This pilot study will enroll 20 patients with septic shock and require emergent vasopressor support in the emergency department (ED). The primary objective of the study is to determine the feasibility of early peripheral administration (within 3 hours of norepinephrine initiation) of angiotensin II for treatment of septic shock in the ED

开始日期2025-01-31

申办/合作机构

University of Iowa

NCT06615102 / Not yet recruiting临床3期IIT

A Prospective Angiotensin II Versus Noradrenaline Trial for Hypotension Management to Reduce Cardiac-surgery Associated Acute Kidney Injury (PAN-AKI)

The study intervention focuses on exploring the use of angiotensin II as a primary vasopressor compared to norepinephrine in cardiac surgery patients to investigate whether angiotensin II can reduce the occurrence of moderate/severe acute kidney injury (AKI). Despite its potential, as suggested by trials involving surgical patients, there is currently no human data confirming its effectiveness in preventing moderate/severe AKI in this context. The intervention aims to address this gap by evaluating angiotensin II's impact compared to norepinephrine.

开始日期2025-01-01

申办/合作机构

Westfälische Wilhelms-Universität Münster

[+1]

NCT06487585 / Not yet recruiting临床4期

Angiotensin II as First-Line Vasopressor Therapy in Cardiac Surgery (ANG-First Trial)

The purpose of this research is to evaluate the use of Angiotensin II in patients with low blood pressure post-surgery. Your information will be collected for 28 days post the procedure and initiation of the study drug to assess for safety events and complications.

开始日期2024-08-20

申办/合作机构

University of Maryland St. Joseph Medical Center, LLC

100 项与血管紧张素II 相关的临床结果

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100 项与血管紧张素II 相关的转化医学

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100 项与血管紧张素II 相关的专利（医药）

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项与血管紧张素II 相关的文献（医药）

2025-01-01·JOURNAL OF HYPERTENSION

Vγ6/Vδ1+ γδ T cells protect from angiotensin II effects on blood pressure and endothelial function in mice

Article

作者: Shokoples, Brandon ; Comeau, Kevin ; Lewis, Julia M. ; Yoshikai, Yasunobu ; Hatano, Shinya ; Paradis, Pierre ; Mahmoud, Ahmad U.M. ; Ferreira, Nathanne S. ; Schiffrin, Ernesto L. ; Tigelaar, Robert E. ; Caillon, Antoine

Objectives::

γδ T cells mediate angiotensin II (AngII)-induced hypertension and vascular injury. γδ T cells expressing specific T-cell receptor (TCR) variable (V) γ chains develop in several waves in the thymus and migrate to specific or diverse tissues. We hypothesized that γδ T cells expressing specific Vγ subtypes in perivascular tissue mediate AngII hypertensive effects.

Methods::

C57BL/6J male mice were infused or not with AngII (490 ng/kg/min, subcutaneously) for 14 days. γδ T-cell Vγ subtypes were profiled by flow cytometry in the spleen, descending thoracic aorta with adherent perivascular adipose tissue (DTAo/PVAT) and mesenteric vessels (MV)/PVAT. Other sets of AngII-infused mice were injected with control or specific anti-Vγ6 or Vγ4 antibodies. Blood pressure (BP) was determined by telemetry, and mesenteric artery function and remodeling by pressurized myography.

Results::

Vγ6/Vδ1+ γδ T cells represented more than 50% of the γδ T-cell Vγ subtypes in DTAo/PVAT and MV/PVAT, whereas Vγ1/2+, Vγ4+ and Vγ6/Vδ1+ γδ T cells were the most abundant Vγ subtypes in the spleen. The frequency of Vγ6/Vδ1+ γδ T cells was increased at least 1.5-fold in the spleen and DTAo/PVAT, and tended to increase in MV/PVAT by AngII. A majority of Vγ6/Vδ1+ γδ T cells were activated in perivascular tissues. Vγ6/Vδ1+ γδ T-cell neutralization caused a steeper BP elevation and greater mesenteric artery endothelial dysfunction in mice infused with AngII. This was associated with more than three-fold increase in activated Vγ6/Vδ1– γδ T cells in perivascular tissues. Depletion of Vγ4+ γδ T cells did not alter AngII detrimental effects.

Conclusion::

Vγ6/Vδ1+ γδ T cells reduce the BP elevation and endothelial dysfunction induced by AngII infusion.

2024-12-31·Clinical and experimental hypertension (New York, N.Y. : 1993)

Emodin ameliorates myocardial fibrosis in mice by inactivating the ROS/PI3K/Akt/mTOR axis

Article

作者: Zhang, Yaolei ; Zhou, Longfu ; Huang, Wei ; Zou, Xinyun ; Zhou, Peiting ; Liu, Yunchuan

BACKGROUND:

Emodin is a traditional medicine that has been shown to exert anti-inflammatory and anti-oxidative effects. Previous research has indicated that emodin can alleviate myocardial remodeling and inhibit myocardial hypertrophy and fibrosis. However, the mechanism by which emodin affects myocardial fibrosis (MF) has not yet been elucidated.

METHODS:

Fibroblasts were treated with ANGII, and a mouse model of MF was established by ligation of the left anterior descending coronary artery. Cell proliferation was examined by a Cell Counting Kit-8 (CCK8) assay. Dihydroethidium (DHE) was used to measure reactive oxygen species (ROS) levels, and Masson and Sirius red staining were used to examine changes in collagen fiber levels. PI3K was over-expressed by lentiviral transfection to verify the effect of emodin on the PI3K/AKT/mTOR signaling axis. Changes in cardiac function in each group were examined by echocardiography.

RESULTS:

Emodin significantly inhibited fibroblast proliferation, decreased intracellular ROS levels, significantly upregulated collagen II expression, downregulated α-SMA expression, and inhibited PI3K/AKT/mTOR pathway activation in vitro. Moreover, the in vivo results were consistent with the in vitro. Emodin significantly decreased ROS levels in heart tissue and reduced collagen fibrillogenesis. Emodin could regulate the activity of PI3K to increase the expression of collagen II and downregulate α-SMA expression in part through the PI3K/AKT/mTOR pathway, and emodin significantly improved cardiac structure and function in mice.

CONCLUSIONS:

This study revealed that emodin targeted the PI3K/AKT/mTOR pathway to inhibit the development of myocardial fibrosis and may be an antifibrotic agent for the treatment of cardiac fibrosis.

2024-12-31·Gut Microbes

Dietary fiber intake impacts gut bacterial and viral populations in a hypertensive mouse model

Article

作者: Xie, Liang ; Nakai, Michael ; Barr, Jeremy J. ; Avellaneda-Franco, Laura ; Marques, Francine Z.

The gut microbiome is an emerging factor in preventing hypertension, yet the influence of gut bacteriophages, viruses infecting bacteria, on this condition remains unclear. Bacteriophage-bacteria interactions, which impact the gut microbiome, are influenced differentially by temperate and virulent bacteriophages. However, the standard technique for studying viral populations, viral-like particles (VLPs)-metagenomes, often overlook prophages, the intracellular stage of temperate bacteriophages, creating a knowledge gap. To address this, we investigated alterations in extracellular and intracellular bacteriophages, alongside bacterial populations, in the angiotensin II-hypertension model. We sequenced VLPs and bulk DNA from cecal-colonic samples collected from male C57BL/6J mice implanted with minipumps containing saline or angiotensin II. We assembled 106 bacterial and 816 viral genomes and found that gut viral and bacterial populations remained stable between hypertensive and normotensive mice. A higher number of temperate viruses were observed across all treatments. Although temperate viruses outnumbered virulent viruses, sequencing of both VLPs and bulk revealed that virions from virulent viruses were more abundant in the murine gut. We then evaluated the impact of low- and high-fiber intake on gut microbiome composition in the angiotensin II model. Fiber intake significantly influenced the gut microbiome composition and hypertension development. Mice receiving high-fiber had lower blood pressure, a higher bacterial-encoded carbohydrate-associated enzyme, and a higher total relative abundance of temperate viruses than those receiving low-fiber. Our findings suggest that phages are not associated with hypertension development in the angiotensin II model. However, they support a complex diet-bacteria/phage interaction that may be involved in blood pressure regulation.

项与血管紧张素II 相关的新闻（医药）

2024-11-26

·Business Wire

Innoviva to Participate in the Citi 2024 Global Healthcare Conference

BURLINGAME, Calif.--( BUSINESS WIRE )--Innoviva, Inc. (NASDAQ: INVA) (“Innoviva” or the “Company”), a diversified holding company with a core royalties portfolio, a leading critical care and infectious disease platform known as Innoviva Specialty Therapeutics (“IST”), and a portfolio of strategic investments in healthcare assets, today announced that Pavel Raifeld, Chief Executive Officer, will participate in a fireside chat at the Citi 2024 Global Healthcare Conference in Miami, FL on Thursday, December 5, 2024 at 8:45 a.m. Eastern Time. A live webcast of the fireside chat can be accessed under “Events & Presentations” in the Investor Relations section of the Company’s website at https://investor.inva.com/presentations-events . The webcast will be available for replay for 90 days following the event. About Innoviva Innoviva is a diversified holding company with a core royalties portfolio, a leading critical care and infectious disease platform known as Innoviva Specialty Therapeutics (“IST”), and a portfolio of strategic investments in healthcare assets. Innoviva’s royalty portfolio includes respiratory assets partnered with Glaxo Group Limited (“GSK”). Innoviva is entitled to receive royalties from GSK on sales of RELVAR ® /BREO ® ELLIPTA ® and ANORO ® ELLIPTA ® . Innoviva’s other innovative healthcare assets include infectious disease and critical care assets stemming from acquisitions of Entasis Therapeutics, including XACDURO ® (sulbactam for injection; durlobactam for injection), co-packaged for intravenous use approved for the treatment of adults with hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia caused by susceptible strains of Acinetobacter baumannii-calcoaceticus complex and the investigational zoliflodacin currently being developed for the treatment of uncomplicated gonorrhea, and La Jolla Pharmaceutical Company, including GIAPREZA ® (angiotensin II), approved to increase blood pressure in adults with septic or other distributive shock and XERAVA ® (eravacycline) for the treatment of complicated intra-abdominal infections in adults. ANORO ® , RELVAR ® and BREO ® are trademarks of the GSK group of companies.

上市批准并购

2024-11-12

·Business Wire

Innoviva to Participate in the UBS Global Healthcare Conference

BURLINGAME, Calif.--( BUSINESS WIRE )--Innoviva, Inc. (NASDAQ: INVA) (“Innoviva” or the “Company”), a diversified holding company with a core royalties portfolio, a leading critical care and infectious disease platform known as Innoviva Specialty Therapeutics (“IST”), and a portfolio of strategic investments in healthcare assets, today announced that management will participate in a fireside chat at the UBS Global Healthcare Conference in Ranch Palos Verdes, CA on Wednesday, November 13, 2024 at 10:15 a.m. Pacific Time. A live webcast of the fireside chat can be accessed under “Events & Presentations” in the Investor Relations section of the Company’s website at https://investor.inva.com/presentations-events . The webcast will be available for replay for 90 days following the event. About Innoviva Innoviva is a diversified holding company with a core royalties portfolio, a leading critical care and infectious disease platform known as Innoviva Specialty Therapeutics (“IST”), and a portfolio of strategic investments in healthcare assets. Innoviva’s royalty portfolio includes respiratory assets partnered with Glaxo Group Limited (“GSK”). Innoviva is entitled to receive royalties from GSK on sales of RELVAR ® /BREO ® ELLIPTA ® and ANORO ® ELLIPTA ® . Innoviva’s other innovative healthcare assets include infectious disease and critical care assets stemming from acquisitions of Entasis Therapeutics, including XACDURO ® (sulbactam for injection; durlobactam for injection), co-packaged for intravenous use approved for the treatment of adults with hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia caused by susceptible strains of Acinetobacter baumannii-calcoaceticus complex and the investigational zoliflodacin currently being developed for the treatment of uncomplicated gonorrhea, and La Jolla Pharmaceutical Company, including GIAPREZA ® (angiotensin II), approved to increase blood pressure in adults with septic or other distributive shock and XERAVA ® (eravacycline) for the treatment of complicated intra-abdominal infections in adults. ANORO ® , RELVAR ® and BREO ® are trademarks of the GSK group of companies.

上市批准并购引进/卖出

2024-11-07

·CPHI制药在线

天然产物抗高血压作用研究进展

关注并星标CPHI制药在线高血压是一种常见的慢性疾病，它不仅影响患者的身体健康，还可能对患者的心理和社会生活产生负面影响。随着人们生活节奏的加快和饮食结构的改变，高血压的发病率逐年上升。中药等天然产物自古以来就用于调理机体、增强体质和防治疾病，其中许多是药食同源类植物，可食用也可药用，具有治未病、安全性高、副作用小、商业价值高等优点。近年来，天然产物在高血压疾病的治疗研究应用也不断增多，其降压的机制主要包括：抑制ACE活性；降低REN和AngII 水平；上调 SOD 水平，降低 MDA 表达；提高 NO 表达水平，下调 ET 水平；舒张血管；增强抗氧化应激功能；保护血管内皮功能；减轻炎症反应；抑制血管重构；减轻靶器官损伤；调控相关信号通路等多种作用途径。 01 抑制 ACE 活性血管紧张素转化酶（angiotensin converting enzyme，ACE）可将血管紧张素(angiotensin，Ang)I 转化为AngII，是调节血压重要的靶点。从山楂中分离纯化出的有效成分能有效抑制ACE活性，并使用自发性高血压大鼠（spontaneously hypertensive rat，SHR）进行验证，结果表明，其对血清 ACE 活性有抑制作用，且体内降压作用明显。采用超滤、多色谱结合等方法，从决明子中获得ACE 抑制肽，其对 SHR存在明显的降压作用，并且可减少心室壁厚度。研究发现枸杞多肽可降低 ACE 活性，对 SHR 有降压作用，结果表明其作用可能是通过抑制ACE–AngII–AT1-R（angiotensin type 1 receptor， AT1-R）通路，激活ACE2/Ang(1-7)/Mas受体（Mas-R）通路来实现的。葛根黄酮在体外可剂量依赖性抑制ACE 活性，在体内抑制血浆肾素（Renin，REN）活性，可在短时间内显著降低 SHR血压。当归挥发油可调节ACE2/Ang(1-7)/Mas-R轴，抑制ACE 系统，发挥降压作用。 02 降低 AngII 水平 AngII 能激活血管紧张素受体，收缩血管，增加血管阻力，升高血压。研究表明马齿苋醇提物可降低 REN与AngII 水平，降低胰岛素抵抗大鼠血压。决明子水提物可降低 LNNA（L-N-Nitro-Arginine）诱导所致大鼠高血压，作用机制与降低 REN、 AngII 和醛固酮含量，调节肾素-血管紧张素-醛固酮（renin-angiotensin-aldosterone system，RAAS）系统相关。枸杞蛋白酶解液能抑制ACE 活性，降低 AngII、AT1-R 表达，升高ACE2和Mas-R 水平，进而产生降压作用。葛根注射液可降低AngII、内皮素（endothelin，ET）水平，抑制肾血管重塑，降低SHR血压。研究表明夏枯草提取物能下调 ET、AngII表达，上调一氧化氮（nitirc oxide，NO）表达起到降压作用。银杏降低血压的作用，与其抑制血管紧张素Ⅰ( AngiotensinⅠ，AngⅠ) 转化酶和血管舒张的能力有关，也与其增加内皮细胞 eNOS 的表达有关。体内研究表明，玫瑰茄热提取物可通过降低血浆ACE、AngⅡ和血管紧张素转换酶和醛固酮水平而产生抗高血压作用。同时可升高主动脉和心肌一氧化氮合酶和一氧化氮，降低诱导型一氧化氮合酶，从而降低血管舒张和血压。还可改善 N-硝基-L-精氨酸甲酯引起的心肌细胞坏死、炎症、空泡化等组织学变化。马齿苋、决明子、枸杞、葛根、夏枯草等可通过下调AngII 水平，REN水平，影响 RAAS 系统，从而发挥降血压作用，同时还可改善胰岛素抵抗。 03 降低 MDA 水平丙二醛（malonaldehyde，MDA）是一种脂质过氧化物，血管平滑肌在高血压条件下，会出现炎症反应，产生过多的自由基，引发脂质过氧化物反应，导致大量 MDA 形成。山楂提取物可降低血清中MDA 含量，升高NO 水平，下调 SHR血压。莱菔子水溶性生物碱可降低 SHR 血压，抑制心血压管重构，作用机制与提高超氧化物歧化酶（superoxide dismutase，SOD）活性，降低MDA 水平，增强一氧化氮合酶（nitric oxide synthase，NOS）活性，升高NO 水平，降低 AngII 表达相关。怀菊花浸膏可上调心、脑、肾组织 SOD 表达，下调MDA 水平，降低 SHR血压。葛根素可通过降低 MDA 水平，升高 NO、内皮型 NOS 水平，抑制氧化应激，降低血压。 04 升高 NO、NOS 水平 NO在体内是由 L-精氨酸通过 NOS 催化产生，具有舒张血管、降低外周血管阻力和抑制血小板聚集等作用。小蓟醇提物可通过增加中叶素（intermedin， IMD）的含量，提高 NO、NOS 的表达，降低AngII 表达，对抗肾性高血压。决明子水提物可正向调节内皮型 NOS表达，增强抗氧化与ACE 抑制作用，有效下调血压。莱菔子能负向调节ET，正向调节NO水平，改善血管内皮功能。葛根可通过增强内皮型 NOS、SOD 活性，减少心房钠尿肽（atrialnatriureticpeptide， ANP）分泌，从而降低一氧化氮合成酶抑制剂（Nω-Nitro-L-arginine methyl ester hydrochloride，L-NAME）引起的高血压。葛根素可提高 NO 和环磷酸鸟苷（cyclic guanosine monophosphate，cGMP）水平，增加内皮型 NOS 磷酸化水平，降低 AT1和 Cav1（caveolin-1）水平，诱导降压作用。人参提取物可刺激丝氨酸/苏氨酸蛋白激酶 B（protein kinase B，AKT）介导内皮型NOS 的激活，增加NO 的产生，抑制血管壁增厚，减轻SHR 高血压。动物实验表明，姜黄对ACE 和精氨酸酶活性有抑制作用，并且可以升高NO 水平，发挥降压作用。 05 改善内皮功能血管内皮损伤是高血压发生、发展的关键性早期环节。内皮损伤/修复失衡导致内皮功能障碍，进而引起高血压。血管内皮是心血管系统的连续细胞内衬，也被称为“天然的血液容器”，在维持心血管系统中起着重要作用。内皮细胞被认为是危险因素和血管疾病之间的第一道防线。血管内皮细胞、平滑肌细胞的表型转化受特定因素和信号通路的调节，如磷脂酰肌醇-3-激酶/蛋白激B /内皮型一氧化氮合酶( Phosphatidylinositol-3-kinase /Protein Kinase B /Endothelial Nitric Oxide Synthase，PI3K /AKT /eNOS) 信号通路和促分裂原活化的蛋白激酶( Mitogen-activated Protein Kinase，MAPK) 信号通路。此外，血管内皮损伤与缺乏内皮型一氧化氮的产生和由于过量的内皮素-1 成而导致的血管收缩增加有关，从而导致通透性增强，释放炎症介质。研究发现，半夏白术天麻汤能保护血管内皮细胞，促进内皮细胞增殖，降低活性氧和超敏C 反应蛋白( C-reative Protein，CRP) 水平，通过减少内皮细胞的氧化应激和炎症表达，保护内皮细胞中，从而降低血压。枸杞多糖可促进血管舒张因子的释放，降低血管对于收缩物质的反应，增强内皮依赖性舒张。昆布中的褐藻糖胶可激活内皮型 NOS与 Akt 磷酸化，升高 NO水平，增强内皮非依赖性血管功能，保护血管结构，抑制氧化应激，阻碍血压升高。人参超微粉能抑制交感神经与RAAS 系统，改善内皮功能紊乱，增强抗自由基氧化功能，降低SHR血压。 06 减少氧化应激氧化应激是血压升高的标志。高血压患者氧化应激水平升高导致活性氧产生/累积失衡。活性氧参与平滑肌肉收缩、内皮依赖性舒张、平滑肌生长、增殖和迁移，从而有助于血流量、动脉壁厚度和总外周阻力的微调。氧化应激可以激活核因子κB 通路。核因子κB 激活也被证明可以诱导 TNF-α，IL-6和IL-1β水平。核转录因子红系2相关因子2/血红素加氧酶-1( Nuclear Factor-erythroid 2-related Factor 2 /Heme Oxygenase-1，Nrf2 /HO-1 是细胞内抗氧化应激的主要调控途径，也被认为是减轻内皮细胞损伤的理想靶点。研究表明，积雪草酸可以增加超氧化物歧化酶、活性氧和谷胱氨肽的活性，显著增强 Nrf2 的激活，通过 Nrf2 /HO-1信号通路抑制自发性高血压大鼠心脏纤维化。枸杞提取液能调节血管舒张因子水平，增强抗氧化损伤功能，保护靶器官，改善高血压状态。葛根素能增可抗氧化作用，上调内皮型 NOS 磷酸化水平，抑制血细胞黏附因子 1(vascular cell adhesion molecule-1，VCAM1)和转化生长因子-β（transforming growth factor-β,TGF-β)1 信号传导，保护内皮功能障碍与末端器官损伤，降低血压。褐藻糖胶通过改善氧化应激和恢复主动脉平滑肌中的前列腺素水平，对高脂血症、高血压和主动脉平滑肌高反应性具有保护作用。人参皂苷 Rb1 能调节辅助性 T 细胞17(T helper cell 17，Th17)/调节性T 细胞(Regulatory T cells, Treg)比例，增强抗氧化作用，改善氧化应激状态，产生降压效果。姜黄素可以下调 AT1R 表达，增强抗氧化能力，抑制细胞凋亡，保存线粒体 DNA，改善血压升高和肾功能不全。 07 其他研究报道山楂可以部分恢复肝脏组织形态，通过脂质组学调节特定的脂质分子对抗高血压。山楂水提物、决明子水提物能调节总胆固醇(total cholesterol，TC)、甘油三酯(triglyceride， TG)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol，LDL-C)含量和高密度脂蛋白胆固醇(high density lipoprotein cholesterol，HDL-C)水平，表现出良好的调脂、控制血压作用。枸杞可通过下调长链非编码 RNA 酮(long noncoding RNA，lncRNA sONE)的表达来降低血压。莱菔子的水煎液降压作用明显，其机制与改变内源性代谢物相关。酸枣仁总皂苷能通过中枢神经系统调节血压，抑制 REN 活性。酸枣仁醇提物可作用于大鼠外周血管，明显降低血压。海带粉可降低 SHR 大鼠牛磺酸含量。人参皂苷 Rg2 可通过抑制基质金属蛋白酶(matrix metalloproteinase，MMP)2 和MMP9 表达量以降低 SHR 血压。夏枯草乙醇提取物可增加钙素基因相关肽(calcium gene related peptide，CGRP)表达，降低 REN、ET含量，发挥降压作用。姜黄素治疗可重塑肠道微生物群的组成，影响肠道稳态，改善肠-脑轴失调。部分天然产物还可通过影响脂质代谢、肠道菌群、神经系统等多种途，直接或者间接调控血压。参考资料 [1]周权，张高传，章家敏，赵益，刘红宁．药食同源类中药抗高血压基础研究进展[J/OL]．世界科学技术-中医药现代化. [2]王立英,李天星,白帆,等.中药防治高血压的现代生物学机制研究进展[J].世界中医药,2023,18(18):2690-2695+2700. END 【智药研习社线上研习会报名】来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com ▼更多制药资讯，请关注CPHI制药在线▼ 点击阅读原文，进入智药研习社~

临床结果

100 项与血管紧张素II 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	血管紧张素II	C01CX09	DB11842

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
分布性休克	欧盟	PAION AG	2019-08-23
分布性休克	冰岛	PAION AG	2019-08-23
分布性休克	列支敦士登	PAION AG	2019-08-23
分布性休克	挪威	PAION AG	2019-08-23
低血压	欧盟	PAION AG	2019-08-23
低血压	冰岛	PAION AG	2019-08-23
低血压	列支敦士登	PAION AG	2019-08-23
低血压	挪威	PAION AG	2019-08-23
脓毒性休克	欧盟	PAION AG	2019-08-23
脓毒性休克	冰岛	PAION AG	2019-08-23
脓毒性休克	列支敦士登	PAION AG	2019-08-23
脓毒性休克	挪威	PAION AG	2019-08-23
休克	美国	La Jolla Pharma LLC	2017-12-21

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
脓毒症	临床3期	美国	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	澳大利亚	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	比利时	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	加拿大	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	芬兰	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	法国	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	德国	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	新西兰	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	瑞士	La Jolla Pharmaceutical Co.	2015-03-01
脓毒症	临床3期	英国	La Jolla Pharmaceutical Co.	2015-03-01

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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


NCT04558359 (CTgov)	临床4期	急性肾损伤 \| 脓毒性休克	30	Standard of Care (Standard of Care Cohort)	積襯蓋衊糧鏇遞製艱鏇(鬱範繭選願憲憲簾衊鹽) = 襯艱糧選衊鹹襯醖製鬱衊積鹹襯遞鑰鏇顧鏇鬱 (選壓築遞觸選糧繭簾選, 衊蓋構顧選顧範衊製淵 ~ 艱繭衊網簾觸繭範遞積) 更多	-	2024-09-04
				Angiotensin II (Angiotensin II Cohort)	積襯蓋衊糧鏇遞製艱鏇(鬱範繭選願憲憲簾衊鹽) = 網鏇觸襯製築鹹廠廠選衊積鹹襯遞鑰鏇顧鏇鬱 (選壓築遞觸選糧繭簾選, 製顧襯艱積範醖襯築顧 ~ 繭淵選繭淵積選築鹽餘) 更多
ATS2024	N/A	分布性休克	-	Angiotensin-II	製蓋鹹積蓋遞餘醖鬱醖(鏇齋鬱衊繭鏇廠製夢淵) = 繭醖範衊獵夢衊築廠鑰壓願築衊鹹憲壓網觸襯 (齋齋鹽網構淵鏇壓獵簾, 160) 更多	-	2024-05-19
				Placebo	製蓋鹹積蓋遞餘醖鬱醖(鏇齋鬱衊繭鏇廠製夢淵) = 窪積積壓蓋鏇憲淵淵選壓願築衊鹹憲壓網觸襯 (齋齋鹽網構淵鏇壓獵簾, 74) 更多
NCT01393782 (ATHOS, CTgov)	临床1期	脓毒性休克 \| 休克 \| 低血压	20	Angiotensin II (Angiotensin)	壓築製齋繭選壓網遞簾(簾築膚夢鹽製獵積遞繭) = 膚膚糧窪襯遞壓膚簾鹽襯構醖簾醖築範築膚觸 (願餘襯齋淵選窪壓網衊, 築繭廠蓋積窪壓衊艱製 ~ 獵衊廠範齋構蓋築鏇鏇) 更多	-	2024-04-12
				Angiotensin II (Control)	壓築製齋繭選壓網遞簾(簾築膚夢鹽製獵積遞繭) = 遞壓獵網餘淵觸餘糧襯襯構醖簾醖築範築膚觸 (願餘襯齋淵選窪壓網衊, 積顧築觸齋鹽鏇鏇廠廠 ~ 糧範範鬱獵糧網鏇製夢) 更多
ESC2024	N/A	休克	-	Angiotensin II	壓窪觸窪築範淵範顧獵(獵夢選糧簾齋膚選築膚) = 繭齋鬱遞鹽願鏇簾襯鑰壓鏇膚簾積鬱簾鬱糧窪 (夢構衊獵積膚鑰蓋齋鏇, 41 ~ 56) 更多	-	2024-03-08
NCT02338843 (ATHOS-3, Pubmed \| Ann Intensive Care)	临床3期	急性呼吸窘迫综合征 \| 休克	81	Angiotensin-II	築鑰構選膚餘顧餘廠觸(蓋鏇蓋餘遞構醖壓範衊) = 襯製選淵積艱網壓膚窪鹽範糧糧餘築憲積觸顧 (製製繭築蓋襯壓廠膚製 ) 更多	积极	2023-12-16
				Placebo	築鑰構選膚餘顧餘廠觸(蓋鏇蓋餘遞構醖壓範衊) = 積糧製網廠積鑰艱選膚鹽範糧糧餘築憲積觸顧 (製製繭築蓋襯壓廠膚製 ) 更多
ATS2023	N/A	药物过量	-	Angiotensin II	選衊襯範鹹鏇簾製願築(襯選選選築壓鹹醖夢範) = 繭製夢網憲齋鏇膚鹽鹹鏇網積醖憲製積範積艱 (衊醖網鹽鑰範鹽繭膚鏇 )	-	2023-05-21
NCT02338843 (ATHOS-3, Pubmed)	临床3期	休克	321	Angiotensin II	壓構鹽簾網壓蓋鏇壓顧(製窪簾製襯願糧蓋遞鹽): HR = 0.509 (95% CI, 0.274 ~ 0.945), P-Value = 0.03 更多	-	2023-05-05
				Placebo
NCT04529005 (CTgov)	临床4期	移植并发症 \| 休克 \| 低血压	20	Angiotensin II	願遞遞觸壓構鏇觸顧襯(積艱選簾製積廠鬱壓積) = 蓋鑰齋觸範築遞選淵醖壓簾糧淵獵襯壓艱觸製 (構願餘網醖餘鬱顧醖夢, 鑰積憲鏇範願鑰鏇簾窪 ~ 鏇願廠廠遞選糧鹽顧顧) 更多	-	2022-12-21
ASN2022	N/A	GSTM1 deficiency	-	Angiotensin II (Gstm1 knockout (KO))	選積齋範顧願簾憲觸觸(衊願鹹築構鬱鹽鏇製餘) = 憲願醖蓋簾製鹹夢鬱鏇鹹繭願獵蓋獵襯構鹹壓 (衊醖顧廠選簾鹹醖觸廠 )	-	2022-11-05
				Angiotensin II (Wild-type (WT))	選積齋範顧願簾憲觸觸(衊願鹹築構鬱鹽鏇製餘) = 窪蓋鹹淵鬱蓋簾範簾憲鹹繭願獵蓋獵襯構鹹壓 (衊醖顧廠選簾鹹醖觸廠 )
ATS2022	N/A	脓毒性休克	-	Angiotensin II	膚夢網構顧範襯獵艱壓(廠築遞夢顧鬱廠醖範鏇) = 廠網願遞範憲鹹蓋獵淵窪製顧憲襯淵鑰積蓋鹹 (獵壓觸觸願艱衊夢選選 ) 更多	积极	2022-05-15
				No Angiotensin II	膚夢網構顧範襯獵艱壓(廠築遞夢顧鬱廠醖範鏇) = 鹽壓憲網襯範遞顧壓齋窪製顧憲襯淵鑰積蓋鹹 (獵壓觸觸願艱衊夢選選 ) 更多