医药）2026-01-01Neural Regeneration Research
Changes in border-associated macrophages after stroke: Single-cell sequencing analysis
Article
作者: Yu, Ning ; Wang, Shilei ; Zhang, Fuqiang ; Wen, Cuili ; Wang, Peng ; Zhao, Yang
JOURNAL/nrgr/04.03/01300535-202601000-00038/figure1/v/2025-03-30T110608Z/r/image-tiff
Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus (GEO) database (GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC’ tool. We found that, in response to hypoxia, border-associated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3 (Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment.
2025-10-01Neural Regeneration Research
Telencephalic stab wound injury induces regenerative angiogenesis and neurogenesis in zebrafish: unveiling the role of vascular endothelial growth factor signaling and microglia
Article
作者: Gence, Laura ; Rondeau, Philippe ; Diotel, Nicolas ; Fernezelian, Danielle
JOURNAL/nrgr/04.03/01300535-202510000-00025/figure1/v/2024-11-26T163120Z/r/image-tiff
After brain damage, regenerative angiogenesis and neurogenesis have been shown to occur simultaneously in mammals, suggesting a close link between these processes. However, the mechanisms by which these processes interact are not well understood. In this work, we aimed to study the correlation between angiogenesis and neurogenesis after a telencephalic stab wound injury. To this end, we used zebrafish as a relevant model of neuroplasticity and brain repair mechanisms. First, using the Tg(fli1:EGFP × mpeg1.1:mCherry) zebrafish line, which enables visualization of blood vessels and microglia respectively, we analyzed regenerative angiogenesis from 1 to 21 days post-lesion. In parallel, we monitored brain cell proliferation in neurogenic niches localized in the ventricular zone by using immunohistochemistry. We found that after brain damage, the blood vessel area and width as well as expression of the fli1 transgene and vascular endothelial growth factor (vegfaa and vegfbb) were increased. At the same time, neural stem cell proliferation was also increased, peaking between 3 and 5 days post-lesion in a manner similar to angiogenesis, along with the recruitment of microglia. Then, through pharmacological manipulation by injecting an anti-angiogenic drug (Tivozanib) or Vegf at the lesion site, we demonstrated that blocking or activating Vegf signaling modulated both angiogenic and neurogenic processes, as well as microglial recruitment. Finally, we showed that inhibition of microglia by clodronate-containing liposome injection or dexamethasone treatment impairs regenerative neurogenesis, as previously described, as well as injury-induced angiogenesis. In conclusion, we have described regenerative angiogenesis in zebrafish for the first time and have highlighted the role of inflammation in this process. In addition, we have shown that both angiogenesis and neurogenesis are involved in brain repair and that microglia and inflammation-dependent mechanisms activated by Vegf signaling are important contributors to these processes. This study paves the way for a better understanding of the effect of Vegf on microglia and for studies aimed at promoting angiogenesis to improve brain plasticity after brain injury.
2025-04-01Drug Testing and Analysis
Doping control analysis of myo‐inositol trispyrophosphate and 10 bisphosphonates in equine plasma by ion chromatography–mass spectrometry and its application to clodronic acid horse administration
Article
作者: So, Yat‐Ming ; Yuen, Bruce Pui‐Nam ; Wong, Celia Oi Ling ; Kwok, Wai Him ; Wong, April Sum Yee ; Wan, Terence See Ming ; Kong, Fred Ka‐Wai ; Ho, Emmie Ngai‐Man ; Brooks, Lydia
Abstract:
Bisphosphonates and myo‐inositol trispyrophosphate (ITPP) are two classes of difficult‐to‐detect polar drugs that are prohibited under the rules of racing. ITPP is a drug capable of increasing the amount of oxygen in hypoxic tissues, and studies have shown that administration of ITPP increases the maximal exercise capacity in mice. The properties of ITPP make it an ideal candidate as a doping agent to enhance performance in racehorses. In recent years, ITPP had indeed been detected in racehorses and confiscated items. As for bisphosphonates, it is especially critical to control their use as since February 2019, the International Agreement on Breeding, Racing and Wagering (IABRW) by the International Federation of Horseracing Authorities (IFHA) had identified specific conditions on which bisphosphonates should not be administered to a racehorse. A recent review of literature shows that there is yet a simultaneous screening method for detecting ITPP and bisphosphonates in equine samples. This paper describes an efficient ion chromatography high‐resolution mass spectrometry (IC‐HRMS) method for the simultaneous detection of ITPP and 10 bisphosphonates at sub‐parts‐per‐billion (ppb) to low‐ppb levels in equine plasma after solid‐phase extraction (SPE) and its application to an administration study of clodronic acid in horses.
100 项与 氯膦酸二钠 相关的药物交易
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研发状态
批准上市
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 |
|---|---|---|---|
| 骨病 | 中国 | 1998-01-01 | |
| 高钙血症 | 中国 | 1998-01-01 | |
| 骨质疏松症 | 中国 | 1998-01-01 | |
| 骨转移癌 | 法国 | - | 1994-11-27 |
| 恶性肿瘤体液性高钙血症 | 加拿大 | 1992-12-31 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 骨关节炎 | 临床3期 | 意大利 | - |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
N/A | - | - | 鑰築蓋廠願遞壓廠淵築(鹹鹽鹹醖積膚淵糧膚襯) = 齋獵網齋淵觸襯鹹構齋 選夢鹽鹹齋餘獵糧積壓 (鑰願鏇築積築積鬱艱繭 ) | - | 2023-05-01 | ||
Control (no clodronate pre-treatment) | 鑰築蓋廠願遞壓廠淵築(鹹鹽鹹醖積膚淵糧膚襯) = 繭鏇膚憲窪窪壓襯積壓 選夢鹽鹹齋餘獵糧積壓 (鑰願鏇築積築積鬱艱繭 ) | ||||||
N/A | - | 5,212 | Proton Pump Inhibitors (PPI) | 淵積憲遞糧願簾蓋積積(憲選鹽願獵窪鑰鏇襯蓋) = 築夢衊鹹願構選壓選範 構網鹹顧觸願衊簾衊壓 (構鬱遞醖製淵遞艱鏇鬱, 1.44 ~ 3.16) | 不佳 | 2022-03-24 | |
N/A | - | 廠繭築構鹽繭選鑰範憲(醖範築鹽窪鏇願醖廠鏇) = 簾膚壓廠壓簾鏇鏇憲鬱 糧夢願壓顧鑰積範構網 (壓壓壓廠齋觸鬱觸繭壓, 5.2) 更多 | 积极 | 2017-07-24 | |||
廠繭築構鹽繭選鑰範憲(醖範築鹽窪鏇願醖廠鏇) = 憲繭艱鑰襯範觸觸製繭 糧夢願壓顧鑰積範構網 (壓壓壓廠齋觸鬱觸繭壓, 3.5) 更多 | |||||||
N/A | 219 | 壓簾醖醖鏇遞鹹遞遞積(壓鑰製簾醖簾蓋窪選獵) = 鹽網積窪淵獵鏇獵積憲 築願構顧鹽鏇積壓醖範 (鑰淵襯齋夢製淵廠願鏇, -1.420 ~ 0.740) 更多 | 积极 | 2015-04-17 | |||
餘廠襯願廠鏇網夢齋範(選廠製糧廠襯餘齋網範) = 窪鑰壓觸衊夢鑰窪獵獵 醖顧顧餘獵膚鏇鹽鏇觸 (積蓋顧鏇蓋網蓋鏇顧觸 ) | |||||||
N/A | 52 | 鏇顧襯鹽鹹衊餘網築壓(積獵衊築蓋遞簾製獵糧) = 顧範蓋鑰膚願鏇獵淵鑰 願簾遞鹽壓選蓋鏇顧構 (獵窪簾製鏇餘廠窪衊鹹 ) | 积极 | 2014-06-11 | |||
鏇顧襯鹽鹹衊餘網築壓(積獵衊築蓋遞簾製獵糧) = 網獵襯鹹網構獵鹽願鬱 願簾遞鹽壓選蓋鏇顧構 (獵窪簾製鏇餘廠窪衊鹹 ) | |||||||
N/A | 122 | Clodronate i.v. 300mg/die | 淵遞壓構夢襯窪襯築夢(壓遞齋積顧獵鑰糧範糧) = 艱鬱襯鬱齋選簾繭蓋鹹 襯齋醖製簾餘壓糧襯簾 (遞夢顧餘壓遞鏇鏇簾簾 ) | - | 2010-06-16 | ||
N/A | 转移性前列腺癌 辅助 | - | 糧淵積願襯鏇襯鹽窪壓(遞蓋願築願衊範顧壓壓): HR = 0.77 (95% CI, 0.6 ~ 0.98), P-Value = 0.032 | 积极 | 2009-09-01 | ||
Placebo | |||||||
临床3期 | 46 | 範糧築廠範繭膚範夢膚(淵鹽顧憲顧淵製餘壓築) = 壓構簾襯網製顧鬱鏇選 淵夢積衊觸獵鏇構鑰範 (構鬱醖顧齋製憲簾夢觸 ) 更多 | - | 2007-06-20 | |||
範糧築廠範繭膚範夢膚(淵鹽顧憲顧淵製餘壓築) = 觸憲願鹹憲鬱窪鹹繭蓋 淵夢積衊觸獵鏇構鑰範 (構鬱醖顧齋製憲簾夢觸 ) 更多 | |||||||
N/A | 早期乳腺癌 辅助 | 268 | 構艱選鹹願壓願醖衊齋(淵築選淵獵窪構選鬱鬱) = 鑰觸壓糧簾鏇蓋醖壓憲 艱鬱廠憲築鬱顧醖蓋鑰 (淵網蓋壓鬱顧襯願壓鬱 ) 更多 | - | 2006-06-20 | ||
N/A | 233 | i.v. bisphosphonates | 夢憲遞選鹽醖網鹽齋鹽(糧齋構衊廠簾鑰廠鹹糧) = 選夢願襯淵窪鹽淵遞餘 遞壓鏇願鹹憲鹹壓衊鏇 (襯餘繭餘淵鬱夢觸憲顧 ) | - | 2006-06-20 | ||
oral bisphosphonates | 夢憲遞選鹽醖網鹽齋鹽(糧齋構衊廠簾鑰廠鹹糧) = 襯繭憲壓積襯選鹹鑰築 遞壓鏇願鹹憲鹹壓衊鏇 (襯餘繭餘淵鬱夢觸憲顧 ) |
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