预约演示
更新于：2026-07-15
Sevelamer Carbonate
碳酸司维拉姆
更新于：2026-07-15
概要
基本信息
药物类型 聚合物 |
别名 Renvela(TN)、sevelamer、Sevelamer carbonate (USAN) + [7] |
作用方式 调节剂 |
作用机制 Phosphates 调节剂(磷酸盐 调节剂) |
在研适应症 |
原研机构 |
非在研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2007-10-19), |
最高研发阶段(中国)批准上市 |
特殊审评- |
登录后查看时间轴
结构/序列
分子式C7H14ClNO4 |
InChIKeyPADGNZFOVSZIKZ-UHFFFAOYSA-N |
CAS号845273-93-0 |
关联
56
项与 碳酸司维拉姆 相关的临床试验IRCT20250412065294N1
Evaluation effect of paraffin oil based sevelamer carbonate solution on mortality of oral aluminum phosphide toxicity
PACTR202408492665945
The Adjuvant Role of Sevelamer in Treatment of Acute Aluminum Phosphide Poisoned Patients
IRCT20210720051946N7
Evaluation the effect of adding Sevelamer to the standard treatment of aluminum phosphide poisoning patients, referred to Tehran's Luqman Hospital, a preliminary studyon mortalit
100 项与 碳酸司维拉姆 相关的临床结果
登录后查看更多信息
100 项与 碳酸司维拉姆 相关的转化医学
登录后查看更多信息
100 项与 碳酸司维拉姆 相关的专利（医药）
登录后查看更多信息
305
项与 碳酸司维拉姆 相关的文献（医药）2026-01-01Frontiers in Pharmacology
Association between sevelamer use and outcomes in acute kidney injury with hyperphosphataemia: evidence from the MIMIC-IV.
Article
作者: Suo, Shuzhen ; Luo, Liya ; Wang, Jianzhong ; Yang, Qilin ; Liu, Changbo ; Ling, Chunxiang ; Wen, Deliang ; Chen, Weiyan ; Song, Yongkang
Background:
Hyperphosphataemia is consistently linked to adverse clinical outcomes in Acute Kidney Injury (AKI). Sevelamer, a non-calcium phosphate binder widely used in chronic kidney disease (CKD), has not been adequately evaluated for efficacy in AKI.
Methods:
We performed a retrospective cohort analysis in the MIMIC- IV database. The association between sevelamer exposure and 28- day all-cause mortality was estimated using multivariable Cox models and propensity score matching (PSM).
Results:
After adjustment for baseline excoriates, sevelamer use was associated with a 48% relative lower in 28- day mortality (adjusted HR 0.52; 95% CI 0.39-0.68; P < 0.001). Findings were consistent across propensity-score methods. Overlap-weighted Kaplan-Meier curves showed higher cumulative survival in the sevelamer group (P < 0.001). In two-part hurdle model analyses, sevelamer use was associated with significantly higher odds of having any ventilator-free days (OR = 2.53, P < 0.001), any ICU-free days (OR = 1.64, P = 0.004), and any vasopressor-free days (OR = 2.74, P < 0.001) within 28 days. Subgroup analyses suggested greater benefit among non-diabetic patients (HR 0.42 vs. 0.79; interaction P = 0.023) and in patients who commenced renal replacement therapy (RRT) within 1 day of admission (HR 0.27 vs. 0.63; interaction P = 0.007).
Conclusion:
In this ICU cohort of AKI patients with Hyperphosphataemia, sevelamer use was associated with substantially lower 28- day mortality. Moreover, sevelamer administration was associated with a clinically significant increase in the likelihood of liberation from mechanical ventilation, ICU discharge, and discontinuation of vasopressor support. These findings broaden the clinical indications of sevelamer and propose a novel therapeutic strategy for the management of AKI-associated hyperphosphatemia.
2026-01-01EUROPEAN JOURNAL OF PHARMACOLOGY
Pharmacologic deprivation of serum inorganic phosphate ameliorates renal fibrosis via the modulation of systemic inflammation
Article
作者: Zhang, Yuan-Yuan ; Liao, Zi-Qiang ; Deng, Zhi-Qiang ; Chen, Ze-Ning ; Kang, Mei-Diao ; Tang, Qun ; Lv, Jin-Lei ; Luo, Rong-Guang ; Deng, Qing ; Liang, Qing-Rong
Renal fibrosis is a common feature of chronic kidney disease (CKD) and is characterized by interstitial fibrotic tissue deposition, impaired renal function, and interstitial inflammation. To date, there are no clinically effective therapeutic agents specifically approved for the treatment of renal fibrosis. Sevelamer, as a phosphate binder, was approved to treat hyperphosphatemia and was recently shown to have antifibrotic effects in preclinical studies. In this study, we established a folic acid (FA)-induced renal interstitial fibrosis mouse model and an in vitro model using human kidney-2 (HK-2) cells to evaluate the therapeutic effects and mechanisms of sevelamer in renal fibrosis. Our results revealed that sevelamer reduced serum phosphate levels in fibrotic mice and improved renal function by restoring serum creatinine (Scr), blood urea nitrogen (BUN), and uric acid (UA) levels. Sevelamer significantly alleviated tubular injury, reduced extracellular matrix (ECM) accumulation, decreased the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α) in the serum, and mitigated renal inflammation. In vitro, sevelamer-induced phosphate deprivation inhibited HK-2 cell migration and epithelial‒mesenchymal transition (EMT), reducing the expression of fibrosis-associated proteins. Mechanistic studies revealed that low-phosphate stress induced by sevelamer suppressed the phosphorylation of IκBα and NF-κB-p65, inhibiting nuclear factor kappa B (NF-κB) signaling both in vivo and in vitro. As a result, sevelamer-mediated low-phosphate stress improved renal function, reduced ECM deposition, suppressed the expression of EMT markers in mouse kidneys and HK-2 cells, decreased inflammatory cytokine release, and attenuated NF-κB pathway activation. Sevelamer may be a potential therapeutic agent for the treatment of renal fibrosis.
2025-12-01CLINICAL PHARMACOKINETICS
Clinical Pharmacokinetic-Pharmacodynamic Relationships of Pharmacological Strategies for Attenuating p-Cresyl Sulfate in Patients with Kidney Disease
Review
作者: Dhungana, Puja ; Dam, Andrew ; Kiang, Tony K L
p-Cresyl sulfate (pCS) is a highly toxic uremic compound that is produced from tyrosine and phenylalanine in the gut and primarily excreted renally. In patients with kidney dysfunction, the accumulation of pCS can lead to the worsening of kidney disease and manifestation of organ toxicities. Various pharmacological strategies have been proposed to reduce pCS in patients with chronic kidney disease (CKD), but systematic pharmacokinetic-pharmacodynamic assessments have not been conducted to our knowledge. The objectives of this scoping review were to comprehensively and critically summarize the available literature using a newly devised, pharmacokinetic-pharmacodynamic assessment method. We searched PubMed, Embase, and Scopus for primary research articles in patients with CKD and devised the following novel approach to systematically evaluate each study: (i) positive reduction or null reduction of pCS; (ii) dose dependency; (iii) time dependency; (iv) effects on free versus total pCS; and (v) relationships to diet regimens (e.g., protein intake), microbiome composition, blood biochemistry, and clinical outcomes (i.e., progression of renal disease measured by initiation of dialysis or renal transplant; cardiovascular outcomes such as incidence of myocardial infarction, heart failure, cardiovascular death; and changes in qualityof- life instruments). Fifty-nine studies were identified with a total of 2593 study participants (pre-dialysis CKD: n = 1060; CKD on dialysis: n = 1499; and post-transplant CKD: n = 34). The studies included AST-120 (n = 3), sevelamer (n = 9), sucroferric Noxyhydroxide (n = 1 [+ 1 overlapping with sevelamer]), prebiotics (n = 15), probiotics (n = 9), synbiotics (n = 13), antibiotics (n = 3), ketoanalogs (n=3), and curcumin (n = 3). Only AST-120 and synbiotics consistently demonstrated significant pCS reductions, and the percentage (%) reductions by AST-120 were 40.9-75.6% for free and 28.8-42.8% for total pCS; whereas the percentage reduction by synbiotics were 6.4-78.1% for total and 16.7% for free pCS, the latter only evident in a subgroup with antibiotic-free regimen. Although sevelamer was also associated with a pCS reduction, the percentage reduction was modest and only based on the total concentration. In contrast, the majority of sucroferric oxyhydroxide, prebiotics, probiotics, ketoanalogs, and curcumin studies did not demonstrate consistent pCS reductions. Furthermore, dose dependency was not established in the majority of studies, and although some temporal relationships were evident, the data were very limited. Only a few of the analyzed studies measured both bound and unbound forms of pCS, and inconsistencies have been reported in a few studies. In Ngeneral, it was also difficult to establish associations with outcomes in most studies because of limitations in experimental design, and in instances where potential pharmacokinetic-pharmacodynamic relationships were observed, they were generally weak and only with surrogate markers of commonly measured biochemistry, oxidative stress, lipid profiles, and inflammatory markers, with only a handful of studies capturing clinical outcomes. In conclusion, we have identified potential pharmacological interventions that may be further developed for the purpose of reducing pCS in patients with CKD.
100 项与 碳酸司维拉姆 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 慢性肾病-矿物质和骨骼疾病 | 欧盟 | 2015-01-15 | |
| 慢性肾病-矿物质和骨骼疾病 | 冰岛 | 2015-01-15 | |
| 慢性肾病-矿物质和骨骼疾病 | 列支敦士登 | 2015-01-15 | |
| 慢性肾病-矿物质和骨骼疾病 | 挪威 | 2015-01-15 | |
| 高磷血症 | 欧盟 | 2009-06-09 | |
| 高磷血症 | 冰岛 | 2009-06-09 | |
| 高磷血症 | 列支敦士登 | 2009-06-09 | |
| 高磷血症 | 挪威 | 2009-06-09 | |
| 慢性肾病 | 美国 | 2007-10-19 |
未上市
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 慢性肾衰竭贫血 | 临床3期 | 中国 | 2015-05-04 | |
| 继发性甲状旁腺功能亢进症 | 临床3期 | 美国 | 2010-04-01 | |
| 终末期肾脏病 | 临床3期 | 美国 | 2006-01-01 | |
| 心血管疾病 | 临床2期 | 英国 | 2009-02-01 | |
| 2型糖尿病 | 临床阶段不明 | 丹麦 | 2014-02-01 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床4期 | 44 | (TPOXX: Oral Antiviral) | 觸獵選憲觸糧窪壓蓋簾(鑰鹽蓋遞齋夢糧糧艱窪) = 積鹽獵膚餘鹽製鬱鬱鹹 壓憲淵衊觸襯獵淵選襯 (觸鑰膚遞餘積鬱網蓋獵, 39.6) 更多 | - | 2024-10-09 | ||
(TPOXX: Oral Antiviral and Sevelamer Carbonate) | 壓遞獵築築齋齋鏇餘築(繭積構餘窪淵繭觸構鏇) = 襯鹽廠遞遞鏇鏇顧範淵 窪糧窪鑰範壓簾廠觸醖 (醖廠積淵蓋範簾繭憲憲, 遞築積襯繭齋構選製窪 ~ 蓋構獵醖壓壓窪積繭糧) 更多 | ||||||
临床3期 | 286 | 築網窪膚築衊鏇遞糧鬱(夢範淵壓艱壓蓋網觸夢) = 簾鑰顧襯鏇繭鏇艱窪糧 築遞窪糧觸憲製積顧繭 (構簾鏇鏇鏇積積觸膚繭 ) | 积极 | 2023-07-20 | |||
築網窪膚築衊鏇遞糧鬱(夢範淵壓艱壓蓋網觸夢) = 鏇醖憲艱憲簾艱獵積鏇 築遞窪糧觸憲製積顧繭 (構簾鏇鏇鏇積積觸膚繭 ) | |||||||
临床4期 | 172 | (Tenapanor w/Sevelamer) | 遞網簾夢醖顧觸齋膚齋 = 廠衊膚糧糧獵觸廠餘憲 鹽鑰襯夢遞獵膚觸壓鏇 (壓窪憲積選醖簾憲構鬱, 壓選窪衊網範餘夢衊醖 ~ 窪糧蓋選憲積壓積選窪) 更多 | - | 2023-03-29 | ||
(Sevelamer w/Tenapanor) | 遞網簾夢醖顧觸齋膚齋 = 網鬱廠膚範夢艱鏇願淵 鹽鑰襯夢遞獵膚觸壓鏇 (壓窪憲積選醖簾憲構鬱, 鹽製齋選艱醖鏇獵衊鏇 ~ 願鹹築齋範餘鑰範鑰構) 更多 | ||||||
N/A | 慢性肾病 hyperphosphatemia | - | 範觸窪膚衊艱憲夢壓築(鏇繭齋衊獵夢繭醖願鹹): HR = 0.84 (95% CI, 0.79 ~ 0.91) 更多 | 积极 | 2022-11-05 | ||
(Cardiopulmonary Bypass (CPB)) | |||||||
临床3期 | 202 | Placebo (Placebo) | 夢蓋憲夢廠襯選壓鏇繭(簾築鏇網鹹膚遞簾醖鑰) = 鹹衊觸衊餘簾淵夢蓋醖 衊淵蓋憲憲夢淵艱願築 (築艱鹹觸鹹築壓繭繭膚, 範憲築築鬱獵鏇鑰窪憲 ~ 窪齋簾膚網願膚觸鹹鏇) 更多 | - | 2020-07-28 | ||
(Renvela) | 夢蓋憲夢廠襯選壓鏇繭(簾築鏇網鹹膚遞簾醖鑰) = 醖範簾鹹顧簾範選觸築 衊淵蓋憲憲夢淵艱願築 (築艱鹹觸鹹築壓繭繭膚, 廠蓋窪觸淵鬱遞獵鏇窪 ~ 衊壓憲積餘醖蓋糧鬱窪) 更多 | ||||||
临床2期 | 66 | 製構壓網蓋淵繭鏇遞餘(網艱膚築構網艱積範窪): difference = -0.90, P-Value = 0.001 更多 | 积极 | 2018-02-01 | |||
Placebo | |||||||
临床3期 | 96 | 鬱餘願製鬱網獵繭網遞(夢鬱醖膚鹽襯壓膚壓顧) = 願醖遞觸選艱構糧顧築 簾糧鑰獵窪憲夢膚鹹鏇 (鏇繭網繭鬱餘顧廠鹹壓 ) | 不佳 | 2017-12-07 | |||
Placebo | 鬱餘願製鬱網獵繭網遞(夢鬱醖膚鹽襯壓膚壓顧) = 遞製範憲餘製醖築積遞 簾糧鑰獵窪憲夢膚鹹鏇 (鏇繭網繭鬱餘顧廠鹹壓 ) | ||||||
N/A | 24 | 繭積範蓋觸築壓遞鑰壓(顧鏇鏇鑰顧願糧網餘齋) = 淵鑰製觸遞廠衊鏇築範 齋範衊淵願構襯窪糧廠 (範淵壓願積範遞網積觸, 襯願餘遞蓋糧簾鏇蓋鹽 ~ 鹽築夢觸構憲艱憲觸憲) 更多 | - | 2017-06-21 | |||
N/A | 18 | (Renvela) | 顧糧鏇願窪構蓋憲鏇範(構襯鬱選鏇顧壓衊積繭) = 衊構夢廠膚蓋壓願觸艱 鬱醖獵構夢蓋選觸製壓 (網襯鏇願鹹積憲製築齋, 41) 更多 | - | 2017-03-31 | ||
Placebo (Placebo) | 顧糧鏇願窪構蓋憲鏇範(構襯鬱選鏇顧壓衊積繭) = 製構襯壓鏇鹹繭積蓋顧 鬱醖獵構夢蓋選觸製壓 (網襯鏇願鹹積憲製築齋, 46) 更多 | ||||||
临床2期 | 101 | 窪膚積製積築窪築鏇網(網構簾膚艱壓衊製廠醖) = 鹽遞繭鹹淵遞廠構齋廠 膚衊觸餘積遞蓋範選淵 (鹽蓋膚製壓選廠範夢淵 ) | 积极 | 2016-11-15 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
芽仔
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用