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更新于：2025-12-02
Charcoal
炭素
更新于：2025-12-02
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 日本 (1991-10-04), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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关联
45
项与 炭素 相关的临床试验NCT07220031
Effect of Activated Charcoal on Serum Osmolality, Osmolal Gap, and Enzymatic Ethylene Glycol Assay
NCT07182422
Impact of Kremezin on Renal Recovery and Uremic Toxin Levels in Patients With Acute Kidney Disease
NCT06595121
Comparative Bioavailability Study of Budesonide After Inhalation of Budesonide 1 Mg / 2 Ml Nebuliser Suspension (Test Product 08P1707F0): Administration Without and with Activated Charcoal and Inhalation of Pulmicort® 1.0 Mg / 2 Ml Suspension (Reference Product) in Healthy Subjects
100 项与 炭素 相关的临床结果
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100 项与 炭素 相关的转化医学
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100 项与 炭素 相关的专利（医药）
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238
项与 炭素 相关的文献（医药）2025-12-31RENAL FAILURE
Adynamic bone disorder in chronic kidney disease: meta-analysis and narrative review of potential biomarkers as diagnosis and therapeutic targets
Review
作者: Chao, Chia-Ter ; Hung, Kuo-Chin ; Tsai, Kuo-Wang ; Shih, Li-Jane ; Hou, Yi-Chou ; Lu, Kuo-Cheng ; Liao, Min-Tser
Adynamic bone disorder, common in chronic kidney disease (CKD), results from reduced bone turnover, often due to medications such as calcimimetics or high-dose vitamin D analogs that induce low parathyroid hormone (PTH) levels. Numerous factors contributing to PTH hyporesponsiveness, which also induces low bone turnover, include deficient PTH, uremic toxins like indoxyl sulfate, malnutrition, inflammation, and diabetes. Diagnosis typically involves bone biopsy, although it is inconvenient. Biomarkers like bone-specific alkaline phosphatase (BALP) and intact PTH (iPTH) show promise in distinguishing between low and high bone turnover. Meta-analysis suggests that levels of iPTH below 150 pg/mL or BALP levels below 20 μg/l indicate low bone turnover. Treatments aim to improve bone density without hindering repair, with osteo-anabolic medications being favored for low PTH levels and anti-resorptive agents being cautioned. Romosozumab, while effective, has safety concerns that limit its use. Uremic toxins are reduced by AST-120 treatment, which alleviates PTH hypo-responsiveness and bone toxicity. Adjunctive measures include addressing vitamin D deficiency, and diabetes, and utilizing antioxidant and anti-inflammatory therapies. Overall, BALP and iPTH appear as potential promising biomarkers for diagnosing and monitoring adynamic bone disorder in CKD, effectively guiding therapeutic interventions.
2025-09-01Kidney360
Indoxyl Sulfate Contributes to Selenium Deficiency and Renal Ferroptosis by Decreasing the Expression of Selenium Transport Protein Selenoprotein P
Article
作者: Kitazato, Yutaka ; Shintani, Yuhi ; Matsushita, Kazutaka ; Nakano, Takehiro ; Tanaka, Motoko ; Yoshitake, Takuma ; Maeda, Hitoshi ; Tokumaru, Kai ; Maruyama, Toru ; Ogawa, Takumu ; Watanabe, Hiroshi ; Yasuno, Kohei
Key Points:
Indoxyl sulfate (IS) is involved in the liver-kidney axis by inducing renal ferroptosis by selenium deficiency due to suppression of selenoprotein P (SEPP1) expression in the liver.IS concentrations were negatively associated with selenium concentrations and SEPP1 concentrations in serum from patients on dialysis.We propose the potential therapeutic strategy targeting the IS/SEPP1/glutathione peroxidase 4 pathway for CKD.
Background:
The relationship between the progression of CKD and trace element deficiencies has attracted considerable attention. However, many aspects of trace element deficiency and the molecular mechanisms of CKD pathology remain unclear. In this study, we hypothesized that uremic toxins are involved in trace element deficiencies, which contribute to the progression of CKD.
Methods:
Adenine-induced CKD mice were used for in vivo study. Cultured hepatocytes were used for in vitro study.
Results:
Seventeen trace elements in plasma of CKD mice were measured using inductively coupled plasma mass spectrometry. Among these, selenium (Se) was identified as the trace element most significantly affected by the administration of oral spherical activated carbon (AST-120), an oral spherical activated carbon. CKD mice displayed reduced levels of Se in plasma, which was restored after the administration of AST-120. In vivo and in vitro experiments showed the uremic toxin indoxyl sulfate (IS) decreased expression of the Se transport protein selenoprotein P (SEPP1) in the liver. IS suppressed SEPP1 expression through increased production of reactive oxygen species by the organic anion transporting polypeptide/aryl hydrocarbon receptor/NADPH oxidase pathway. Increased reactive oxygen species led to the downregulation of transcription factors for SEPP1, such as AMP-activated protein kinase/PGC-1α and microRNA-34a/HNF4α. Analysis of serum from patients on hemodialysis also suggested that IS is involved in reducing serum SEPP1 levels and exacerbating Se deficiency. Combination therapy with AST-120 and sodium selenite restored the supply of Se to the kidneys and increased glutathione peroxidase 4 expression, thereby exerting renoprotective effects by suppression of ferroptosis.
Conclusions:
This study highlights the key role IS plays in Se deficiency and renal ferroptosis by suppressing hepatic SEPP1 expression. The findings suggest potential therapeutic strategies that target IS and Se deficiency for the management of CKD.
2025-06-01KIDNEY INTERNATIONAL
Mitochondrial dysfunction and mitophagy blockade contribute to renal osteodystrophy in chronic kidney disease-mineral bone disorder
Article
作者: Freeman, Tom C ; Macrae, Vicky E ; Stephen, Louise A ; Farquharson, Colin ; Phadwal, Kanchan ; Emelianova, Katie ; Hsu, Shun-Neng ; Carter, Roderick ; Amin, Anish K ; Morton, Nicholas M ; Dillon, Scott ; Luijten, Ineke ; Hsu, Yu-Juei ; Staines, Katherine A
Chronic kidney disease-mineral and bone disorder (CKD-MBD) presents with extra-skeletal calcification and renal osteodystrophy (ROD). However, the pathophysiology of ROD remains unclear. Here we examine the hypothesis that stalled mitophagy within osteocytes of CKD-MBD mouse models contributes to bone loss. RNA-seq analysis revealed an altered expression of genes associated with mitophagy and mitochondrial function in tibia of CKD-MBD mice. The expression of mitophagy regulators, p62/SQSTM1, ATG7 and LC3, was inconsistent with functional mitophagy, and in mito-QC reporter mice with ROD, there was a two- to three-fold increase in osteocyte mitolysosomes. To determine if uremic toxins were potentially responsible for these observations, treatment of cultured osteoblasts with uremic toxins revealed increased mitolysosome number and mitochondria with distorted morphology. Membrane potential and oxidative phosphorylation were also decreased, and oxygen-free radical production increased. The altered p62/SQSTM1 and LC3-II expression was consistent with impaired mitophagy machinery, and the effects of uremic toxins were reversible by rapamycin. A causal link between uremic toxins and the development of mitochondrial abnormalities and ROD was established by showing that a mitochondria-targeted antioxidant (MitoQ) and the charcoal adsorbent AST-120 were able to mitigate the uremic toxin-induced mitochondrial changes and improve bone health. Overall, our study shows that impaired clearance of damaged mitochondria may contribute to the ROD phenotype. Targeting uremic toxins, oxygen-free radical production and the mitophagy process may offer novel routes for intervention to preserve bone health in patients with CKD-MBD. This would be timely as our current armamentarium of anti-fracture medications for patients with severe CKD-MBD is limited.
100 项与 炭素 相关的药物交易
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外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| - | - | - |
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 |
|---|---|---|---|
| 瘙痒 | 中国台湾 | - | 2020-07-26 |
| 慢性肾病 | 日本 | 1991-10-04 | |
| 慢性肾病 | 日本 | 1991-10-04 |
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 |
|---|---|---|---|---|
| 尿毒症 | 申请上市 | - | - | |
| 炎症性肠病 | 临床3期 | 奥地利 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 比利时 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 捷克 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 法国 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 德国 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 匈牙利 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 荷兰 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 波兰 | 2006-03-01 | |
| 炎症性肠病 | 临床3期 | 英国 | 2006-03-01 |
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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 | 外周动脉疾病 indole | indoxyl sulfate | 30 | AST-120 6 gram/day | 淵艱鑰憲醖餘築齋膚壓(壓鹽網遞齋繭鬱糧範製) = did not change during study period 淵齋選夢膚遞網鏇築獵 (願遞積餘齋齋鏇鬱鹹衊 ) 更多 | 积极 | 2019-11-05 | |
临床4期 | 225 | 糧簾襯膚遞築壓蓋鏇齋(蓋選選築齋壓築廠夢選) = 簾顧遞艱衊膚獵網壓觸 齋網獵餘衊憲餘廠襯衊 (蓋選醖膚簾鏇選衊蓋網 ) 更多 | 积极 | 2019-11-05 | |||
临床3期 | 2,035 | 觸蓋艱鏇鹹鹽艱壓網構(鹹窪製製積鏇顧網襯鹹): Hazard Ratio = 0.74 (95% CI, 0.56 ~ 0.97) | - | 2016-09-30 | |||
Placebo | |||||||
临床3期 | 2,035 | 繭網鬱艱顧鏇鏇範窪糧(醖願鹽選窪範窪蓋憲鹹): HR = 0.91 (95% CI, 0.74 ~ 1.12), P-Value = 0.37 | 不佳 | 2015-07-01 | |||
Placebo | |||||||
临床3期 | 1,015 | (AST-120) | 襯積選鬱築衊齋網鏇壓 = 鬱繭艱網簾淵積淵醖窪 選襯廠蓋餘衊艱鏇艱襯 (築鏇壓餘積廠醖製衊獵, 範膚壓鏇艱淵齋蓋積窪 ~ 鑰繭膚鹹簾顧糧膚鏇夢) 更多 | - | 2015-03-02 | ||
Placebo (Placebo) | 襯積選鬱築衊齋網鏇壓 = 廠遞夢夢壓鹹積壓築繭 選襯廠蓋餘衊艱鏇艱襯 (築鏇壓餘積廠醖製衊獵, 積糧衊廠憲顧餘膚憲網 ~ 夢獵窪衊壓鹽艱鹽網窪) 更多 | ||||||
临床3期 | 1,020 | (AST-120) | 獵襯齋選觸範鏇選憲膚 = 醖夢鬱窪簾蓋繭憲窪製 製壓憲艱觸網壓餘顧顧 (夢廠鏇糧顧簾蓋衊鑰選, 繭糧鏇築範齋憲鏇蓋廠 ~ 襯襯網獵鬱鑰製構淵築) 更多 | - | 2015-03-02 | ||
Placebo (Placebo) | 獵襯齋選觸範鏇選憲膚 = 夢淵齋衊鹽簾簾壓製壓 製壓憲艱觸網壓餘顧顧 (夢廠鏇糧顧簾蓋衊鑰選, 築蓋獵繭積廠廠餘夢鏇 ~ 鏇網廠壓膚齋膚衊選窪) 更多 |
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