预约演示
更新于：2026-02-27
Clodronate Disodium
氯膦酸二钠
更新于：2026-02-27
概要
基本信息
原研机构- |
权益机构- |
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
26
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
ISRCTN34217298
Randomised controlled trial of PENTOCLO (pentoxifylline, tocopherol and clodronate) in mandibular osteoradionecrosis
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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2,175
项与 氯膦酸二钠 相关的文献（医药）2026-04-01BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Vesicular nucleotide transporter (VNUT)-dependent ATP secretion by hepatic stellate cells promotes liver fibrosis
Article
作者: Niimoto, Tomohiro ; Nomura, Seiji ; Kabashima, Masaharu ; Gobaru, Mizuki ; Tokubuchi, Rie ; Rikitake, Junjiro ; Wang, Lixiang ; Inoguchi, Yukihiro ; Moriyama, Sawako ; Moriyama, Yoshinori ; Hasuzawa, Nao ; Nagayama, Ayako ; Ashida, Kenji ; Ohta, Keisuke ; Nomura, Masatoshi
Although liver fibrosis presents a substantial global health challenge, therapeutic options that directly target liver fibrosis remain limited. Hepatic stellate cells (HSCs) are key contributors to fibrosis through extracellular matrix production. This study uncovers a previously unrecognized function of HSCs: ATP secretion. We found that HSCs express the vesicular nucleotide transporter (VNUT) on secretory vesicles and actively release ATP. In mouse HSCs, VNUT is localized to the cytosol and around lipid droplets. In a thioacetamide-induced liver fibrosis model, VNUT inhibition with clodronate suppressed HSC proliferation and fibrosis progression, while restoring AMPK phosphorylation. In human hepatic stellate LX-2 cells, VNUT colocalized with v-SNARE proteins VAMP3 and VAMP7 and the vesicular proton pump V-ATPase. ATP secretion from LX-2 cells was observed upon stimulation with the Ca2+ ionophore ionomycin and was inhibited by Ca2+ chelation or low temperature, supporting an exocytotic mechanism. Clodronate and VNUT-targeting siRNA significantly reduced ATP release. Thapsigargin, an inducer of endoplasmic reticulum Ca2+ release, upregulated VNUT expression, suggesting a transcriptional regulation of VNUT-dependent ATP release by Ca2+ signaling. TGF-β1 stimulation also upregulated VNUT expression, suggesting its involvement in TGF-β1-induced fibrogenesis pathway. Additionally, serotonin was identified as an ATP secretion stimulator in LX-2 cells, and this effect was blocked by clodronate. Platelets-a major peripheral serotonin source-were increased in TAA-treated liver and found adjacent to serotonin receptor 5-HT2B-positive HSCs. Clodronate treatment reduced CD41-positive platelets in liver tissue. These findings highlight VNUT-mediated ATP secretion as a key regulator of HSC function and a potential therapeutic target for liver fibrosis.
2026-03-01THROMBOSIS RESEARCH
Monocyte depletion reduces late experimental post-thrombotic fibrotic injury in a stasis mouse model
Article
作者: Henke, Peter K ; Shea, Lonnie ; Cai, Qing ; Pellerito, Antonio M ; Jaffer, Farouc ; Quang, Andrew ; Pellerito, Mattea ; Dowling, Abigail R ; Luke, Catherine E ; Obi, Andrea
BACKGROUND:
Post thrombotic syndrome is a fibrotic disease related to inflammation resolution. There are no direct therapies that can ameliorate this disease. Monocyte/macrophages (Mo/MØ) are the primary leukocyte involved with later venous resolution, and likely direct vein wall responses and healing. Herein, we explored the vein wall response with Mo/MØ depletion by two methods.
METHODS:
Using two mouse models of venous thrombosis (VT), complete stasis and a flow restricted model, Mo/MØ depletion was accomplished using CD11b-DTR mice administered diphtheria toxin, and clodronate micelle administration in wild type mice. Tissue assays for structural histology, immunohistochemistry and western blotting were performed.
RESULTS:
Mo/MØ depletion resulted in significantly less vein wall fibrotic thickness, in the stasis model at day 14 in both the CD11b-DTR mice and those receiving clodronate micelles. No significant effect of Mo/MØ depletion was observed in the flow restricted VT model. The decrease in vein wall fibrosis was associated with fewer DDR2+ vein wall cells in the CD11b-DTR mice, but no difference in endothelial luminal coverage. Decreased cytokine and growth factor expression of IL-6, FSP-1, and VEGFa were associated with Mo/MØ depletion. Lastly, PMN depletion was associated with increased proinflammatory Mo/MØ, and a trend towards increased vein wall fibrosis as compared with controls.
CONCLUSION:
Mo/MØ direct the post VT late fibrotic response, possibly by affecting fibroblasts and inflammatory cytokine expression. This effect was only found with the complete stasis model and is consistent with worsened PTS in humans with complete venous obstruction.
2026-02-24ACS Nano
Selective Depletion of Tumor-Associated Macrophages with Biomineralized Erythrocyte Nanoghosts to Boost Neoadjuvant Radioimmunotherapy
Article
作者: Wen, Kexin ; Qu, Xinran ; Wang, Lianhui ; Fan, Qin ; Dong, Ziliang ; Zhang, Jinqiao ; Ren, Yingjie ; Li, Jifeng ; Liu, Yang
Neoadjuvant radiotherapy (NRT) is widely applied to reduce tumor burden and improve surgical outcomes. However, accumulating evidence indicates that radiation, at certain dose levels, paradoxically promotes the infiltration and polarization of tumor-associated macrophages (TAMs), especially the immunosuppressive M2-like subtype, thereby fostering an immunosuppressive tumor microenvironment (TME) and compromising long-term therapeutic efficacy. To overcome this limitation, we developed a biomineralized nanoghost platform (SBC@CaP) derived from senescent erythrocyte vesicles and coated with a pH-responsive calcium phosphate (CaP) shell. In the acidic TME, the CaP layer gradually dissolves, exposing the senescent erythrocyte membrane for selective recognition and uptake by TAMs, particularly those enriched after radiotherapy. Functioning as a universal TAM-targeting carrier, SBC@CaP can be modularly loaded with agents, such as disodium clodronate to induce apoptosis or ferrous ions to trigger ferroptosis in TAMs. In addition, released CaP buffers intratumoral acidity and enhance radiosensitization. This modular strategy enables precise TAMs clearance, TME remodeling, and immune activation. In multiple tumor models, SBC@CaP effectively reprograms the immune landscape and suppresses tumor progression, offering a versatile platform to mitigate the drawbacks of NRT and potentiate macrophage-targeted cancer therapy.
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
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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 | - | |
| 膝关节炎 | 临床2期 | 意大利 | - | 2019-02-21 |
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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 | 转移性前列腺癌 辅助 | - | 齋醖鏇遞製積積鹽襯艱(艱網遞糧襯鏇壓醖夢鑰): HR = 0.77 (95% CI, 0.6 ~ 0.98), P-Value = 0.032 | 积极 | 2009-09-01 | ||
Placebo | |||||||
临床3期 | 46 | 繭積衊鏇鏇構築廠糧獵(鏇構遞膚鬱艱襯憲廠醖) = 鑰鏇簾製鹹醖窪餘鹽窪 鑰膚積顧獵壓選積構夢 (製願衊鹽網廠構積窪衊 ) 更多 | - | 2007-06-20 | |||
繭積衊鏇鏇構築廠糧獵(鏇構遞膚鬱艱襯憲廠醖) = 餘顧製鏇餘願醖襯選顧 鑰膚積顧獵壓選積構夢 (製願衊鹽網廠構積窪衊 ) 更多 | |||||||
临床3期 | 乳腺癌 辅助 | 1,079 | 鹹淵鹽壓醖鹹衊襯廠鏇(鏇壓鹽憲選鑰鬱廠鹹願) = 醖鹹築窪顧鬱醖選觸襯 憲齋鹹艱鑰衊構夢鑰遞 (鹽獵觸顧遞觸製網鑰繭 ) 更多 | - | 2003-01-01 | ||
Placebo | 鹹淵鹽壓醖鹹衊襯廠鏇(鏇壓鹽憲選鑰鬱廠鹹願) = 醖製醖艱衊壓選選醖構 憲齋鹹艱鑰衊構夢鑰遞 (鹽獵觸顧遞觸製網鑰繭, 4.0 ~ 15.6) 更多 | ||||||
临床3期 | 3,323 | 夢鑰鬱夢鑰淵築構鹹觸(膚廠觸鹹廠糧壓鏇糧糧): HR = 0.77 (95% CI, 0.56 ~ 1.08) | 积极 | 2002-08-01 | |||
Placebo |
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