The investigator-initiated international clinical trial on efficacy and safety of recombinant factor VIIa for hyperacute intracerebral hemorrhage - FASTEST

开始日期2022-07-20

申办/合作机构-

NCT03496883

/ Recruiting临床3期IIT

Recombinant Factor VIIa (rFVIIa) for Acute Hemorrhagic Stroke Administered At Earliest Time (FASTEST) Trial

The objective of the rFVIIa for Acute Hemorrhagic Stroke Administered at Earliest Time (FASTEST) Trial is to establish the first treatment for acute spontaneous intracerebral hemorrhage (ICH) within a time window and subgroup of patients that is most likely to benefit. The central hypothesis is that rFVIIa, administered within 120 minutes from stroke onset with an identified subgroup of patients most likely to benefit, will improve outcomes at 180 days as measured by the Modified Rankin Score (mRS) and decrease ongoing bleeding as compared to standard therapy.

开始日期2021-12-03

申办/合作机构

National Institute of Neurological Disorders & Stroke

[+1]

NCT04444856

/ CompletedN/A

Clinical Outcomes of NovoSeven® Treatment in Severe Postpartum Haemorrhage - a Retrospective Single-centre Cohort Study at the University Hospital of Bern

This non-interventional study will compare the clinical outcomes in women with an event of severe postpartum haemorrhage treated with NovoSeven® to clinical outcomes in women with an event of severe postpartum haemorrhage not treated with NovoSeven®. The study will be a single centre retrospective cohort study of women with an event of severe postpartum haemorrhage, defined as 1.5 L of blood loss within 24 hours of delivery, in the period of 2005-2016.

开始日期2020-06-29

申办/合作机构

Novo Nordisk A/S

100 项与依他凝血素α 相关的临床结果

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100 项与依他凝血素α 相关的转化医学

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100 项与依他凝血素α 相关的专利（医药）

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项与依他凝血素α 相关的文献（医药）

2025-12-31·PLATELETS

Management of a twin pregnancy patient with Glanzmann thrombasthenia might be caused by a novel ITGA2B gene mutation (c.2822G>A): a case report and family investigation

Article

作者: Li, Ping ; Liao, Xiangcheng ; Yang, Zhigang ; Liu, Liling ; Huang, Yucong ; Mo, Zhuning ; Zhu, Ruikai ; Qin, Aiqiu

Mutations in the ITGA2B or ITGB3 gene that encodes for the αIIbβ3 platelet integrin usually cause Glanzmann thrombasthenia (GT). This study aims to investigate the clinical characteristics of a pedigree exhibiting an inherited hemorrhagic disorder resembling GT, elucidate its molecular pathogenesis and evaluate the efficacy of blood management strategies for a proband who is pregnant with twins. The clinical data of the pedigree with inherited hemorrhagic disorder were collected, including the assessment of clinical, laboratory and thromboelastography (TEG) profiles. DNA samples were obtained for next-generation sequencing, encompassing the exons and flanking sequences of the ITGA2B and ITGB3 genes, as well as other genes associated with blood and immune deficiency. Bioinformatics software tools, such as PolyPhen-2, SIFT and MutationTaster, were employed to analyze the functional impact of mutations. Protein structural models for the new mutation type were generated using PyMOL. The phenotype of the proband in this pedigree with inherited platelet dysfunction and bleeding disorder was in accordance with GT. The proband shows persistent blood accumulation in the uterine cavity. Laboratory findings indicate normal PLT morphology, PLT count, MPV, and PDW. However, there is a decreased PLT aggregation induced by agonists ADP, collagen, and AA while maintaining a normal response to ristocetin. The initial TEG examination results indicated that the patient presented with a hypocoagulable state, characterize d by a reduction in α angle (46.9), an extended K value (4.6) and a decreased maximum amplitude (35.1). The younger sister demonstrated comparable TEG performance to that of the proband and has a documented history of abnormal bleeding. A novel heterozygous mutation of ITGA2B at position c.2822 G>A (p.Trp941*) was identified in the proband and her familial counterparts-father, brother and sister. MutationTaster software predicted the new mutation to be pathogenic; however, PolyPhen-2 and SIFT software did not provide correlated predictions. The p.Trp941* mutation resulted in the premature termination of translation at residue 940Trp, leading to impaired protein function. Successful management was achieved during the perioperative period by administration of human immunoglobulin, platelets and antifibrinolytic drugs, followed by recombinant factor VIIa (rFVIIa), according to the thromboelastography tracings. The laboratory findings of the proband are consistent with GT, and a novel mutation in the ITGA2B gene at position c.2822 G>A (p.Trp941*) has been identified as a potential cause of GT. However, since GT is a recessive disorder and both the proband and her family members are heterozygous, it cannot be excluded that they may possess additional bleeding risk factors, including the presence of other undetected variants. This study also illustrates the significance of multidisciplinary planning, TEG analysis and judicious utilization of rFVIIa to minimize operative bleeding risk.

2025-07-01·Neurohospitalist

Factor XIa Inhibitor Reversal in Intracranial Hemorrhage: A Case Report

Article

作者: Strohm, Tamara ; Key, Nigel ; Smalley, Sierra ; John, Kayla ; Jones, Lee Ann ; Al-Obeidi, Arshed ; Garavito, Draia

Background/Objectives:

There is currently no consensus regarding the optimal strategy for reversal of anticoagulation in life-threatening hemorrhage associated with factor XIa (FXIa) inhibitors.

Methods:

For this clinical case report, informed consent was obtained from surrogate.

Results and Discussion:

Here, we present the case of an 82-year-old female who sustained a large subdural hematoma after a fall. Her aPTT on admission was elevated at 90.4 s and remained persistently prolonged at 90.9 s 12-hour after receiving an adequate dose of 4-factor prothrombin complex concentrate (PCC). She was found to have received a factor XIa inhibitor in a clinical trial, and subsequently received recombinant activated factor VII (rFVIIa) 2 mg (45 mcg/kg) as a one-time dose, and tranexamic acid (TXA) 1 g intravenously for reversal given her intracranial bleeding in the setting of trauma complicated by recent factor XIa inhibitor use. However, given her clinical decline and high surgical risk, the patient’s family elected to withdraw care and she expired three days later. Reversal of FXIa inhibitors is challenging but may best be achieved using a combination of rFVIIa and TXA.

Practical Implications:

Clinicians should consider administration of low dose recombinant activated factor VII (rFVIIa) in conjunction with an anti-fibrinolytic inhibitor such as tranexamic acid (TXA) for reversal of life-threatening hemorrhage in bleeding patients with exposure to novel factor XIa inhibitors that are currently in clinical trials.

2025-07-01·THROMBOSIS RESEARCH

In vitro effects of Mim8 and combined Mim8-bypassing therapy on thrombin generation, thromboelastography and fibrin clot ultrastructure

Article

作者: Dargaud, G Yesim ; Nougier, Christophe ; Josset, Laurie ; Lund, Jacob ; Rezigue, Hamdi

INTRODUCTION:

Mim8, a fully human bispecific IgG4 antibody, FVIIIa mimetic, which emerges as a promising prophylactic treatment option for patients with hemophilia A (HA).

AIM:

This study investigates the in vitro hemostatic activity of Mim8 in blood samples from six patients with severe hemophilia A using a thrombin generation assay (TGA) and thromboelastography. The results were compared to those obtained with emicizumab.

MATERIALS AND METHODS:

TG was assessed in both platelet-poor (PPP) and platelet-rich plasma (PRP). Fibrin clots formed during TG were collected, and clot ultrastructure was examined using scanning electron microscopy (SEM). Whole blood samples were analyzed using ROTEM-NATEM.

RESULTS:

Mim8 significantly improved the TG capacity of severe HA plasma samples. Mim8 6 μg/mL demonstrated higher TG capacity compared to emicizumab 50 μg/mL. In PRP samples fortified with Mim8 6 μg/mL and rFVIIa 90 μg/kg together, ETP levels were fully normalized. No synergistic effect was observed when FVIII concentrate was combined with Mim8 at therapeutic doses due to the higher affinity of FVIII for FIXa and FX compared to Mim8. ROTEM-NATEM in whole blood confirmed the TGA results. SEM showed a more robust fibrin clot structure with thinner fibrin fibers in the presence of Mim8 compared to emicizumab.

CONCLUSIONS:

Mim8 significantly improves TG in vitro in both PPP and PRP from patients with severe HA, with ETP levels comparable to those of FVIII at 100 IU/dL. The TGA can effectively monitor the combined treatment with Mim8 and either rFVIIa or APCC, which is not possible with currently available routine laboratory tests.

项与依他凝血素α 相关的新闻（医药）

2025-05-07

·PRNewswire

TiumBio and Daewon Pharmaceutical Successfully Complete Phase 2 Clinical Trial of 'Merigolix (TU2670/DW4902)' for Uterine Fibroids

Primary Endpoint Met: Statistically significant reduction in heavy menstrual bleeding achieved in all dosage of Merigolix groups compared to placebo Broader Therapeutic Potential: Positive Phase 2 results in both uterine fibroids and endometriosis could place Merigolix as a strong best-in-class candidate for novel drug approval and global licensing opportunities Multi-Indication Development: Clinical trials are underway for three indications enhancing the asset value-uterine fibroids, endometriosis, and assisted reproductive technology (ART), the latter in collaboration with Hansoh Pharma in China SEONGNAM, South Korea, May 7, 2025 /PRNewswire/ -- TiumBio (KRX: 321550.KQ), a clinical-stage biopharmaceutical company focused on discovering and developing innovative therapeutics for patients with rare and incurable disease, today announced that Merigolix (code name: TU2670, Daewon's code name: DW4902) has successfully met the primary endpoint of reducing heavy menstrual bleeding in a Phase 2 clinical trial for uterine fibroids. In this trial, Merigolix demonstrated statistically significant improvements across all dosage groups compared to placebo in patients with uterine fibroids. Merigolix is an investigational, once-daily, oral gonadotropin-releasing hormone (GnRH) receptor antagonist. Unlike traditional GnRH agonists, which require injection and often lead to an initial hormone surge, Merigolix offers a more patient-friendly oral administration without an initial hormonal flare, providing a faster onset of action and improved treatment adherence. The Phase 2 clinical trial of Merigolix in uterine fibroids was conducted by TiumBio's partner, Daewon Pharmaceutical, and enrolled a total of 71 women diagnosed with uterine fibroids. Participants were randomly assigned to receive high, medium, or low doses of Merigolix, or placebo, administered orally once daily for 12 weeks, followed by a 12-week observation period. The results showed that Merigolix led to statistically significant improvements in heavy menstrual bleeding (HMB)—a validated clinical endpoint—across all dosage groups compared to the placebo. In addition to the primary endpoint, Merigolix demonstrated statistically and clinically meaningful improvements in several key secondary endpoints, including fibroid size reduction, increased hemoglobin levels (indicating improved anemia), and relief of pelvic pain. The safety and tolerability profile of Merigolix was consistent with prior clinical data, with no new safety signs. The mechanism of action of Merigolix can be used in various disorders, including endometriosis, uterine fibroids, ART, precocious puberty, and prostate cancer. Notably, in a separate Phase 2 clinical trial for endometriosis completed in 2024, Merigolix also showed excellent therapeutic efficacy and safety, further reinforcing its potential as a promising new treatment. "We are very excited that Merigolix has demonstrated excellent therapeutic efficacy not only in endometriosis but also in uterine fibroids," said Hun-Taek Kim, Ph.D., MBA, CEO of TiumBio. "successfully achieving both efficacy and safety in Phase 2 significantly increases the probability of regulatory approval and licensing opportunities. We plan to accelerate development and expand into the global uterine fibroid treatment market," he added. "Uterine fibroids are a condition that causes significant suffering for many women, and we believe Merigolix has the potential to become an important new oral treatment that addresses this unmet medical need," said Jonathan In Baek, President of Daewon Pharmaceutical. "We are pleased with the positive results in uterine fibroids and will continue our efforts to provide patients with a convenient and effective new treatment option," he continued. Uterine fibroids are benign tumors that develop in the uterus, primarily affecting women of reproductive age, particularly those in their 30s and older. The condition has a high prevalence rate of approximately 20% among women over the age of 35. The most common symptom is heavy menstrual bleeding, but it can also cause abnormal uterine bleeding, pelvic pain, and anemia. Meanwhile, TiumBio entered into a licensing agreement with Daewon Pharmaceutical in 2019, granting Daewon the rights to develop and commercialize Merigolix in South Korea. About TiumBio Co., Ltd. TiumBio (KRX: 321550.KQ) is a clinical-stage biopharmaceutical company focused on the discovery and development of innovative therapeutics for patients with rare and incurable diseases. Its mission is to expand the hope and happiness of mankind through our science. TiumBio has three leading pipeline assets: Merigolix (code name: TU2670), TU2218, and TU7710, all in various stages of clinical development. Merigolix is a once-daily, oral GnRH receptor antagonist being developed for the treatment of endometriosis, uterine fibroids, and assisted reproductive technology. TU2218 is a first-in-class oral immune-oncology therapy targeting TGF-β and VEGF pathways to promote response rates in cancer patients when used in combination with immune checkpoint inhibitors. TU7710 is a novel rFVIIa designed to extend its half-life in order to provide more clinical benefits to hemophilia patients with inhibitors. With its expertise in drug development, TiumBio is committed to the discovery and development of innovative treatments to ease the burden of debilitating diseases. For further information, visit our website at and connect with us on LinkedIn. Contacts: Junseok Jang, Head of Corporate Communications & Investor Relations [email protected] Da-ye Song, Manager, Corporate Communications & Investor Relations [email protected] SOURCE TiumBio WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

临床结果引进/卖出临床2期免疫疗法

2025-04-24

·FierceBiotech

Bioxodes halts phase 2 stroke trial after successful interim review, plots registrational study

BIOX-101 is derived from a protein found in the salivary glands of a tick. \n Bioxodes has stopped enrolling people in a phase 2a stroke study after hitting the safety and efficacy endpoints, positioning the Belgian biotech to power into a potentially registrational trial.The interim phase 2a analysis included data on 16 intracerebral hemorrhagic stroke (ICH) patients. Some patients received a single intravenous dose of BIOX-101, also known as Ir-CPI, on top of standard of care. Other people only received standard of care. Bioxodes’ primary endpoints looked at safety outcomes. The biotech’s secondary endpoints assessed efficacy in the 10 days after randomization.At the interim analysis, the biotech saw positive changes in hematoma and edema volume, a secondary efficacy endpoint, and said inflammation biomarkers were encouraging. No patients died, and no serious adverse events were attributed to the drug. The treatment was well tolerated with no signs of increased bleeding.Hans Warrinnier, chief medical officer at Bioxodes, said in a statement that the results are preliminary but all point in the right direction. The biotech believes generating more phase 2a data won’t change the interim conclusions, leading it to stop enrollment in the study early. Bioxodes will now start raising a series B financing round and making BIOX-101 ready for a phase 2b trial. The process will take around one year, Bioxodes CEO Marc Dechamps said, putting the company on track to start enrolling patients in the potentially pivotal study in the first half of 2027. Bioxodes said the phase 2b could support filings for conditional marketing authorization in the U.S. and Europe before 2030.BIOX-101 is derived from a protein found in the salivary glands of a tick. The tick secretes the protein to stop the host’s blood from clotting and allow it to feed. Repurposed for treating ICH, the approach could tackle blood clots without causing bleeding. There are currently no approved treatments for ICH. Efforts to change that include a phase 3 study of recombinant factor VIIa (rFVIIa) that has an estimated complete date of January 2028. An earlier phase 3 trial found rFVIIa failed to improve survival or functional outcomes. That trial allowed patients to receive rFVIIa up to four hours after stroke onset. The ongoing rFVIIa trial has a treatment window of two hours.

临床结果临床2期临床3期

2025-03-22

·DrugAI

KGML-xDTD：基于知识图谱的药物治疗预测和机制描述机器学习框架

今天我想给大家介绍的论文是《KGML-xDTD: A Knowledge Graph-based Machine Learning Framework for Drug Treatment Prediction and Mechanism Description》，是一个基于知识图谱的机器学习框架，用于药物再利用预测和作用机制解释。一、背景传统药物开发是一个耗时的过程，从最初的化学鉴定到临床试验，最后到食品药品监督管理局批准，大约需要10-15年，并伴随着数十亿美元的投资开销和较高的失败率。考虑到新型疾病进化的速度很快，人们迫切需要找到一种更高效、更经济的药物发现方法。好消息是，一种药物通常可以有效治疗多种疾病。例如，沙利度胺最初被用作抗焦虑药物，后来人们发现它有治疗癌症的能力。因此，药物再利用也被称为“探索现有药物的新用途”，寻求“老药新用”的可能性，可为我们带来希望。阅读大量的文献后，我找到了一个不错的方法——KGML-xDTD：一种基于知识图谱的机器学习框架，用于可解释地预测治疗疾病的药物。它有两个模块，第一个模块可以预测某种药物治疗某种疾病的概率，第二个模块可以通过知识图谱的路径从生物学上解释该药物的作用机制。它可以有效减少“黑箱”问题，进一步加速新兴疾病药物研发的进程。二、数据准备首先是数据准备。随着生物医学数据库的可用性不断提高，将数据整合到生物医学知识图谱(Biomedical Knowledge Graph) 用于药物发现的做法近年变得流行起来。本方法采用的BKG是RTX-KG2c（the canonicalized version of the Reasoning Tool X Knowledge Graph 2），它是最大的开源BKG之一，包含约640万个节点和3930万条边，整合了约70个公共生物医学数据源，其中所有生物学概念（例如“布洛芬”）都表示为顶点，所有谓词概念（例如“布洛芬 - 增加 - GP1BA 基因的活性”）都表示为边。经过数据清洗后，剩下3659165个节点（33 个不同类别，如图）和18291237条边（74个不同类别）。除了RTX-KG2c，作者还用其他人工制作的数据和NLP衍生的数据集扩展BKG数据。 Ground Truth采用DrugMechDB，这是第一个由人工整理的基于路径的数据库，用于解释从一种药物到一种疾病的作用机制，其中有3593条路径，对应3327个独特的药物-疾病对。这些路径是从DrugBank、维基百科和其他文献中提取，然后由专家整理，保证权威。作者通过Node Synonymizer函数将它们与RTX-KG2c中使用的结点和边匹配。由于KGML-xDTD预测的作用机制路径的长度固定为3，即一共涉及4个结点。所以作者规定若这4个结点都完整出现在同一条DrugMechDB路径中，则被认为是正确匹配的路径。三、模型模块模型框架由两个模块组成：一个是药物再利用预测模块，另一个是作用机制路径预测模块，利用强化学习，有四个可学习的网络。首先看药物再利用预测模块，输入药物A和疾病B，输出药物A可用于治疗疾病B的概率。对于每个节点，其嵌入的向量信息为节点属性和节点邻域。节点属性信息由PubMedBERT模型提供，这是一种针对生物医学文本设计的预训练语言模型，根据节点名称和类别为每个节点生成节点属性嵌入。节点邻域信息由GraphSAGE提供。之后，使用PCA将每个节点的嵌入向量压缩到100维，然后药物A和疾病B的向量拼接起来，形成一个更长的向量，作为随机森林模型的输入。随机森林模型将每个药物-疾病对输出为“不治疗”、“治疗”和“未知”类别之一，并给出每个类别的概率。当药物再利用预测模块确定了药物A能治疗疾病B，另一个至关重要的问题随之而来：我们能否从生物学上解释这个预测？A到底是通过什么方法治疗B的？这就用到了作用机制路径预测模块。首先需要有“演示路径（Demonstration Paths，如图）”作为强化学习的指导，即一组生物学上可能的路径（如药物K-> 基因G -> 蛋白质P-> 疾病D），它们是作者依照一定标准从BKG中提取出来的，一共396705条，演示路径可以辅助结点移动。该模块的最终会输出n条路径来解释A如何治疗B。强化学习模型采用对抗性演员-评论家（Adversarial Actor-Critic）模型，其奖励如公式所示。从药A结点开始，不断移动，最终会停留到某一个结点——反复重复这个过程。如果最终停留到疾病B，则奖励为1；如果停留到某个疾病结点，且被药物再利用预测模块归为“治疗”类，则奖励为该模块给出的治疗概率ptreat，证明该路径的起始药物可以治疗一些潜在疾病，但还没有被人们发现；如果停留到某个疾病结点，且被药物再利用预测模块归为“非治疗”类，则奖励为0；如果最终留到某个和疾病无关的结点，则奖励为-1，代表错误决策。对抗性演员-评论家强化学习模型由四个子网络组成，它们使用相同的多层感知机架构，但每个子网络有自己独立的参数，如图： i代表每一个子网络的id：1）i为a时代表Actor网络——主要目标是学习一个路径寻找策略，智能体能够根据奖励指导自己在BKG中找到最佳路径。2）i为c时代表Critic网络——主要目标是估计在当前状态st下，采取动作at后所能获得的预期奖励QΦ(st,at)。3）i为p时代表Path Discriminator网络——主要目标是解决强化模型仅在路径终点收到奖励的问题，增加了中间奖励，具体操作为判别一个路径片段是来自演示路径（正样本）还是Actor网络自己生成的路径（负样本），通过提供判别结果并给予正负奖励，引导 Actor 网络寻找更合理的生物学的路径。4）i为m时代表Meta-Path Discriminator网络——该网络也提供了一个中间奖励，具体操作为判别一个Actor网络自己生成的路径（负样本）和来自演示路径（正样本）是否相似来给予正负奖励，如果相似则负样本就可以转变成正样本，从而增强Actor网络探索路径的能力。Path Discriminator网络、Meta-Path Discriminator网络提供的中间奖励与到达路径终点收到最终奖励并称为综合奖励。四、结果作者采用基于分类准确性的指标——Accuracy、Macro F1 score与基于排序的指标——平均倒数排名（Mean Reciprocal Rank，计算第一个相关答案的倒数排名，MRR越高，表示真实正样本在排序中越靠前）和前K名排名比例（Hit@K，计算真实正样本出现在前K个预测中的比例，Hit@K越高代表预测越准确）。对于药物再利用模块的概率预测，使用了八个基于知识图谱的药物再利用。SOTA模型作为baseline，和KGML-xDTD及其变体进行比较，结果如图所示：八个baseline的实验超参数如图所示：五、实际案例为了进一步评估KGML-xDTD模型在药物再利用预测与作用机制路径预测上的表现，作者通过两个不同的案例研究来展示该模型的潜力。两个案例研究关注的是两种罕见遗传病，即血友病B（Hemophilia B）和亨廷顿舞蹈症（Huntington’s disease）。血友病B也被称为IX因子缺乏症或圣诞病，是一种罕见的遗传性疾病，患者容易发生持续性出血。它是由位于X染色体上的IX因子（F9）基因的突变引起的。该表列出了由KGML-xDTD模型预测的前十种药物/治疗方法，包括在训练集中使用的药物（用红色标出）和未在训练集中使用的药物：除了训练集中已知的药物/治疗方法外，列表中剩下的七种药物/治疗方法大部分得到了已发布的研究支持，并有潜力用于治疗血友病B。例如，活化的人源性凝血因子VII（Factor VIIa）和重组活化因子VII（rFVIIa）是促进血液凝固的关键蛋白，凝血酶（Thrombin）是维持正常止血功能的关键酶，作为Ground Truth的DrugMechDB仅提供了Eptacog Alfa和Nonacog Alfa这两种治疗血友病B的药物作用机制路径，如图右半部分所示；作者使用它们与KGML-xDTD给出的前10条BKG路径解释路径进行比较，如图左半部分所示，两者相对应的生物学实体用红色高亮显示：由于路径长度的限制以及自定义BKG中缺失某些语义关系，预测路径无法完全与DrugMechDB的路径匹配，但在预测的前10个路径的子图中，仍然可以找到对治疗血友病B至关重要的生物学实体（如factor VII, factor IX, and factor X）。

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-	依他凝血素α	B02BD08	DB00036

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适应症	国家/地区	公司	日期
出血	澳大利亚	Novo Nordisk Pharmaceuticals Pty Ltd.	2013-05-01
常染色体显性遗传性血小板减少症	韩国	Novo Nordisk Pharma Korea Ltd.	2010-05-31
凝血因子Ⅶ缺乏症	日本	Novo Nordisk Pharma Ltd.	2000-03-10
血友病A	日本	Novo Nordisk Pharma Ltd.	2000-03-10
血友病B	日本	Novo Nordisk Pharma Ltd.	2000-03-10
获得性血友病	美国	Novo Nordisk, Inc.	1999-03-25
血友病	欧盟	Novo Nordisk A/S	1996-02-23
血友病	冰岛	Novo Nordisk A/S	1996-02-23
血友病	列支敦士登	Novo Nordisk A/S	1996-02-23
血友病	挪威	Novo Nordisk A/S	1996-02-23
血小板无力症	欧盟	Novo Nordisk A/S	1996-02-23
血小板无力症	冰岛	Novo Nordisk A/S	1996-02-23
血小板无力症	列支敦士登	Novo Nordisk A/S	1996-02-23
血小板无力症	挪威	Novo Nordisk A/S	1996-02-23

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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
产后出血	申请上市	欧盟	Novo Nordisk A/S	2022-04-23
出血性卒中	临床3期	美国	Novo Nordisk A/S	2021-12-03
出血性卒中	临床3期	日本	Novo Nordisk A/S	2021-12-03
出血性卒中	临床3期	加拿大	Novo Nordisk A/S	2021-12-03
出血性卒中	临床3期	德国	Novo Nordisk A/S	2021-12-03
出血性卒中	临床3期	西班牙	Novo Nordisk A/S	2021-12-03
出血性卒中	临床3期	英国	Novo Nordisk A/S	2021-12-03
创伤和损伤	临床3期	美国	Novo Nordisk A/S	2005-10-01
创伤和损伤	临床3期	巴西	Novo Nordisk A/S	2005-10-01
创伤和损伤	临床3期	捷克	Novo Nordisk A/S	2005-10-01

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临床结果

适应症

分期

评价

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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


ISTH2020	N/A	血小板无力症	-	Novoseven	鬱蓋願鏇鹽選顧憲蓋鹽(淵鹹夢窪簾壓夢願簾淵) = 齋選艱憲蓋鏇淵壓鏇簾築夢獵鏇範範醖醖齋衊 (醖襯膚觸鏇襯遞範範廠 ) 更多	-	2020-07-12
EHA2015	N/A	-	-	Recombinant Activated Factor VII (NovoSeven)	鹽鏇鬱積餘艱範醖獵鏇(築襯齋繭糧鹽鹹顧鏇膚) = 顧構壓築網範顧鏇網餘膚鹹鏇淵淵鬱選餘獵鑰 (糧衊範選築製鏇製糧築 )	-	2015-05-21
NCT00710619 (DOSE, Pubmed \| Haemophilia)	N/A	血友病一线	52	recombinant activated factor VII (rFVIIa) (Paediatric patients)	願鏇壓繭構選糧繭網鹹(蓋壓觸廠遞遞淵齋鬱衊) = 簾範繭鑰築鹹範淵觸獵顧醖選壓積淵選鹹醖構 (鏇繭積製簾鑰壓觸繭鏇 )	-	2013-07-01
				recombinant activated factor VII (rFVIIa) (Adult patients)	願鏇壓繭構選糧繭網鹹(蓋壓觸廠遞遞淵齋鬱衊) = 艱選鑰齋鹹獵衊壓餘鏇顧醖選壓積淵選鹹醖構 (鏇繭積製簾鑰壓觸繭鏇 )
ASCO2012	N/A	肿瘤 \| 血友病A	-	Recombinant human activated FVII	網鏇餘蓋鹽衊積觸襯遞(夢醖顧觸膚淵觸鏇選願) = 鑰網膚醖遞願廠觸獵憲膚築蓋顧範憲繭願積齋 (選範襯鬱觸餘窪糧鹹廠 )	-	2012-05-20
NCT00127283 (Pubmed \| N Engl J Med)	临床3期	脑出血	841	Placebo	鹽繭窪鏇選繭糧淵製淵(夢積範鹽範齋淵鹽鬱淵) = 顧簾膚鹽積壓顧糧願鑰構衊艱鹹築遞願膚淵願 (襯齋積夢鹽壓淵廠憲製 ) 更多	不佳	2008-05-15
				rFVIIa 20 microg/kg	鏇鏇憲簾觸淵積鏇築鹹(蓋衊艱繭鑰網築廠醖觸) = 獵築遞鏇繭鏇鏇鏇觸網窪鏇淵膚襯築製糧顧築 (糧糧顧獵積衊憲膚壓築 )
NCT00102037 (Pubmed \| Spine (Phila Pa 1976))	临床2期	-	50	Placebo	鏇願襯艱醖壓獵願糧憲(壓憲遞鏇鏇蓋繭獵壓鹽) = 鬱壓餘繭網願蓋築獵衊鏇壓衊窪襯膚衊壓積淵 (願鹹窪簾窪壓範蓋醖齋 ) 更多	积极	2007-10-01
				30 microg/kg rFVIIa	鏇願襯艱醖壓獵願糧憲(壓憲遞鏇鏇蓋繭獵壓鹽) = 蓋窪簾鹹憲鬱憲遞鏇鑰鏇壓衊窪襯膚衊壓積淵 (願鹹窪簾窪壓範蓋醖齋 ) 更多
NCT00426803 (Pubmed \| Cerebrovasc Dis)	临床2期	脑出血	399	Recombinant activated factor VII (rFVIIa)	憲簾積鏇蓋鹽範願鑰鹹(鏇窪憲蓋醖艱鑰遞蓋繭) = 製壓鑰憲網網製衊淵窪壓積築範積夢顧廠淵鑰 (選獵淵繭齋獵糧齋願鏇 )	积极	2007-01-01
				Placebo	憲簾積鏇蓋鹽範願鑰鹹(鏇窪憲蓋醖艱鑰遞蓋繭) = 淵醖壓廠夢鹽簾鏇顧膚壓積築範積夢顧廠淵鑰 (選獵淵繭齋獵糧齋願鏇 )
NCT01562821 \| NCT01563458 \| NCT01563523 \| NCT01563471 (Pubmed \| Transfusion)	临床1/2期	纤维化 \| 创伤和损伤 \| 凝血障碍	-	Recombinant factor VIIa	壓鏇鏇鹹製築願窪餘鏇(網廠夢繭願網鹹鹽觸觸) = 齋蓋願製襯願淵積襯範鹹夢鏇糧網鹹蓋鬱艱築 (簾淵齋齋構繭衊鏇顧獵 )	-	2006-06-01
				Placebo	壓鏇鏇鹹製築願窪餘鏇(網廠夢繭願網鹹鹽觸觸) = 鹹顧夢糧艱齋鬱艱壓膚鹹夢鏇糧網鹹蓋鬱艱築 (簾淵齋齋構繭衊鏇顧獵 )
NCT01563445 (Pubmed \| Neurocrit Care)	临床2期	脑出血	40	Placebo	觸築獵窪構衊夢積積醖(夢夢衊範鏇餘獵積糧鑰) = 蓋構壓簾鬱廠襯鹽鏇醖襯網選衊鬱艱鹽顧蓋夢 (獵範網觸夢壓選鹽築鹹 )	积极	2006-01-01
NCT01601613 (Pubmed \| Blood Coagul Fibrinolysis)	临床2期	严重登革热	25	rFVIIa	網選製膚製鬱淵艱憲鹽(選獵壓淵鹹醖艱獵獵憲) = 繭鑰醖選顧選艱淵鹽網廠積範夢餘齋齋製選遞 (遞選膚窪鹹遞蓋糧膚膚 ) 更多	积极	2005-11-01
				Placebo	網選製膚製鬱淵艱憲鹽(選獵壓淵鹹醖艱獵獵憲) = 衊繭艱獵鏇齋鏇觸構鹹廠積範夢餘齋齋製選遞 (遞選膚窪鹹遞蓋糧膚膚 ) 更多