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

开始日期2024-03-20

申办/合作机构

Shahid Beheshti University of Medical Sciences

100 项与碳酸司维拉姆相关的临床结果

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100 项与碳酸司维拉姆相关的转化医学

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100 项与碳酸司维拉姆相关的专利（医药）

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331

项与碳酸司维拉姆相关的文献（医药）

2026-01-01·EUROPEAN 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.

2025-12-01·CLINICAL 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.

2025-09-01·JOURNAL OF RENAL NUTRITION

Gastrointestinal Mucosal Cell Injury Caused by Sevelamer Crystals: Case Series and Literature Review

Review

作者: Ali, Umair ; Singh, Manisha ; Karakala, Nithin ; Elbahnasawy, Enas ; Elkalashy, Ahmed ; Rainwater, Randall R

In end-stage kidney disease (ESKD), hyperphosphatemia occurs secondary to decreased renal elimination with continued intestinal absorption of dietary phosphate. Even in chronic kidney disease, glomerular filtration rate lower than 30 mL/min markedly decreases the filtration of inorganic phosphate and increases its serum level. Sevelamer, a noncalcium phosphate binder, is commonly used to control hyperphosphatemia. Available in 2 forms, sevelamer hydrochloride and sevelamer carbonate, it absorbs phosphate in the gastrointestinal tract and is known to have minimal adverse effects. These are limited to nausea, vomiting, flatulence, and metabolic acidosis, with infrequent significant adverse outcomes. We present a series of 2 patients with ESKD on sevelamer, with lower gastrointestinal bleeding and endoscopic findings of colonic mucosal injuries with histopathological findings of sevelamer crystals deposition. Although reported in gastrology literature, nephrology reports show a paucity of discussion around this increasingly common adverse effect and the need for vigilance in ESKD.

176

项与碳酸司维拉姆相关的新闻（医药）

2026-07-28

·梅斯医学

碳酸司维拉姆干混悬剂：高效安全降磷，延缓血管钙化

引言我国慢性肾脏病（CKD）疾病负担沉重，成人患病率已达10. 8%1，患病总人数约1.56亿2。高磷血症是CKD患者常见并发症之一，其患病率随肾功能下降而急剧攀升，显著增加CKD患者心血管事件及全因死亡的发生风险。因此，主动、严格管控血磷，延缓血管钙化进程，对改善CKD患者预后、降低心血管死亡率有重大的临床意义1。 1 我国CKD高磷血症管理面临两大难题：血管钙化风险高、用药负担重 1.1 CKD 患者血管钙化高发且风险严峻血磷升高贯穿CKD全程1，是血管钙化的重要因素之一。血磷每升高1 mg/dL，心血管事件风险增加20%3、4。我国透析患者血管钙化患病率77.4%5，高于国际报道的平均水平（68.5%）6。血磷水平与冠状动脉、主动脉及瓣膜钙化患病率呈正相关7，其多部位血管钙化患病率超过50%8。CKD G3a期至G5期已存在血管或瓣膜钙化的患者，心血管事件风险最高9。图1：血磷水平与冠状动脉、主动脉及瓣膜钙化患病率相关性图2：CKD患者中多部位血管钙化患病率 ♥ ♥ ♥ 1.2 磷结合剂约占日服药五成，加重CKD患者用药负担磷结合剂是目前临床治疗CKD高磷血症的常用药物，透析患者平均每天服用10. 8片磷结合剂，占每日总服药量的近一半10，用药负担较重。此外，目前常用磷结合剂在口服便利性和药物安全性上仍有不足之处，降磷疗效或患者用药依从性仍有较大提升空间11。图3：CKD患者不同药物片剂负荷比例 2 碳酸司维拉姆干混悬剂：高效降磷并延缓血管钙化 2.1 碳酸司维拉姆干混悬剂覆盖成年CKD患者全周期血磷管控，高效降磷 Meta分析表明，与安慰剂相比，碳酸司维拉姆可显著降低血磷水平12。图4：Meta分析中碳酸司维拉姆与安慰剂对比在非透析患者中，一项纳入202例中国CKD非透析高磷血症患者的III期随机对照研究证实，治疗8周后，碳酸司维拉姆组血磷水平较安慰剂组显著下降，疗效明确13。图5：CKD非透析者血清磷相对基线的均值（标准误）变化在维持性血液透析患者中，一项为期3个月的随机对照研究比较了碳酸司维拉姆与含钙磷结合剂的疗效。结果显示，碳酸司维拉姆组的总有效率为91.3%，钙磷代谢指标控制也更优14。图6：透析患者疗效与钙磷代谢的临床观察可见，对于成年CKD非透析及透析患者，使用碳酸司维拉姆可得到较好的钙磷调节和血磷控制。 ♥ ♥ ♥ 2.2 碳酸司维拉姆干混悬剂延缓血管钙化，为CKD患者带来肾心双重获益碳酸司维拉姆对血管钙化的疗效已有研究证明。Meta分析显示，与含钙磷结合剂相比，使用碳酸司维拉姆等非含钙磷结合剂的患者冠状动脉钙化评分更低15。图7：Meta分析中冠状动脉钙化情况（纳入18项研究，其中8项涉及冠状动脉钙化评分）另一项52周随机对照试验证明使用碳酸司维拉姆后，冠状动脉钙化积分的百分比由0变化为6%，对应主动脉钙化积分由1%变化为5%，钙化进展被延缓16。图8：含钙磷结合剂与碳酸司维拉姆治疗26周、52周后钙化积分百分比变化临床硬终点中，3年期前瞻性队列研究（966名非透析CKD G4 - G5期患者）指出：相较于未接受碳酸司维拉姆治疗的患者，接受碳酸司维拉姆治疗的患者全因死亡风险降低了33%17。图9：碳酸司维拉姆治疗组与非碳酸司维拉姆治疗组患者的生存曲线比较此外，一项针对非透析CKD合并高磷血症患者的真实世界研究表明：使用碳酸司维拉姆治疗时，肾脏替代治疗启动率比用含钙磷结合剂减少16%，主要不良心血管事件发生风险减少9%18。图10：含钙磷结合剂组与碳酸司维拉姆组患者RRT、MACE终点的Kaplan-Meier生存曲线对比 3 碳酸司维拉姆干混悬剂与片剂控磷疗效相当，与原研参比剂等效，服用更安心碳酸司维拉姆的降磷效果呈现剂量依赖性：若每日用2.4g、4.8g或7.2g剂量，血磷减少分别为0.87、1.27、2.01mg/dL19。血磷控制不佳患者往往需提升片剂给药剂量以达标，然而片剂因剂型体积大、口感粗糙等，易导致老年等CKD患者吞咽障碍，显著降低长期治疗依从性，不利于长期规范管理血磷。图11：碳酸司维拉姆不同剂量组从基线到治疗结束血磷的平均变化干混悬剂以冲服方式给药，既保证疗效，又方便剂量调整，可有效提升患者用药依从性与便利性。在临床疗效方面，碳酸司维拉姆干混悬剂在降磷疗效上与同剂量片剂相当20，且与原研参比制剂相比生物等效21。一项多中心、随机、交叉设计研究显示，干混悬剂与片剂在血磷控制方面具有一致的临床效果20。图12：干混悬剂与片剂血磷水平随时间的变化（纳入31例血液透析患者）在安全性方面，三期研究显示碳酸司维拉姆干混悬剂治疗相关不良事件发生率仅9.7%，低于盐酸司维拉姆片剂的22.6%。此外，碳酸司维拉姆片剂胃肠道不良事件发生率也低于盐酸司维拉姆片剂，干混悬剂整体胃肠道耐受更优20 。图13：不同司维拉姆制剂不良事件发生率总结 ◆ 碳酸司维拉姆干混悬剂作为非钙非金属磷结合剂，覆盖成年CKD患者全病程血磷管理，有效调节钙磷代谢，实现血磷高效管控、心肾双重获益 ◆ 碳酸司维拉姆干混悬剂高效安全降磷的同时不增加钙负荷，有效降低心血管不良事件的发生风险 ◆ 干混剂型为吞咽困难及老年等CKD患者提供了更优的给药选择，显著提高患者长期治疗依从性参考文献： [1] 慢性肾脏病高磷血症临床管理中国专家共识(2025版)工作组, 等. 慢性肾脏病高磷血症临床管理中国专家共识(2025版)[J]. 中国血液净化, 2025, 24(7): 529-547 [2] He G, et al. Chronic kidney disease burden from 1990 to 2023 in China: national and provincial insights from the Global Burden of Diseases study 2023. Lancet Reg Health West Pac. 2025 Dec 19; 68: 101776 [3] Cozzolino M, et al. Role of calcium-phosphate product and bone-associated proteins on vascular calcification in renal failure. J Am Soc Nephrol. 2001 Nov;12(11):2511-2516 [4] Martin KJ, et al. Metabolic bone disease in chronic kidney disease. J Am Soc Nephrol. 2007 Mar;18(3):875-85. [5] Liu ZH, et al; China Dialysis Calcification Study Group. Prevalence and risk factors for vascular calcification in Chinese patients receiving dialysis: baseline results from a prospective cohort study. Curr Med Res Opin. 2018 Aug;34(8):1491-1500. [6] Yao Z, et al. Prevalence of abdominal artery calcification in dialysis patients with end-stage renal disease: a systematic review and meta-analysis. Int Urol Nephrol. 2017 Nov;49(11):2061-2069. [7] Adeney KL, et al. Association of serum phosphate with vascular and valvular calcification in moderate CKD. J Am Soc Nephrol. 2009 Feb;20(2):381-7. [8] Hutcheson JD, et al. Cardiovascular Calcification Heterogeneity in Chronic Kidney Disease. Circ Res. 2023 Apr 14;132(8):993-1012. [9] Zhang H, et al. Progression of Vascular Calcification and Clinical Outcomes in Patients Receiving Maintenance Dialysis. JAMA Netw Open. 2023 May 1;6(5):e2310909. [10] Fishbane SN, et al. Phosphate Absorption and Hyperphosphatemia Management in Kidney Disease: A Physiology-Based Review. Kidney Med. 2021 Aug 27; 3(6): 1057-1064. [11] 《中国高磷血症医患诊疗现状蓝皮书》. 2026-01-22. [12] Zeng Q, et al. Meta-analysis of the efficacy and safety of sevelamer as hyperphosphatemia therapy for hemodialysis patients. Ren Fail. 2023 Dec; 45(1): 2210230. [13] Chen W, et al. Efficacy and Safety of Sevelamer Carbonate in Chinese Nondialysis Chronic Kidney Disease Patients with Hyperphosphatemia: A Randomized, Double-Blind, Parallel-Group Study. Kidney Dis (Basel). 2022 Dec 15;9(2):82-93. [14] 刘康,赵锦,王凡,等.司维拉姆与醋酸钙治疗维持性血液透析患者高磷血症的效果对比[J].四川大学学报(医学版),2025,56(3):798-803. [15] Jamal SA, et al. Effect of calcium-based versus non-calcium-based phosphate binders on mortality in patients with chronic kidney disease: an updated systematic review and meta-analysis. Lancet. 2013 Oct 12;382(9900):1268-77. [16] .Chertow GM, et al. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int. 2002 Jul;62(1):245-52 [17] Molina P, et al. Nephrol Dial Transplant. 2022; 37 (Supplement 3): i397-i398. [18]Li P, et al. Real-World Evidence for Sevelamer vs Calcium-Containing Phosphate Binders in Long-Term Effectiveness and Safety Among Patients with Non-Dialysis CKD: The REVEAL Study. Adv Ther. 2026 Apr 15. [19] Moustafa M, et al. A randomized, double-blind, placebo-controlled, dose-ranging study using Genz-644470 and sevelamer carbonate in hyperphosphatemic chronic kidney disease patients on hemodialysis. Int J Nephrol Renovasc Dis. 2014 Apr 7;7:141-52.. [20] Fan S, et al. A randomized, crossover design study of sevelamer carbonate powder and sevelamer hydrochloride tablets in chronic kidney disease patients on haemodialysis. Nephrol Dial Transplant. 2009 Dec; 24(12): 3794-9 [21] 司维拉姆干混悬剂BE实验数据——非公开免责声明：本文仅作最新前沿信息交流之目的，仅供医疗卫生行业专业人士阅读参考，文中所有观点不代表梅斯医学立场，亦不代表梅斯医学支持或反对文中观点。如需获得治疗方案指导，请前往正规医院就诊！

2026-07-24

·药通社

复杂铁剂，正大天晴争首仿

7月18日，江苏知原药业的枸橼酸铁片的上市申请被受理，这是江苏知原药业第二次申请此品种上市。 2024年1月，江苏知原药业提交了枸橼酸铁片上市申请，历经2年多审评，在今年2月被下发了通知件，当时此品种给了资料发补的机会，但最终未成功上市。几个月后，江苏知原药业重新提交了上市申请，枸橼酸铁片原研未上市，目前也只有江苏知原在挑战此品种。枸橼酸铁片，顾名思义就是含铁制剂，但它不是补铁剂，而是一款治疗慢性肾病（CKD）患者高磷血症的药物，用含铁制剂吸附胃肠道的磷是肾科常用的方式。另一款更有名的铁制剂降磷产品是蔗糖羟基氧化铁咀嚼片，这两款药都属于铁基-非钙磷结合剂，肾科用药，成分相似，命运相似，同属于研发难度高，仿制难度大的品种。仿制药立项已经到了立无可立的地步，这种治疗领域偏窄，难度偏高的品种也开始被关注。更多立项建议然而这两款药仿制进展都不太顺利。先来看一下枸橼酸铁片，这一品种虽然目前只有江苏知原药业有提交上市，但在十年前，扬子江，恒瑞这些大公司都获得过这一品种的临床批件，可惜进度都搁置了。江苏知原药业在2019年到2022年完成了疗效和安全性III期临床试验，又过了两年，在2024年提交了上市申请。其实除了江苏知原药业之外，泰州朗润也完成了III期临床试验，2023年底完成，但到了现在也没有提交上市。国内有一款枸橼酸铁胶囊已上市，原研是台湾宝龄富锦生技，今年4月才在国内获批上市，属于进口5.1类，台湾宝龄富锦生技与山东威高合资成立山东威高宝龄制药，负责国内商业化。从这些停滞和失败的研究就可以看出枸橼酸铁口服制剂难度颇高。蔗糖羟基氧化铁咀嚼片难度也不遑多让，2023年2月，此品种进口注册获批，持证商为瑞士Vifor Fresenius，填补国内12-18岁CKD4-5期或接受透析治疗的CKD患儿的降磷药物空白。蔗糖羟基氧化铁咀嚼片为儿童提供了降血磷药物，当时上市时走的优先审批。 6月23日，丽彩药业的蔗糖羟基氧化铁咀嚼片上市失败，继南京恒生之后，这款复杂制剂再次有企业冲击首仿失败。图源：摩熵医药这款产品目前尚有正大天晴、民生药业、四川国为、昂利康、湖南明瑞、湖南埃威格林的上市申请在审。经查询，只有正大天晴的上市申请进入了资料发补阶段，其余的都进度缓慢。陕西丽彩和湖南明瑞还有一款蔗糖羟基氧化铁颗粒，已提交了3类仿制申请，选择的参比制剂依旧是Vifor公司产品，只怕也不简单。这两款药难在哪里显而易见，首先是原料药难度，蔗糖羟基氧化铁属于复杂化学原料，要求与制剂关联申报。而至今没有谁家仿制成功，原研是纯进口，暂无企业的原料药顺利转A。图源：CDE 枸橼酸铁没有列入举例，但与复杂化学原料共性太多，大概率也归属于这类，目前只有台湾宝龄富锦生技已经转A，该企业的胶囊剂已上市。其次是生物等效性研究难度，这两款铁制剂FDA都发过指导原则，略有不同，但综合就是难在生物等效性研究。蔗糖羟基氧化铁咀嚼片做不了体内生物利用度试验，该药成分几乎不入血，体内生物利用度试验主要靠得就是测血药浓度，对一款几乎不入血的产品而言，测血药浓度毫无意义。蔗糖羟基氧化铁咀嚼片FDA指导原则只推荐两项体外研究，体外平衡结合试验和体外动力学结合试验。从指导要求看，3个PH值控制下，多个样本，每15分钟检测，每项重复12次的要求，加起来是相当大的工作量，且要求完整药片进行试验，蔗糖包裹的多核羟基氧化铁本身就会因为处方工艺变动而出现波动。枸橼酸铁则有两个，方案一：体外生物等效性研究（对比溶出度）和方案二：两项体外生物等效性研究（磷酸盐结合）以及一项比较性临床终点生物等效性研究。江苏知原药业没有登记BE临床试验，大概率也选了体外生物等效性研究。这两款铁制剂虽然治疗领域偏窄和专业，但是相对应的竞品也少，临床常用竞品仅司维拉姆和碳酸镧都已被集采，铁基-非钙磷结合剂在国内销量增长很快，自是进入了仿制企业的视野。蔗糖羟基氧化铁咀嚼片与司维拉姆片相比，磷结合能力是后者的2.6倍，适合儿童等，上市后市场也很好，2023年就被纳入了国家谈判目录，国内商业化由康哲药业负责，2024年销售额七千多万，2025年销售额就到了2.6亿。而枸橼酸铁片，降磷的同时还能补铁，台湾宝龄富锦生技枸橼酸铁胶囊2026年国谈初审已通过。目前就看进度最快的正大天晴这一首仿收割机，凭借其强悍研发实力，能否顺利获批了。这类高壁垒的固体制剂难在哪里？又该如何突破？ 9月4日，CMC固体制剂大会，现场交流 ↓⭐关注药通社，洞见行业趋势↓

2026-07-24

·制药网

7 月下旬，礼邦医药、恒瑞医药等密集发布临床喜讯

【制药网行业动态】 2026年以来，国内药企在新药临床方面进展密集。7月下旬，又有多家企业集中披露了临床试验获批或取得积极数据的公告，覆盖了从代谢、抗感染到肿瘤等多个治疗领域。　　近日，礼邦医药宣布，其口服泛磷转运蛋白抑制剂AP306用于接受维持性血液透析的高磷血症患者的全球IIb期多区域临床试验(NCT06712654)已完成首例受试者随机入组并给药。该试验正在美国及中国的多个临床中心开展，由礼邦医药与R1Therapeutics,Inc.("R1")共同申办。　　AP306是一款口服泛磷转运蛋白抑制剂，由日本中外制发现，礼邦医药获授权引进并取得其全球开发、生产及商业化权利。该IIb期试验是一项多中心、随机、双盲、安慰剂对照研究，计划招募约168名接受维持性血液透析的高磷血症受试者，研究旨在评估固定剂量AP306的安全性、耐受性及降低血清磷的效果。　　据悉，在从前已完成的中国II期临床试验(NCT05764590)中，AP306单药治疗组的血清磷水平较基线平均降低2.51mg/dL，而试验中的阳性对照药碳酸司维拉姆组平均降低1.08mg/dL。此外，中国国家药品监督管理局也已于2024年6月授予其用于治疗慢性肾脏病患者高磷血症的突破性治疗药物认定。　　7月23日，中国生物制药发布公告，公司附属公司正大天晴开发的国家 1 类创新药(886015)IM-101 注射液 "PreS1 重组融合蛋白 " 已获得中国国家药品监督管理局 ( NMPA ) 的临床试验批准，拟用于治疗慢性乙型肝炎 ( CHB ) 。　　IM-101 是一款靶向 PreS1 的创新型重组融合蛋白，具有打破免疫耐受、重建慢性乙型肝炎病毒 ( HBV ) 特异性免疫应答的潜力。该药若能顺利落地，将进一步丰富公司在主动免疫治疗领域的管线布局，并为更广泛的肝病患者提供多元化的治疗选择。　　7月20日，恒瑞医药宣布，GLP-1/GIP双重受体激动剂瑞普泊肽(HRS9531，大中华区外称KAI-9531)注射液治疗中国2型糖尿病初治人群的Ⅲ期临床试验 (HRS9531-302)取得积极顶线结果，主要终点及所有关键次要终点均达到优效。　　瑞普泊肽是一款新型靶向GIPR和GLP-1R的双激动剂，其用于成人长期体重管理的上市申请已于2025年9月获国家药监局受理。恒瑞医药计划近期在中国提交瑞普泊肽注射液用于成人2型糖尿病患者血糖控制的新药上市申请(NDA)。　　除了以上企业，近期悦康药业、康缘药业等企业也已披露了临床新进展。业内分析认为，这波新药临床密集获批，以及临床进展覆盖了从传统生物药到前沿核酸药物的多元技术路线，充分体现出国产创新药正从“仿制跟随”向“源头创新”的明确转向。　　免责声明：在任何情况下，本文中的信息或表述的意见，均不构成对任何人的投资建议。

100 项与碳酸司维拉姆相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D06642	碳酸司维拉姆	V03AE02	DB00658

研发状态

批准上市

10 条最早获批的记录,

后查看更多信息

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	Sanofi Winthrop Industrie SA	2015-01-15
慢性肾病-矿物质和骨骼疾病	冰岛	Sanofi Winthrop Industrie SA	2015-01-15
慢性肾病-矿物质和骨骼疾病	列支敦士登	Sanofi Winthrop Industrie SA	2015-01-15
慢性肾病-矿物质和骨骼疾病	挪威	Sanofi Winthrop Industrie SA	2015-01-15
高磷血症	欧盟	Sanofi Winthrop Industrie SA	2009-06-09
高磷血症	冰岛	Sanofi Winthrop Industrie SA	2009-06-09
高磷血症	列支敦士登	Sanofi Winthrop Industrie SA	2009-06-09
高磷血症	挪威	Sanofi Winthrop Industrie SA	2009-06-09
慢性肾病	美国	Genzyme Corp.	2007-10-19

未上市

10 条进展最快的记录,

后查看更多信息

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	南京恒生制药有限公司	2015-05-04
继发性甲状旁腺功能亢进症	临床3期	美国	Genzyme Corp.	2010-04-01
终末期肾脏病	临床3期	美国	Genzyme Corp.	2006-01-01
心血管疾病	临床2期	英国	Genzyme Corp.	2009-02-01
2型糖尿病	临床阶段不明	丹麦	Sanofi	2014-02-01

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临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04485039 (CTgov)	临床4期	天花	44	Tecovirimat (TPOXX: Oral Antiviral)	築築齋鬱壓鑰憲觸淵簾(艱齋遞壓淵繭鹽鬱願蓋) = 醖艱遞範構膚淵衊願簾壓築糧鹹選廠願簾願積 (鑰網襯憲範鑰襯構選獵, 39.6) 更多	-	2024-10-09
				Tecovirimat+sevelamer carbonate oral tablet (TPOXX: Oral Antiviral and Sevelamer Carbonate)	齋壓蓋齋鏇窪糧繭壓蓋(淵築鹹選築製鏇獵鬱獵) = 憲觸築醖壓範憲築壓鬱顧網範鬱鏇選築壓遞獵 (願餘鑰鹹壓鏇構網鬱鑰, 壓淵蓋淵顧憲蓋築鹹鬱 ~ 選鬱窪鬱築齋製餘艱壓) 更多
NCT03644264 (Pubmed)	临床3期	高磷血症	286	Sucroferric oxyhydroxide	獵簾膚糧築網積壓製範(鑰艱鑰夢夢願艱選構夢) = 觸鑰衊醖衊壓襯襯遞淵醖艱壓鑰選積築齋網壓 (憲範膚夢製膚網窪憲顧 )	积极	2023-07-20
				Sevelamer carbonate	獵簾膚糧築網積壓製範(鑰艱鑰夢夢願艱選構夢) = 艱壓夢餘獵膚觸憲獵窪醖艱壓鑰選積築齋網壓 (憲範膚夢製膚網窪憲顧 )
NCT03988920 (NORMALIZE, CTgov)	临床4期	高磷血症 \| 终末期肾脏病	172	Sevelamer Carbonate+Tenapanor (Tenapanor w/Sevelamer)	製築簾積壓鬱構糧衊憲 = 遞壓顧獵襯壓遞獵窪齋餘簾蓋選積襯蓋壓觸夢 (窪鬱夢顧選壓廠齋壓積, 範鹹窪醖鑰憲艱構蓋夢 ~ 醖繭齋壓獵襯糧製餘願) 更多	-	2023-03-29
				Sevelamer Carbonate+Tenapanor (Sevelamer w/Tenapanor)	製築簾積壓鬱構糧衊憲 = 觸窪醖積壓餘鹽醖繭顧餘簾蓋選積襯蓋壓觸夢 (窪鬱夢顧選壓廠齋壓積, 夢鬱齋願夢築觸範觸夢 ~ 鬱網範築製範鏇廠蓋蓋) 更多
ASN2022	N/A	慢性肾病 hyperphosphatemia	-	Sevelamer	醖遞憲衊築蓋艱壓鬱鬱(構夢鬱鏇襯膚範夢窪醖): HR = 0.84 (95% CI, 0.79 ~ 0.91) 更多	积极	2022-11-05
				Sevelamer (Cardiopulmonary Bypass (CPB))
NCT03001011 (RECOVER \| P0880, CTgov)	临床3期	高磷血症 \| 慢性肾病	202	Placebo (Placebo)	鑰鑰構艱簾繭構觸觸製(網鏇齋鹹醖憲蓋蓋鑰鹹) = 齋廠築廠鏇遞網衊壓顧積膚網範襯廠範鑰鑰糧 (積鹹鹽鏇願淵範壓醖餘, 衊願顧艱遞窪衊醖鬱鹽 ~ 獵艱糧鹽鬱製糧鑰廠憲) 更多	-	2020-07-28
				Sevelamer Carbonate (GZ419831) (Renvela)	鑰鑰構艱簾繭構觸觸製(網鏇齋鹹醖憲蓋蓋鑰鹹) = 顧鹽餘獵遞壓簾糧鹽築積膚網範襯廠範鑰鑰糧 (積鹹鹽鏇願淵範壓醖餘, 衊窪壓簾壓餘網顧襯齋 ~ 蓋觸遞鏇願顧遞窪製夢) 更多
NCT01574326 (Pubmed \| Pediatr Nephrol) 人工标引	临床2期	高磷血症 \| 慢性肾病	66	sevelamer carbonate	憲蓋選範鑰選醖鑰鏇製(蓋鑰蓋鏇艱膚遞鑰鬱襯): difference = -0.90, P-Value = 0.001 更多	积极	2018-02-01
				Placebo
NCT01220843 (FRENCH, Pubmed) 人工标引	临床3期	慢性肾病	96	Sevelamer	壓廠構淵構構醖餘選鑰(膚夢繭鹹選窪鏇鬱餘淵) = 製願遞築鏇選鹹構餘膚鬱範遞顧糧製夢衊鹽顧 (範膚製糧蓋壓餘顧鏇顧 )	不佳	2017-12-07
				Placebo	壓廠構淵構構醖餘選鑰(膚夢繭鹹選窪鏇鬱餘淵) = 鹹範觸鹽範艱糧糧憲繭鬱範遞顧糧製夢衊鹽顧 (範膚製糧蓋壓餘顧鏇顧 )
NCT01238588 (CTgov)	N/A	高磷血症 \| 炎症 \| 动脉粥样硬化斑块	24	Renvela+Sevelamer Carbonate	簾壓壓遞構襯簾膚衊繭(醖鬱廠願窪餘願襯壓積) = 觸糧壓範繭膚觸鬱醖鬱蓋遞糧衊製窪鑰蓋艱夢 (鑰積壓製夢鏇淵簾鏇壓, 製構築鹹醖鬱築範夢衊 ~ 糧鹽積蓋糧夢製繭構製) 更多	-	2017-06-21
NCT00999037 (CTgov)	N/A	继发性甲状旁腺功能亢进症 \| 慢性肾病	18	Sevelamer Carbonate (Renvela)	遞齋糧鑰鏇顧鏇顧構鏇(餘鬱築遞糧衊願蓋顧鑰) = 繭網構鑰壓顧積糧範網襯憲壓願製製選簾襯鏇 (廠襯醖糧獵觸製選遞蓋, 41) 更多	-	2017-03-31
				Placebo (Placebo)	遞齋糧鑰鏇顧鏇顧構鏇(餘鬱築遞糧衊願蓋顧鑰) = 選網鏇艱鬱獵壓夢衊衊襯憲壓願製製選簾襯鏇 (廠襯醖糧獵觸製選遞蓋, 46) 更多
NCT01574326 (phase 2 study, ASN2016)	临床2期	高磷血症 \| 慢性肾病	101	Sevelamer Carbonate	糧糧遞窪齋憲獵廠積淵(憲窪淵窪糧鹹壓蓋淵製) = 淵糧齋網鹽願醖繭願鏇簾繭蓋鹹鬱餘網範壓選 (簾繭繭淵網範襯顧糧艱 )	积极	2016-11-15