Effects of Ziltivekimab Versus Placebo on Coronary Atherosclerosis in Patients With Acute Myocardial Infarction. A Serial, Multivessel, Intravascular Ultrasound, Near-infrared Spectroscopy and Optical Coherence Tomography Imaging Study

Despite improvements in the treatment, coronary artery disease (CAD) remains one of the leading causes of death worldwide. Around 20% of people who have suffered a heart attack (myocardial infarction) need to be hospitalized again within a year, and 10% experience another heart attack. Despite currently available medication, patients remain at risk of further episodes after a heart attack. Scientists have discovered that inflammation in the body plays a decisive role in the development and narrowing of arterial blockages (atherosclerosis). This study aims to investigate whether a new treatment that reduces inflammation can help improve the arteries of patients with CAD.
This study will examine whether blocking certain inflammation-related substances with a new medicinal product called ziltivekimab affects the buildup and composition of plaques (fatty deposits) in the coronary arteries. Special imaging diagnostic techniques will be used to look inside the arteries and check whether the treatment helps reduce the narrowing caused by dangerous plaques, which can lead to future heart attacks.
This is a clinical study in which participants are randomly divided into two groups (randomization): one group will receive the new treatment ziltivekimab and other group will receive a placebo (a harmless substance with no active ingredients). Both groups will continue to receive standard treatment for heart attacks. The study lasts approximately 15 months per participant.
The full scientific title of the trial is: Effects of ziltivekimab versus placebo on coronary atherosclerosis in patients with acute myocardial infarction. A study with serial multi-vessel imaging obtained using intravascular ultrasound, near-infrared spectroscopy, and optical coherence tomography techniques.

开始日期2025-12-19

申办/合作机构

ECRI-1 BV

[+3]

NCT06118281

/ Active, not recruiting临床3期

ARTEMIS - Effects of Ziltivekimab Versus Placebo on Cardiovascular Outcomes in Patients With Acute Myocardial Infarction

The research study is being done to see if ziltivekimab can be used to treat people who were admitted to hospital because of a heart attack. Ziltivekimab might reduce development of heart disease, thereby preventing new heart attacks or strokes. Participants will either get ziltivekimab (active medicine) or placebo (a dummy medicine which has no effect on the body). Which treatment participants get is decided by chance. The chance of getting ziltivekimab or placebo is the same. The participant will need to inject the study medicine into a flat skin surface in there stomach, thigh, or upper arm once every month. Ziltivekimab is not yet approved in any country or region in the world. It is a new medicine that doctors cannot prescribe. The study will last for about 2 years.

开始日期2024-06-25

申办/合作机构

Novo Nordisk A/S

[+1]

NCT06263244

/ Completed临床3期IIT

Specifying the Anti-inflammatory Effects of Ziltivekimab With Diverse Imaging Modalities and In-depth Cellular Phenotyping

The goal of this randomized, double blind, placebo controlled trial is to study whether ziltivekimab therapy reduces arterial wall inflammation as assessed by imaging, and reduces the systemic inflammatory tone as assessed by circulating monocytes, inflammatory biomarkers and proteomics.

开始日期2024-05-03

申办/合作机构-

100 项与齐替韦单抗相关的临床结果

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100 项与齐替韦单抗相关的专利（医药）

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项与齐替韦单抗相关的文献（医药）

2026-10-01·JOURNAL OF CARDIAC FAILURE

The Comorbidity-Driven Interleukin-6-Mediated Systemic Inflammation Hypothesis of Heart Failure With Preserved Ejection Fraction: A Decade of Testing Ends in Disappointment

Review

作者: Borlaug, Barry A ; Zannad, Faiez ; Packer, Milton ; Vaduganathan, Muthiah ; Butler, Javed

In 2013, Paulus and Tschöpe proposed that the multitude of comorbidities seen in patients with heart failure with preserved ejection fraction (HFpEF) was responsible for triggering an interleukin-6 (IL-6)-mediated systemic inflammatory state that might lead to HFpEF, postulating the intermediary contribution of coronary microvascular disease and deficient nitric oxide/cyclic guanosine monophosphate (NO-cGMP) signaling and cytokine-mediated cardiac hypertrophy and fibrosis. The comorbidity-driven IL-6-systemic inflammation hypothesis has been extensively evaluated in randomized controlled trials. However, in these trials, most comorbidities have not been shown to represent a causal mechanism for systemic inflammation, and the treatment of comorbidities (other than obesity) has not ameliorated HFpEF. Although coronary microvascular dysfunction is common in HFpEF, it is often not endothelium dependent, and it is not a cause of defective NO-cGMP signaling. Numerous randomized clinical trials with NO-cGMP-enhancing drugs (nitrates/nitrites, phosphodiesterase 5 inhibitors and soluble guanylyl cyclase stimulators) have not provided symptomatic or exercise benefits in HFpEF. Mendelian randomization studies link IL-6 to the development of HFpEF; serum levels of IL-6 precede the development and track the severity of HFpEF; and experimental models point to IL-6 as a causal mediator of HFpEF. However, the adipokine hypothesis partitioned IL-6 and other classical cytokines from pathogenic adipokines in identifying molecular mediators of HFpEF based on the observations that systemic IL-6 does not reliably reflect visceral adipose tissue dysfunction, and it is co-secreted with neutralizing cytokine antagonists. These observations suggested that systemic IL-6 represents a distal marker, not a mediator, of adipose tissue inflammation, and thus, it is unlikely to play a role in HFpEF. In proteomics analyses, heightened natural endogenous cytokine antagonists are more prominent and consistent features of HFpEF than circulating levels of the cytokines themselves. The HERMES trial tested the efficacy of the IL-6 antibody, ziltivekimab, in patients with HFpEF who were enriched for cytokine-mediated systemic inflammation, but the trial has been stopped for futility. Therefore, as a result of rigorous testing of each of its mechanistic layers, it is now difficult to support the hypothesis that HFpEF is a comorbidity-driven, IL-6-mediated systemic inflammatory disorder that acts through or independently of an NO-cGMP deficiency mechanism.

2026-09-15·EUROPEAN JOURNAL OF HEART FAILURE

Ziltivekimab in heart failure with preserved and mildly reduced ejection fraction: rationale and design of the ATHENA and HERMES trials

Article

作者: Borlaug, Barry A ; Petrie, Mark C ; Auerbach, Pernille ; Hvelplund, Anders ; Voors, Adriaan A ; Cikes, Maja ; Ducharme, Anique ; Lam, Carolyn S P ; Mendieta, Guiomar ; Fudim, Marat ; Michelsen, Marie Mide ; Ridker, Paul M

Abstract:

Aims:

We hypothesized that targeting interleukin-6—a cytokine central to NOD-like receptor protein 3 (NLRP3) inflammasome activation that is associated with both the onset and progression of heart failure (HF)—may be beneficial in patients with HF and circulating evidence of cardiovascular inflammation but without overtly reduced ejection fraction (EF). We describe the rationale and design of two clinical trials (ATHENA and HERMES) investigating ziltivekimab, a human monoclonal antibody directed against the interleukin-6 ligand, in patients with HF and mildly reduced or preserved EF (HFmrEF/HFpEF) and cardiovascular inflammation.

Methods:

ATHENA (n = 673) and HERMES (n = 4900) are international, multi-centre, double-blind, placebo-controlled trials randomizing adults with HFpEF/HFmrEF and cardiovascular inflammation (high-sensitivity C-reactive protein ≥2 mg/l) to ziltivekimab 15 mg or placebo, administered subcutaneously once monthly on top of standard of care. Eligible participants have a left ventricular EF >40%, elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP), and serum high-sensitivity C-reactive protein ≥2 mg/l. The primary endpoint in ATHENA is the change in Kansas City Cardiomyopathy Questionnaire—Clinical Summary Score at 12 months. The primary endpoint in HERMES is time to first composite of cardiovascular death, hospitalization for HF, or urgent HF visit. ATHENA has a fixed duration of 12 months, whereas the HERMES trial is event driven (∼845 adjudicated primary events) with a minimum exposure of 6 months from randomization to the last treatment visit.

Conclusion:

ATHENA and HERMES will investigate the effect of ziltivekimab in HFpEF/HFmrEF and cardiovascular inflammation. ATHENA will determine the effect of ziltivekimab on health status. HERMES will determine the efficacy and safety of ziltivekimab on morbidity and mortality.

2026-09-02·Expert Opinion on Drug Metabolism & Toxicology

Pharmacokinetics of novel drugs for the treatment of diabetic nephropathy

Review

作者: Mousavi, Taraneh ; Davis, Stephen N. ; Munir, Kashif M. ; Shaya, Fadia T.

INTRODUCTION:

Diabetic kidney disease (DKD) alters drug pharmacokinetics (PK), affecting exposure, pharmacodynamic response, and toxicity. As newer therapies become central to DKD management, understanding their PK profiles is essential for individualized treatment across stages of kidney impairment.

AREAS COVERED:

PubMed/MEDLINE, Embase, and Scopus were searched from database inception through 18 April 2026, for evidence on PK, pharmacodynamics, renal-impairment effects, and drug-drug interactions. Evidence was synthesized for sodium-glucose cotransporter-2 inhibitors (SGLT2i), glucagon-like peptide-1 receptor agonists (GLP-1RA), dual incretin agonists, nonsteroidal mineralocorticoid receptor antagonists (nsMRA), endothelin receptor antagonists (ERA), aldosterone synthase inhibitors (vicadrostat, baxdrostat, and lorundrostat), avenciguat, and ziltivekimab, emphasizing exposure, clearance, metabolism, elimination, and dosing implications.

EXPERT OPINION:

In reduced kidney function, SGLT2i show modest increases in drug exposure but attenuated glucose-lowering effects. Finerenone demonstrates modest exposure increases despite minimal renal clearance. Some ERAs, particularly zibotentan may have larger esposure increases, poentially narrowing the therapeutic window. Newer incretin-based therapies generally maintain stable exposure. However, eGFR alone may not fully capture changes in drug disposition. Factors such as uremia, altered protein binding, and nonrenal clearance can also affect exposure. The next advance will likely be drug-specific decision support integrating eGFR trajectory, potassium levels, dialysis status, body composition, and concomitant medications, rather than universal therapeutic drug monitoring.

239

项与齐替韦单抗相关的新闻（医药）

2026-11-10

·药讯小知

生物医药行业动态 · 2026-11-10（周二）

生物医药行业动态 · 2026-11-10 今日摘要卫健委等四部门发文：双目录内 1 类新药"入院不带枷锁" —— 1 类新药不计入"一品两规"、不纳入五项绩效监测指标，商保创新药目录药品可豁免按病种支付并走特例单议，国内创新药商业化兑现的政策摩擦成本进一步下降。（影响：高）FDA 要求全类 GLP-1 药物标签增补 NAION 罕见视神经病变警告 —— 绝对风险差仅 6.4 vs 3.8 例/10 万人年，临床冲击有限、情绪冲击更大，但这是 GLP-1 大叙事落地以来第一处标签级风险提示。（影响：高）礼来口服 GLP-1 Foundayo 攻下 OSA 第三适应症 —— ATTAIN-OSA 两项 III 期达标（AHI 降幅 43.8% vs 6.3%），年内递交申报；口服小分子 GLP-1 正把"一粒胶囊替代呼吸面罩"变成可定价的支付叙事。（影响：高）一、政策与监管本节速览卫健委 / 国家医保局等四部门 — 发文优化双目录创新药配备使用：1 类新药不计入"一品两规"、豁免绩效指标，商保目录药品不纳入按病种支付，入院与支付摩擦同步拆除美国国防部 / 药明康德 — 药明康德被正式移出 1260H"中国军工企业"名单，地缘不确定性压制落地解除美国 CMS — IRA 药价谈判新规终稿敲定（2029 年生效）：改给药途径产品与原产品同列谈判，"改剂型避谈判"路径被堵死 ← 左右滑动查看 → 二、IND 申报与获批本节速览恒瑞医药 · SHR-1139（IL-23p19×IL-36R 双抗） — 自免双通路新药获批临床（掌跖脓疱病），国内自免军备竞赛再加一条期权恒瑞医药 · HRS-5346（口服 Lp(a) 抑制剂） — 获批开展 III 期临床，在 pelacarsen/ ziltivekimab 双证伪后仍获监管放行，机制风险定价的关键样本上海莱士 · SR604（活化蛋白 C 抗体）（简报） — 血小板无力症预防治疗 IND 获受理并拟纳入"关爱计划-延伸"试点，稀有出血赛道持续加宽瑞博生物 · SR122（简报） — 双靶点小核酸，混合型血脂异常及重度高甘油三酯血症 I 期临床申请提交港交所公告 ← 左右滑动查看 → 三、临床与研发本节速览礼来 · Foundayo（orforglipron，口服 GLP-1） — OSA III 期 ATTAIN-OSA 双研究达标（AHI -43.8% vs -6.3%），年内递交，口服 GLP-1 第三适应症落地Immunovant · IMVT-1402（imeroprubart，FcRn） — 难治性 RA II 期随机期 ACR20 92.5% vs 75.6%（p=0.0139），FcRn 通路向 RA 扩张成功（股价 +15.1%）信达生物 · 信必乐（托莱西单抗 IBI306，PCSK9） — CREDIT-5 III 期一线单药达主要终点，近期递交新增适应症Zura Bio · tibulizumab（ZB-106，IL-17/BAFF 双抗） — HS II 期 TibuSHIELD 主终点与关键次要终点双败、终止开发（股价 -69.7%）Vir Biotechnology · elebsiran+tobevibart（siRNA+抗体） — 丁型肝炎 III 期 ECLIPSE 1 达主要终点（79% RNA 阴转），siRNA 功能性治愈路线验证（股价 +11.8%） ← 左右滑动查看 → 四、审批与上市本节速览拜耳 · Sunharbo（asundexian，FXIa 抑制剂） — FDA 获批（全球首个 FXIa 抑制剂），继 10-26 中国首批后再下一城，定价 $748.50/30 天百济神州 · Daraxonrasib（RMC-6236，Rasonque） — CDE 拟纳入优先审评（转移性胰腺癌），国内落地提速罗氏 · 伐米奇拜单抗（简报） — 葡萄膜炎性黄斑水肿 IL-6 单抗获 CDE 优先审评资格，有望全球首发（进博会披露，待 CDE 公示核验） ← 左右滑动查看 → 五、资本与交易本节速览荣昌生物 / 荣昌制药 · RCZY-690（泛 RAS(ON) 抑制剂） — 首付 5,000 万元 + 最高 48.7 亿元里程碑引进全球权益，关联交易补齐小分子管线argenx / Unnatural Products — 收购大环肽药物发现平台，最高 11.5 亿美元，补口服/长效免疫疗法能力查尔斯河 / 方达控股（泰格医药旗下） — 收购其美国生物分析与 DMPK 业务，初始 4.7 亿美元 + 最高 7,500 万业绩挂钩Delix Therapeutics · zalsupindole — 1 亿美元 C 轮（JJDC 领投），非致幻性神经塑生素转向"MDD IIb 就绪"，致幻剂路线之争的资本投票Windward Bio（简报） — 瑞士 TSLP 超长效抗体公司设定纳斯达克 IPO 条款，拟募约 1.75 亿美元Heron Therapeutics / CorMedix（简报） — Heron 出售资产给 CorMedix，首付 1.45 亿美元 ← 左右滑动查看 → 六、市场与商业化本节速览ImmunityBio · ANKTIVA（简报） — Q3 产品收入 4,870 万美元（同比 +53%）但环比下滑且不及预期，持续经营存疑表述维持，股价 -15%七、情报与预警本节速览FDA / GLP-1 全类（礼来 Mounjaro/Zepbound、诺和诺德 Ozempic/Wegovy 等） — 标签增补 NAION 罕见视神经病变警告：发生率 6.4 vs 3.8 例/10 万人年，情绪冲击大于临床冲击Alteogen / Halozyme（简报） — Alteogen 11-09 单日 -17.26%：Halozyme 在意大利就 K 药皮下版供应链申请禁令（首次听证 12-02），10 亿美元里程碑款确定性承压复星医药 · AR1001（简报） — 口服 AD 新药 POLARIS-AD III 期顶线定档 11-16 CTAD 大会 OC2 口头报告（1,535 例、88% 完成 52 周双盲期）Arrowhead Pharmaceuticals（简报） — 11-09 股价 -15.3%，具体触发原因待核验诺华 · Zolgensma（简报） — FDA 宣布对 Zolgensma 肿瘤病例启动调查，为 11-09 事件的进展 ← 左右滑动查看 → 免责声明：内容基于公开信息整理，不保证完整性与准确性。

临床3期申请上市临床申请临床2期

2026-11-10

·我就是来科普的

AI制药真的靠谱吗？心脏病新药研发接连失败

诺华和诺和诺德的两款心血管新药，虽然成功降低了致病风险因子和炎症指标，却均未改善患者的临床结局。这也给备受期待的AI制药带来启示。 2026年11月7日，在美国心脏协会(AHA)年会上，两项备受期待的大型临床试验公布了令人失望的结果。诺华和诺和诺德开发的两款心血管新药，虽然成功改变了目标生物学指标，却都未能显著降低患者发生心脏病、中风或死亡的风险。第一款药物是诺华与IonisPharmaceuticals联合开发的pelacarsen，针对脂蛋白(a)，简称Lp(a)。这种主要由遗传因素决定的物质与心血管疾病存在因果联系，全球约20%的人口存在Lp(a)升高的问题。科学家原本希望，通过降低Lp(a)，能够像他汀类药物降低胆固醇一样，减少心血管事件。在涉及8300多名患者的HORIZON临床试验中，pelacarsen成功将Lp(a)水平降低78%，但经过中位4.7年的随访，患者发生心脏病、中风、死亡或接受紧急血管疏通手术的风险，并未显著降低。克利夫兰诊所心脏病专家Steven Nissen坦言，几乎所有人都相信这种治疗会有效，结果却出人意料。研究人员怀疑，问题可能在于治疗时机。试验参与者均已有严重心血管疾病史，降低Lp(a)可能为时已晚。安进和礼来正在测试另外两款能将Lp(a)降低约95%的药物，相关结果预计分别于2028年和2029年公布。第二款药物来自诺和诺德，名为ziltivekimab。它通过阻断白细胞介素6(IL-6)抑制炎症，而慢性炎症长期被认为是心血管疾病的重要推动因素。在涉及6300名患者的ZEUS临床试验中，药物成功降低了炎症指标，却未能减少心脏病发作、中风或死亡。诺和诺德随后终止了另外两项相关晚期临床试验。哈佛大学心脏病专家Paul Ridker认为，参与试验的患者可能已经病得太重，即使阻断炎症信号，也无法逆转已经形成的损伤。两项研究揭示了药物研发中的一个难题：找到疾病的关键机制，并不意味着干预它就能改善患者的健康状况。 STAT资深医学记者Matthew Herper将此与当前的AI制药热潮联系起来。过去，制药业曾寄望于人类遗传学大幅提高新药成功率，但这两项试验表明，即使具有可靠的遗传学或生物学依据，药物仍可能在临床试验中失败。如今，AI被寄予类似期待。它能够加速靶点发现和药物设计，却不能保证这些药物最终有效。人体生物学的复杂性，仍然是任何先进技术必须面对的挑战。

AHA会议临床结果

2026-11-09

·上海女王之舟

2026年11月1日至11月7日全球生物医药重要进展

11月4日，欧洲分子生物学实验室、德国癌症研究中心和英国维康桑格研究所的研究人员在《自然》发表研究论文，深度解析胶质母细胞瘤的可塑性，为未来的癌症治疗带来了希望。胶质母细胞瘤是成人中最常见且致命的恶性脑肿瘤，它几乎无法治愈，原因在于单个肿瘤细胞彼此差异很大，并且会在各种“状态”之间动态转换，这种可塑性使它们能够逃避抗癌治疗。由于治疗方法可能只针对某些细胞状态，而对其他状态无效，这种可塑性有助于癌细胞在治疗中存活下来。过去主流观点认为，这种状态转换是随机的，很难预测。而这次，研究人员通过创建并分析迄今为止最全面的胶质母细胞瘤患者分子数据集之一，对这一观点提出了挑战。他们发现，与此前的认知相反，胶质母细胞瘤在不同细胞状态之间的转换遵循着某些固定且可预测的路径，不同的细胞状态在肿瘤内部也占据不同的空间生态位。接下来，研究人员便开始探究胶质母细胞瘤细胞的状态转换过程是如何调控的。研究人员分析了超过100万个胶质母细胞瘤细胞的基因调控特征，并据此揭示了肿瘤细胞在不同状态间转换的机制。他们发现了一种结构化的调控程序，该程序控制着这些细胞的可塑性，并且具有可预测性和层级性。研究团队还发现了一组“保护机制”，这些调控因子能够将细胞锁定在低可塑性状态，阻止其向其他状态转变，他们发现过表达MYT1L能够降低细胞可塑性和肿瘤恶性程度。将这些“修饰”后的肿瘤移植到小鼠体内，小鼠的存活率高于对照组。这一点尤其引人关注，因为这些调控因子未来有望成为癌症治疗中的基因或药物靶点。 11月6日，中国国家药监局药审中心发布《化学药生物等效性试验备案范围和程序》及共性问题解答的通告。生物等效性试验备案机制优化，明确哪些需要备案、流程简化，对仿制药开发有很大积极影响。 11月7日，由哈佛医学院与诺和诺德研发团队牵头，全球多中心协作研究完成的一项3期临床试验结果发表于《新英格兰医学杂志》。该3期试验纳入6376名合并动脉粥样硬化、慢性肾病、hsCRP升高的高危受试者，使用IL‑6单抗ziltivekimab。结果显示，药物可显著压低IL‑6、hsCRP等炎症标志物，但主要心血管不良事件与安慰剂无差异，且严重感染风险有所上升。该试验虽未达到预设终点，但具备重要的警示意义。它直接证明炎症标志物下降不等于真正临床终点获益，不能简单依靠生物标志物替代临床结局判断，打破了“抑制炎症就一定减少心血管事件”的假说。对比早年另一试验：卡那单抗（IL‑1β抑制剂）在既往心梗、高炎症人群中取得阳性结果，提示不同炎症通路、不同基础疾病人群，抗炎治疗的获益完全不同，不能直接套用既往抗炎策略。该IL‑6单抗阴性结果为后续抗炎靶点临床试验的人群筛选、终点设计提供关键参考，避免同类研究盲目推进。 Global Biomedicine Highlights, Nov 1–7, 2026 On November 4, researchers from the European Molecular Biology Laboratory, the German Cancer Research Center and the Wellcome Sanger Institute published a paper inNature that dissected the plasticity of glioblastoma and offered promising insights for future cancer therapy. Glioblastoma is the most common and lethal malignant brain tumor in adults and is nearly incurable. Its poor prognosis stems from extensive intratumoral heterogeneity and the dynamic switching of tumor cells between distinct cellular states. This plasticity enables cancer cells to evade anticancer treatments, as therapies may only target certain cell populations while leaving others unaffected. The prevailing view had long held that such state transitions were random and unpredictable. Analyzing one of the most comprehensive molecular datasets of patient-derived glioblastoma samples to date, the team challenged this assumption. They demonstrated that state transitions follow defined, predictable trajectories, with individual cell states occupying distinct spatial niches within the tumor. The researchers further explored the regulatory machinery governing these transitions. Profiling gene regulatory features across more than one million glioblastoma cells, they uncovered a structured, hierarchical and predictable regulatory program underlying tumor cell plasticity. The team also identified protective regulatory factors that lock cells into a low-plasticity state and block state switching. Overexpression of MYT1L reduced cellular plasticity and tumor aggressiveness. Mice implanted with these modified tumor cells achieved better survival than control animals. These regulatory factors represent promising genetic or pharmacological targets for future anticancer interventions. On November 6, the Center for Drug Evaluation of the National Medical Products Administration of China released the Scope and Procedures for Filing of Bioequivalence Studies for Chemical Drugs, together with a notice addressing frequently asked questions. The optimized filing framework clarifies which studies require filing and streamlines administrative workflows, delivering substantial benefits for generic drug development. On November 7, a global multicenter phase 3 trial led by investigators from Harvard Medical School and the R&D team at Novo Nordisk was published inThe New England Journal of Medicine. The trial enrolled 6,376 high-risk participants with atherosclerotic cardiovascular disease, chronic kidney disease and elevated hsCRP, who received the IL‑6 monoclonal antibody ziltivekimab. While the drug markedly lowered circulating IL‑6 and hsCRP levels, the incidence of major adverse cardiovascular events was comparable to the placebo group, with a slight increase in serious infections observed. Though the trial missed its primary endpoint, it carries critical implications. It validates that reductions in inflammatory biomarkers do not translate to clinical outcome benefits, and biomarkers cannot substitute hard clinical endpoints. It overturns the simplistic hypothesis that suppressing inflammation will invariably reduce cardiovascular events. Compared with the earlier positive trial of canakinumab, an IL‑1β inhibitor studied in patients with prior myocardial infarction and high inflammation, the finding underscores that therapeutic gains from anti‑inflammatory agents vary widely by inflammatory pathway and patient comorbidities. This negative result provides key guidance for patient selection and endpoint design in future anti‑inflammatory trials, preventing blind advancement of similar programs.

临床3期临床结果

100 项与齐替韦单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D12807	-	-	-

研发状态

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
冠心病	临床3期	奥地利	Novo Nordisk A/S	2025-12-18
冠心病	临床3期	丹麦	Novo Nordisk A/S	2025-12-18
冠心病	临床3期	意大利	Novo Nordisk A/S	2025-12-18
冠心病	临床3期	荷兰	Novo Nordisk A/S	2025-12-18
冠心病	临床3期	西班牙	Novo Nordisk A/S	2025-12-18
冠心病	临床3期	瑞士	Novo Nordisk A/S	2025-12-18
急性心肌梗塞	临床3期	美国	Novo Nordisk A/S	2024-06-25
急性心肌梗塞	临床3期	中国	Novo Nordisk A/S	2024-06-25
急性心肌梗塞	临床3期	日本	Novo Nordisk A/S	2024-06-25
急性心肌梗塞	临床3期	阿根廷	Novo Nordisk A/S	2024-06-25

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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


NCT04626505 (RESCUE-2, CTgov)	临床2期	炎症 \| 慢性肾病	36	Ziltivekimab (Ziltivekimab 15 mg)	鹹窪窪顧顧憲襯繭製遞(窪夢糧構廠壓繭構廠艱) = 築憲衊鑰餘憲廠築壓製艱構鏇窪鏇簾築蓋淵遞 (糧範顧積夢憲齋壓憲夢, 醖鏇夢淵餘鑰觸製繭壓 ~ 淵範鑰膚夢廠獵糧鬱網) 更多	-	2026-05-06
				Ziltivekimab (Ziltivekimab 30 mg)	鹹窪窪顧顧憲襯繭製遞(窪夢糧構廠壓繭構廠艱) = 網觸觸獵壓餘簾醖蓋廠艱構鏇窪鏇簾築蓋淵遞 (糧範顧積夢憲齋壓憲夢, 齋醖壓鑰繭夢選壓獵鏇 ~ 夢構鬱範艱壓窪淵製壓) 更多
NCT03926117 (RESCUE, Pubmed) 人工标引	临床2期	炎症 \| 慢性肾病 C-reactive Protein Expression	261	Ziltivekimab 7.5 mg	襯簾鹹廠齋遞憲鹽鬱齋(簾壓顧簾衊鹹製窪壓願) = 鏇觸壓範願蓋鏇蓋觸鏇簾顧顧構鹹觸糧繭糧淵 (顧鬱鹹構壓蓋廠選衊淵 )	积极	2024-01-01
				Ziltivekimab 15 mg	襯簾鹹廠齋遞憲鹽鬱齋(簾壓顧簾衊鹹製窪壓願) = 憲夢膚願憲醖觸蓋範遞簾顧顧構鹹觸糧繭糧淵 (顧鬱鹹構壓蓋廠選衊淵 )
NCT04626505 (RESCUE-2, Pubmed \| J Cardiol)	临床2期	动脉粥样硬化 high-sensitivity C-reactive protein (hsCRP)	-	Ziltivekimab 15mg	鬱蓋範構蓋衊餘齋積簾(鹹構鏇餘夢製憲醖繭選) = 遞壓膚獵網廠壓醖構選壓襯鹹壓醖蓋膚醖廠壓 (憲鏇築蓋窪鑰鏇蓋鏇襯 )	积极	2023-10-01
				Ziltivekimab 30mg	鬱蓋範構蓋衊餘齋積簾(鹹構鏇餘夢製憲醖繭選) = 遞鬱夢蓋壓膚遞廠憲憲壓襯鹹壓醖蓋膚醖廠壓 (憲鏇築蓋窪鑰鏇蓋鏇襯 )
NCT03926117 (RESCUE \| RESCUE Trial, CTgov)	临床2期	炎症 \| 慢性肾病	264	Ziltivekimab (Placebo)	獵製願願餘壓顧壓襯夢(網構蓋獵顧簾積膚窪膚) = 鬱夢鹽簾淵鏇遞憲獵衊觸製鑰簾鹽蓋壓積餘簾 (憲餘淵窪窪餘醖選遞觸, 膚鏇蓋選淵蓋顧醖製糧 ~ 獵構蓋觸構窪製醖繭醖) 更多	-	2023-08-09
				Ziltivekimab (Ziltivekimab 7.5 mg)	獵製願願餘壓顧壓襯夢(網構蓋獵顧簾積膚窪膚) = 憲製夢顧餘構糧願齋憲觸製鑰簾鹽蓋壓積餘簾 (憲餘淵窪窪餘醖選遞觸, 簾簾遞憲範獵構餘壓選 ~ 鹽顧鬱範遞膚齋蓋憲願) 更多
NCT03926117 (RESCUE Trial, ASN2021)	临床2期	慢性肾病 serum hemoglobin \| iron homeostasis \| high-sensitivity C-reactive protein	-	Ziltivekimab 7.5 mg	齋餘繭製蓋鑰範觸獵艱(餘膚醖憲築繭選觸顧顧) = 壓鏇選繭齋範憲壓襯醖淵窪積鹹範選鏇觸壓簾 (繭鏇衊簾窪廠獵醖夢網 )	积极	2021-10-27
				Ziltivekimab 15 mg	齋餘繭製蓋鑰範觸獵艱(餘膚醖憲築繭選觸顧顧) = 鏇醖艱膚鏇襯鹹艱選淵淵窪積鹹範選鏇觸壓簾 (繭鏇衊簾窪廠獵醖夢網 )
NCT02868229 (CTgov)	临床1/2期	贫血	61	Placebo (Placebo)	築鏇齋簾繭顧鏇範糧構 = 餘醖膚鹽膚醖觸廠艱構糧衊淵齋糧蓋顧醖顧簾 (構顧簾鹹製醖襯鹽積獵, 膚壓鬱遞壓齋膚衊鏇淵 ~ 餘範製製蓋鑰淵選窪選) 更多	-	2021-07-30
				COR-001 (COR-001)	醖糧醖窪築糧壓夢糧襯(艱夢鏇壓簾鏇積艱築壓) = 願選鹽壓構憲壓觸獵糧鏇簾顧艱夢蓋築壓鏇獵 (選鹹衊鑰選艱鹽糧積鑰, 醖襯夢壓糧築製範衊壓 ~ 襯繭憲糧築衊構鬱襯鏇)
NCT03926117 (RESCUE, Pubmed \| Lancet)	临床2期	动脉粥样硬化	264	Placebo	顧蓋製願膚築網願廠繭(選廠顧鹹繭艱築製獵願) = 壓壓憲鹽艱醖觸觸構廠繭選醖簾範積餘淵遞顧 (鑰繭衊蓋糧醖窪鬱壓遞 )	积极	2021-05-14
ASN2019	临床1期	慢性肾病	12	COR-001 5 mg	鹹遞糧積鹽窪餘廠衊膚(糧齋鏇糧襯壓壓壓衊鑰) = 鏇繭鹹艱衊築鹽憲範廠範觸簾網選願鑰願醖願 (壓齋壓廠鏇鹽衊齋壓廠 )	积极	2019-11-05
				COR-001 15 mg	鹹遞糧積鹽窪餘廠衊膚(糧齋鏇糧襯壓壓壓衊鑰) = 窪壓齋廠襯鏇願築膚積範觸簾網選願鑰願醖願 (壓齋壓廠鏇鹽衊齋壓廠 )