Evidence-based medicine research of tonifying qi-blood and regulating tendon and vessel on the prevention and treatment of anemia and thrombosis on added effection of enhanced recovery after surgery of total knee arthroplasty

开始日期2024-05-24

申办/合作机构-

ChiCTR2400084010 / SuspendedN/AIIT

开始日期2024-05-09

申办/合作机构-

100 项与舒洛地特相关的临床结果

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100 项与舒洛地特相关的转化医学

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100 项与舒洛地特相关的专利（医药）

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367

项与舒洛地特相关的文献（医药）

2024-09-01·Journal of Vascular Surgery: Venous and Lymphatic Disorders

Changes of the serum properties and its effect on the endothelial cells restoration in patients with chronic venous disease treated with sulodexide

Article

作者: Jasińska-Sumińska, Katarzyna ; Urbanek, Tomasz ; Kowalska, Katarzyna ; Zieliński, Adam ; Wysocka, Teresa ; Khalil, Raouf A ; Zabel, Maciej ; Raffetto, Joseph D ; Bręborowicz, Andrzej

OBJECTIVEInflammation and endothelial dysfunction are important venous changes in patients with chronic venous disease (CVD). The use of the venoactive drugs remains an important treatment modality for patients with CVD, reducing the severity of the CVD-related symptoms and swelling but also reducing inflammation and protecting endothelial cells. In this research, the effects of the serum obtained from patients with CVD before and after sulodexide treatment were evaluated for in vivo and in vitro inflammatory markers and endothelial cell function.METHODSInflammatory markers (IL-6, matrix metalloproteinase-9 [MMP-9], vascular cell adhesion molecule-1 [VCAM-1], and von Willebrand factor [vWF]) from the incompetent great saphenous veins (GSVs) and from the systemic venous circulation were studied in 10 patients with CVD (C2s) before and after 2 months of sulodexide (2 × 500 lipasemic units/d) therapy. Serum obtained from the vein blood before and after sulodexide treatment was evaluated for in vitro cultured human umbilical vein endothelial cell function.RESULTSThe serum collected from lower leg incompetent GSVs had significantly elevated levels of VCAM-1 (+29%, P < .001) compared with the serum from the systemic circulation. Endothelial cells exposed to the serum from the incompetent lower leg veins of the untreated CVD patients demonstrated higher stimulated synthesis of MMP-9 (+17%, P < .01), as well as increased markers of senescence (prolongation of population doubling time, β-galactosidase activity, and expression of p21 and p53 genes). CVD serum-induced senescent endothelial cells had a higher expression of genes regulating IL-6, MMP-9, VCAM-1, and vWF synthesis. The overall proinflammatory effect on endothelial cells by the serum collected from the incompetent GSVs was stronger as compared with the serum from the systemic circulation. Serum collected from the veins after sulodexide treatment caused lower levels of endothelial cell inflammatory markers as well as respective gene expression than serum obtained at the beginning of the study (before sulodexide treatment). Sulodexide application also reduced the inflammatory secretory activity of the senescent endothelial cells. Sulodexide treatment resulted in the decrease of the majority of the studied inflammatory parameters in both lower limb incompetent vein and systemic blood.CONCLUSIONSIn patients with CVD, there are significant differences between circulating inflammatory markers analyzed from the lower leg incompetent GSV segments compared with the systemic circulation, indicating a higher inflammatory condition in CVD. Treatment with sulodexide reduces the proinflammatory and endothelial cell activation properties of the serum from patients with CVD.CLINICAL RELEVANCEThe study documented the significant proinflammatory human vascular endothelial cell activation when exposed to the serum collected from the varicose veins as compared with the serum from the systemic circulation in patients with chronic venous disease (CVD). The inflammatory marker expression, endothelial dysfunction, and endothelial cell senescence transformation can be successfully controlled and downregulated by patients' exposure to the glycosaminoglycan (sulodexide) treatment. Further studies are needed to confirm if glycosaminoglycan application can prevent further CVD clinical progression due to potential CVD-related pathological processes' modulation and their downregulation.

2024-09-01·Journal of Chromatography A

Structural elucidation of Sulodexide with multidimensional chromatography and online in-source acid-induced dissociation mass spectrometry

Article

作者: Tian, He ; Zhu, Wen ; Ouyang, Yilan ; Zhang, Zhenqing ; Liu, Jinqiu ; Chen, Lei ; Yi, Lin ; Wei, Yuyao

Sulodexide, a heparinoid medicine, is wildly used in clinic for prophylaxis and treatment of thromboembolic diseases and diabetic nephropathy. Despite its widespread use, the structure of Sulodexide remains poorly understood. It consists of various polysaccharides characterized by differing sugar compositions, linkages, and sulfonation patterns, yet they share common features such as strong hydrophilicity, high native charges, and considerable polydispersity, posing significant challenges for conventional chromatographic and online mass spectrometry (MS) characterization. In this work, a novel analytical method combining multiple-heart cut 2D-LC and in-source acid-induced dissociation (inAID) MS was developed. Three polysaccharides in Sulodexide were separated by high efficient strong-anion-exchange chromatography, followed by desalting with the second dimensional size-exclusion chromatography before MS. A novel MS strategy employing inAID technique was utilized for online analysis, leading to the initial identification of Sulodexide polysaccharide components. The results were validated through disaccharide composition analysis of those three polysaccharide components after offline preparation. This advanced strategy, merging various techniques, enable a comprehensive structural elucidation of such complex drugs and provides a viable tool for potential routine analysis of complex biomolecules.

2024-08-01·Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

Sulodexide protects endothelial cells against 4-hydroxynonenal-induced oxidative stress and glutathione-dependent redox imbalance by modulation of sestrin2/nuclear factor erythroid 2-related factor 2 pathway.

Article

作者: Gabryel, B ; Bontor, K

The lipid peroxidation product 4-hydroxynonenal (HNE) may be involved in vascular endothelial cell damage by induction of oxidative stress, apoptosis, and loss of redox homeostasis. There is evidence that stimulation of endothelial cells with 4-HNE induces the activation of the nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2/Keap-1) pathway. Sestrin2 protein (SESN2) is one of the key regulators of Nrf2 and is involved in the cellular response to oxidative stress. However, the function of SESN2 in HNE-induced endothelial injury is not yet understood. Sulodexide (SDX) is a mixture of glycosaminoglycans used in clinical practice in the treatment of chronic venous and arterial diseases. While SDX has well-documented endothelial protective properties, little is known about its antioxidant effects. The aim of this study was to elucidate the molecular mechanisms activated by SDX in human umbilical endothelial cells (HUVECs) under HNE-induced oxidative stress. In this experimental model, we decided to evaluate the anti-apoptotic and antioxidant potential of SDX and its effect on the SESN2/Nrf2/GSH pathway. HUVECs were treated with 25 _M HNE or HNE combined with 0.5 LRU/mL SDX for 4 hours. Cell viability, apoptosis and intracellular reactive oxygen species (ROS) production were assessed by MTT assay and fluorescence microscopy. The expressions of Bax, cleaved caspase-3, Keap-1 and Nrf2 were determined by Western blot analysis. The intracellular concentrations of reduced glutathione (GSH) and oxidized glutathione (GSSG) were measured by colorimetric assay. SESN2, glutamate-cysteine ligase catalytic subunit (GCLc) and glutathione synthase (GSS) were assessed using ELISA. RT-qPCR was performed to detect Nrf2, GCLc and GSS mRNA levels. Transient Nrf2 silencing was obtained by short interfering RNA (siRNA). We have demonstrated that SDX can reduce the negative impact of HNE on HUVECs. SDX significantly protected HNE-treated HUVECs from apoptosis (p<0.001) and oxidative stress (p<0.001). SDX treatment significantly reduced Bax (p<0.05) and cleaved caspase-3 (p<0.01) expression. Co-administration of HNE and SDX increased GSH content (p<0.001) and GSH:GSSG ratio (p<0.001) as well as decreased SESN2 concentration (p<0.001) and Nrf2 (p<0.01), GCLc (p<0.05) and GSS (p<0.01) gene expression compared with the HNE group. Moreover, we revealed a negative correlation between SESN2 levels and GSH concentrations (p<0.001). Nrf2 silencing significantly decreased the effect of HNE and SDX on the induction of GCLc and GSS genes. SDX also significantly ameliorated the increase of nuclear Nrf2 in response to HNE (p<0.05). The results confirmed that SDX may protect against HNE-induced endothelial damage through its antioxidant effect and modulation of the SESN2/Nrf2/GSH signaling pathway.

项与舒洛地特相关的新闻（医药）

2024-11-03

·奇点网

一个个的都不干好事儿！

*仅供医学专业人士阅读参考如果说免疫“热肿瘤”的微环境是同仇敌忾、让癌细胞四面楚歌，那有些以免疫抑制性强出名的冷肿瘤，微环境就是离心离德、全员内鬼了，各种名字前面挂着“肿瘤相关”的细胞都争当带路党，巨噬细胞、中性粒细胞、成纤维细胞们的罪行奇点糕都批判过好多回了，但今天要开庭审判的又换了一个对象——肿瘤相关内皮细胞（TECs）。近日，空军军医大学高源、张英起、张红梅及张存等研究者在Journal of Hepatology发表了最新研究成果，揭示趋化因子CXCL12表达阳性的TECs可促进肝细胞癌（HCC）对免疫治疗耐药，它们既能通过分泌CXCL12，阻碍CD8+幼稚T细胞向CD8+细胞毒性T细胞分化，又能吸引髓系来源的免疫抑制细胞（MDSCs），以两种途径介导免疫抑制，而针对CXCL12进行干预，如以双特异性抗体同时靶向CXCL12和PD-1，则有良好的抑癌作用[1]。一图总结论文核心内容其实从TECs的命名就能看出，它们与肿瘤新生血管有着密切的关系，而在HCC中最早应用的靶向药物就是抗血管生成类药物，因此TECs早早就进入了科研工作者的视野[2]。但在HCC也逐步走进免疫治疗时代后，对TECs作用的认知也是时候翻新一下了[3]，而以HCC微环境的一贯特点，TECs在影响抗肿瘤免疫应答方面，大概率也不是什么正面角色。空军军医大学研究者们首先分析了一个接受PD-1抑制剂治疗的前瞻性HCC患者队列，并从中挑选了两例患者组织样本（均为HBV相关性HCC，1例对免疫治疗有应答，1例未应答），进行单细胞核RNA测序（snRNAseq）和空间转录组学分析，并在未应答患者中识别出了一类与免疫应答相关通路下调，与患者生存预后直接相关的TECs亚群（TECsp）。识别TECsp这一特殊亚群的过程借助外部数据证实TECsp在HCC中普遍存在，且其水平与肿瘤内CD8+T细胞和髓系细胞数量均显著相关后，研究者们就开始分析它们对免疫应答施加负面影响的机制，对比免疫激活和免疫抑制状态的肿瘤免疫细胞组分显示，TECsp往往与CD8+幼稚T细胞和MDSCs并存。细胞相互作用分析则提示，TECsp主要通过CXCL12及其相应配体CXCR4影响其它免疫细胞，而且是HCC微环境内CXCL12的主要分泌源，所以研究者们就将TECsp改称为CXCL12+TECs。空间转录组学分析显示，CXCL12+TECs主要存在于肿瘤边缘部位，且更靠近免疫细胞，它们也基本仅在对免疫治疗不应答的HCC患者肿瘤内富集。CXCL12+TECs主要存在于对免疫治疗不应答的HCC患者肿瘤内而由于在CD8+T细胞中，只有CD8+幼稚T细胞存在CXCR4的特异性高表达，研究者们推测CXCL12+TECs主要影响的对象就是CD8+幼稚T细胞，并通过空间转录组学分析证实了这种猜测，且基因集富集分析显示，CXCL12-CXCR4信号主要影响了与T细胞分化相关的基因和信号通路；细胞实验显示，用CXCL12处理健康人的CD8+幼稚T细胞，就足以打断它们向CD8+细胞毒性T细胞分化的进程，使细胞毒性标志物（如IFN-γ）水平显著下降。CXCL12+TECs可阻碍CD8+幼稚T细胞分化进程，使HCC内CD8+细胞毒性T细胞浸润显著减少此外，由于MDSCs也同样普遍高表达CXCR4，CXCL12+TECs还可通过CXCL12-CXCR4信号将它们吸引到HCC微环境内，发挥免疫抑制作用，那不针对CXCL12进行干预就说不过去了。为了更好地配合现有HCC免疫治疗，研究者们直接一步到位地设计了CXCL12/PD-1双特异性抗体，在实验中取得了良好的抑癌效果，期待它能在后续的临床研究中一展身手吧。CXCL12/PD-1双特异性抗体的设计要点和初步实验表现参考文献：[1]Lu Y, Liu Y, Zuo X, et al. CXCL12+ Tumor-associated Endothelial Cells Promote Immune Resistance in Hepatocellular Carcinoma[J]. Journal of Hepatology, 2024.[2]Wicki A, Rochlitz C, Orleth A, et al. Targeting tumor-associated endothelial cells: anti-VEGFR2 immunoliposomes mediate tumor vessel disruption and inhibit tumor growth[J]. Clinical Cancer Research, 2012, 18(2): 454-464.[3]Nagl L, Horvath L, Pircher A, et al. Tumor endothelial cells (TECs) as potential immune directors of the tumor microenvironment–new findings and future perspectives[J]. Frontiers in cell and developmental biology, 2020, 8: 766.本文作者丨谭硕

免疫疗法

2024-10-25

·Insight数据库

显著降低患者致残率！中国原创脑卒中新药最新数据公布

10 月 24 日，北京天坛医院王拥军教授牵头的一项中国原创脑卒中新药研究 TASTE-2 在世界卒中大会上（WSC）以口头报告形式发表。数据显示：急性缺血型卒中患者在血管内取栓治疗前，联合依达拉奉右莰醇（先必新®）进行脑细胞保护，显著改善了患者 90 天时恢复神经功能独立的患者比例，降低了患者致残比例。脑卒中是我国成年人致死、致残的首位病因，缺血性脑卒中（AIS）约占全部脑卒中的 70%。而其中，又有约四成患者属于大血管闭塞型（large vessel occlusion，LVO）这一危险亚型，致残、致死率更高。卒中发生后，以溶栓、取栓为代表的「再灌注」治疗，能尽快恢复大脑供血。血管内取栓术 (EVT) 是近年来再灌注治疗的重要进展，可为约 70%~ 90% 的 LVO 型卒中患者实现血流再通，但只有近一半的患者功能恢复良好。仍有相当比例 EVT 患者在治疗 90 天后存在不同程度的残疾。先必新®（依达拉奉右莰醇注射用浓溶液）是先声药业自主研发的多靶点脑细胞保护剂，国家 1 类新药。该药物含依达拉奉和右莰醇两种活性成分，可高效透过血脑屏障，通过抗炎和清除自由基双效协同，减少 AIS 引发的级联损伤，并将现有治疗时间窗从 24 小时延长至 48 小时。今年 9 月，该药获美国 FDA 授予「突破性疗法认定」，用于治疗急性缺血性脑卒中（AIS）。 2024WSC 上的口头报告显示，一项多中心、双盲、随机、安慰剂对照的 TASTE-2 研究入组了 1362 名接受 EVT 治疗的中-重度卒中患者。在 EVT 前使用脑细胞保护剂依达拉奉右莰醇治疗，对比安慰剂，患者 90 天后功能评分 2 以下的比例为 55.0% vs. 49.6%，差异具有统计学意义，且安全性良好。这表明，卒中取栓前给予脑细胞保护，可进一步改善大血管闭塞型卒中患者的治疗结局，帮助他们恢复自理能力。 TASTE-2 研究的最新结果，为先必新®作为多靶点脑细胞保护策略联合再灌注治疗急性缺血性脑卒中提供了关键性临床医学证据。封面来源：企业 Logo 免责声明：本文仅作信息分享，不代表 Insight 立场和观点，也不作治疗方案推荐和介绍。如有需求，请咨询和联系正规医疗机构。编辑：馨药 PR 稿对接：微信 insightxb 投稿：微信 insightxb；邮箱 insight@dxy.cn 多样化功能、可溯源数据…… Insight 数据库网页版等你体验点击阅读原文，立刻解锁！

突破性疗法临床研究

2024-10-24

·先声药业

TASTE-2研究亮相世界卒中大会先必新®联合取栓显著降低卒中致残

2024年10月24日，北京天坛医院王拥军教授牵头的一项中国原创脑卒中新药研究TASTE-2在世界卒中大会上（WSC）以口头报告形式发表：急性缺血型卒中患者在血管内取栓治疗前，联合依达拉奉右莰醇（先必新®）进行脑细胞保护，显著改善了患者90天时恢复神经功能独立的患者比例，降低了患者致残比例。 10月24日，北京天坛医院王拥军教授在阿联酋阿布扎比举行的第16届WSC大会最新科学研究（Late Breaking and SRT)专场做口头报告取栓+先必新® 进一步为卒中减残脑卒中是我国成年人致死、致残的首位病因，缺血性脑卒中（AIS）约占全部脑卒中的70%。而其中，又有约四成患者属于大血管闭塞型（large vessel occlusion，LVO）这一危险亚型，致残、致死率更高。卒中发生后，以溶栓、取栓为代表的“再灌注”治疗，能尽快恢复大脑供血。血管内取栓术 (EVT)是近年来再灌注治疗的重要进展，可为约 70%~ 90%的LVO型卒中患者实现血流再通，但只有近一半的患者功能恢复良好。仍有相当比例EVT患者在治疗90天后存在不同程度的残疾。 2024WSC上的口头报告显示，一项多中心、双盲、随机、安慰剂对照的TASTE-2研究入组了1362名接受EVT治疗的中-重度卒中患者。在EVT前使用脑细胞保护剂依达拉奉右莰醇治疗，对比安慰剂，患者90天后功能评分2以下的比例为55.0% vs. 49.6%，差异具有统计学意义，且安全性良好。这表明，卒中取栓前给予脑细胞保护，可进一步改善大血管闭塞型卒中患者的治疗结局，帮助他们恢复自理能力。 TASTE-2主要疗效结果：治疗组与安慰剂组患者功能独立 (90天mRS 0~2分)比例有显著差异，OR=1.24 (1.00-1.54)，p=0.047；RR=1.11 (1.00–1.23)，p=0.047 先必新®（依达拉奉右莰醇注射用浓溶液）是先声药业自主研发的多靶点脑细胞保护剂，国家一类新药。该药物含依达拉奉和右莰醇两种活性成分，可高效透过血脑屏障，通过抗炎和清除自由基双效协同，减少AIS引发的级联损伤，并将现有治疗时间窗从24小时延长至48小时。作为全球脑卒中治疗领域自2015年来唯一获批上市销售的创新药，该药物历时12年研发，并获得2次国家科技部“重大新药创制”专项支持。 TASTE-2研究的最新结果，为先必新®作为多靶点脑细胞保护策略联合再灌注治疗急性缺血性脑卒中提供了关键性临床医学证据，也引发了国际学术界的现场热烈讨论。新证据拓展“脑细胞保护”认知根据卒中治疗学术界圆桌会议 (STAIR) 的建议，脑细胞保护剂可减少缺血性脑损伤，尤其是在与取栓联合时可产生协同作用。各国科学界也都曾长期致力于研究卒中治疗的脑细胞保护剂。然而针对卒中复杂的病理生理机制，单靶点药物疗效有限，临床开发有较大困难。与之相对应的，是多靶点脑细胞保护剂在临床上不断取得进展。此前，北京天坛医院王拥军教授团队主导的TASTE研究，以及北京大学第三医院樊东升教授牵头的TASTE-SL研究，分别证实了依达拉奉右坎醇注射剂型，以及舌下片剂型对非取栓AIS患者的疗效。相关数据于2021年和2024年发表在国际神经病学顶级期刊STROKE（《卒中》）和JAMA Neurology（《美国医学会神经病学杂志》），为医学界重启了卒中脑细胞保护研究的大门。依达拉奉右坎醇舌下片也于近日获美国食品药品监督管理局（FDA）“突破性疗法认定”，用于AIS治疗，是全球脑卒中治疗领域首个被FDA认定为突破性疗法的创新药。天坛医院王拥军教授与王春娟教授代表研究团队在WSC现场介绍TASTE-2研究最新发现为探究脑细胞保护与EVT的结合是否能为取栓的卒中患者带来更多获益，王拥军教授团队又进一步推动了TASTE-2研究，证实了AIS患者在取栓前使用先必新®可进一步获益，以新的临床证据不断拓展着科学对“脑细胞保护”的认知。未来，先必新®有望作为取栓等血管内治疗的联合用药，在再灌注之前给药，进一步提升卒中治疗效果，减少卒中致残。先声药业（2096.HK）是一家创新与研发驱动的制药公司，拥有“神经与肿瘤药物研发全国重点实验室”。本公司重点聚焦抗肿瘤、神经科学、自身免疫及抗感染领域，同时积极前瞻性布局未来有重大临床需求的疾病领域，致力于让患者早日用上更有效药物。本公司以自主研发及协同创新双轮驱动，与多家创新企业、科研院校建立战略合作伙伴关系。 www.simcere.com 撰稿 | 李逸玲编辑 | 郭菁菁审校 | 冯晓飞王岚审核 | 宋洋吴奕涵

申请上市临床结果

100 项与舒洛地特相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D08547	舒洛地特	B01AB11	DB06271

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
动脉粥样硬化	中国	Alfa Wassermann SpA	2003-08-15
糖尿病并发症	中国	Alfa Wassermann SpA	2003-08-15
血栓形成	中国	Alfa Wassermann SpA	2003-08-15

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
静脉血栓栓塞	临床2期	波兰	Alfa Wassermann SpA	-
静脉血栓栓塞	临床2期	葡萄牙	Alfa Wassermann SpA	-
静脉血栓栓塞	临床2期	斯洛伐克	Alfa Wassermann SpA	-
静脉血栓栓塞	临床2期	意大利	Alfa Wassermann SpA	-
静脉血栓栓塞	临床2期	捷克	Alfa Wassermann SpA	-
2型糖尿病	临床1期	荷兰	Keryx Biopharmaceuticals, Inc.	2005-08-01
2型糖尿病	临床1期	澳大利亚	Keryx Biopharmaceuticals, Inc.	2005-08-01
2型糖尿病	临床1期	美国	Keryx Biopharmaceuticals, Inc.	2005-08-01
糖尿病肾病	临床1期	澳大利亚	Keryx Biopharmaceuticals, Inc.	2005-08-01
糖尿病肾病	临床1期	荷兰	Keryx Biopharmaceuticals, Inc.	2005-08-01

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临床结果

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


Code Large Vessel Occlusion Process (ISC2024)	N/A	闭塞 RACE score ≥ 5 \| aphasia \| visual field cut ... 更多	-	Code Large Vessel Occlusion Process (MER with code LVO activation)	網鏇艱鏇艱積憲蓋蓋醖(顧繭壓製窪壓遞壓鏇選) = 齋餘網積夢蓋醖鏇膚鹹窪簾膚窪醖遞餘餘製窪 (廠製廠鹹繭糧衊構築襯 ) 更多	不佳	2024-02-01
AUA2021	N/A	并发症	-	Bipolar vessel sealing system	遞夢鏇糧鑰齋淵繭壓選(觸窪築蓋憲艱壓製範淵) = 鹹衊遞窪憲糧壓夢製網遞簾範窪壓憲艱範鏇醖 (範觸顧壓繭簾廠獵繭淵 ) 更多	-	2021-09-01
				BIPOLAR VESSEL SEALING SYSTEM (Silk ligation)	遞夢鏇糧鑰齋淵繭壓選(觸窪築蓋憲艱壓製範淵) = 鑰窪淵衊醖顧築範繭製遞簾範窪壓憲艱範鏇醖 (範觸顧壓繭簾廠獵繭淵 ) 更多
ISTH2021	N/A	血栓栓塞	-	Sulodexide	願鏇膚顧餘襯築製製醖(製鹽餘顧蓋夢繭鑰範鹽) = 鬱範艱壓膚淵顧觸鑰構願鑰顧壓構廠顧膚製窪 (積顧遞顧蓋壓製壓夢膚 )	-	2021-07-17
ISTH2020	N/A	-	-	Sulodexide	顧鏇壓齋選範構積築廠(衊鬱齋餘鏇網壓壓憲襯) = 觸壓鑰壓鏇糧觸壓範繭糧鹹簾繭觸醖廠齋繭齋 (製醖艱襯齋廠網積遞獵 )	-	2020-07-12
				Porcine Heparin	顧鏇壓齋選範構積築廠(衊鬱齋餘鏇網壓壓憲襯) = 繭鏇繭廠窪膚餘齋遞範糧鹹簾繭觸醖廠齋繭齋 (製醖艱襯齋廠網積遞獵 )
ISTH2020	N/A	-	-	Parenteral Sulodexide	顧繭蓋鑰網鬱衊鏇簾蓋(願顧選衊鏇鹽衊選廠鑰) = 艱鑰繭鬱簾範鹽衊襯繭艱遞艱鑰繭醖網衊顧簾 (鹹壓製廠積鹽蓋夢廠艱 )	-	2020-07-12
				Saline	顧繭蓋鑰網鬱衊鏇簾蓋(願顧選衊鏇鹽衊選廠鑰) = 遞鬱餘鹽窪壓襯簾齋鑰艱遞艱鑰繭醖網衊顧簾 (鹹壓製廠積鹽蓋夢廠艱 )
NCT00130208 (CTgov)	临床3期	2型糖尿病 \| 糖尿病肾病	1,056	Sulodexide (Sulodexide)	壓鑰襯觸蓋願選繭獵觸(糧鏇淵蓋遞製顧衊願觸) = 繭鬱顧窪窪衊糧選廠窪遞選壓襯夢淵積構蓋憲 (選憲築壓選鑰遞艱遞膚, 鹹選積膚鏇簾鏇網願窪 ~ 廠糧鹹鹽齋淵壓鏇選顧) 更多	-	2018-03-23
				Placebo (Placebo)	壓鑰襯觸蓋願選繭獵觸(糧鏇淵蓋遞製顧衊願觸) = 願築齋願餘鹽積窪願衊遞選壓襯夢淵積構蓋憲 (選憲築壓選鑰遞艱遞膚, 遞選鏇鏇壓簾鹹襯顧艱 ~ 鹽願膚遞艱醖網淵淵願) 更多
NCT01295775 (DRESS, Pubmed \| Graefes Arch Clin Exp Ophthalmol)	临床2期	非增殖性糖尿病视网膜病变	130	Sulodexide	(鏇廠窪膚鹹餘蓋選製簾) = 製餘築顧築蓋壓蓋壓顧遞製範繭顧醖衊遞醖憲 (壓遞膚獵構獵鏇製鹹醖 )	积极	2015-06-01
				Placebo	(鏇廠窪膚鹹餘蓋選製簾) = 網簾鑰鑰憲鏇蓋網簾繭遞製範繭顧醖衊遞醖憲 (壓遞膚獵構獵鏇製鹹醖 )
FP585 (ERA2015)	N/A	-	6	Sulodexide	範蓋憲鏇憲艱蓋鬱鑰醖(製繭醖製願襯簾鬱範鏇) = 鹹選艱築窪憲鹹廠製製鹹網願鹽繭鏇築衊鏇觸 (網衊餘蓋觸簾積鹽遞獵 )	积极	2015-05-21
ASN2014	N/A	-	-	Sulodexide treatment	(艱鹹簾窪鏇範壓蓋構衊) = 積網壓鏇顧鹹艱獵簾艱夢蓋願憲顧製鬱糧遞衊 (膚願壓選製夢選窪願網, -3.9 ~ -0.8) 更多	积极	2014-11-11
NCT00130208 (Pubmed \| Am J Kidney Dis)	临床3期	2型糖尿病肾脏病	1,056	Sulodexide	選遞憲蓋膚糧構夢蓋鏇(齋壓廠鹹壓醖鑰夢獵鏇) = 襯選鬱簾鹹衊鏇鹹襯積廠餘窪夢繭夢蓋廠築淵 (淵淵築鏇蓋鹽廠觸網簾 ) 更多	不佳	2011-11-01
				Placebo	選遞憲蓋膚糧構夢蓋鏇(齋壓廠鹹壓醖鑰夢獵鏇) = 鏇築繭顧夢艱鑰獵顧壓廠餘窪夢繭夢蓋廠築淵 (淵淵築鏇蓋鹽廠觸網簾 ) 更多