Alirocumab for Stabilisation of Symptomatic Vulnerable Carotid Plaque: A Multicentre, Randomised, Double-Blind, Placebo-Controlled Trial With High-Resolution Vessel-Wall MRI and Clinical Endpoints

CAROTID-STABILISE is a phase III, multicentre, randomised, double-blind, placebo-controlled trial evaluating whether alirocumab 150 mg subcutaneously every 2 weeks, added to high-intensity statin therapy, produces greater reduction in intraplaque haemorrhage (IPH) volume at 26 weeks compared with placebo in patients with recently symptomatic carotid stenosis of 50-69% harbouring IPH or lipid-rich necrotic core (LRNC) on high-resolution vessel-wall MRI. The study will enroll 280 participants across multiple centres with a 52-week extension for durability and clinical endpoints assessment.

开始日期2027-07-01

申办/合作机构-

NCT07477704

/ Recruiting临床2期

A Randomized, Open-Label, Dose-Ranging Study to Evaluate the Efficacy, Safety, and Pharmacokinetics of Weekly Alirocumab in Adults With Hypercholesterolemia

This study is researching an experimental drug called alirocumab, referred to as "study drug". In the United States, alirocumab is approved for the treatment of hypercholesterolemia (high blood cholesterol levels).
The aim of the study is to see how safe and effective alirocumab is when given weekly to adult participants who have hypercholesterolemia.
The study is looking at several other research questions, including:
* What side effects may happen from taking the study drug once a week
* How much study drug is in the blood at different times

开始日期2026-06-17

申办/合作机构

Regeneron Pharmaceuticals, Inc.

NCT07581808

/ Recruiting临床4期IIT

PCSK9-DUO Trial: Dual PCSK9 Inhibition With Inclisiran and Alirocumab in Patients With High Cardiovascular Risk in Secondary Prevention

This study will evaluate the effectiveness and safety of combining two different types of PCSK9 inhibitors, inclisiran and alirocumab, in patients with high cardiovascular risk who are unable to tolerate statins.
Lowering low-density lipoprotein cholesterol (LDL-C) is essential to reduce the risk of cardiovascular events. While PCSK9 inhibitors are effective, many patients treated with a single agent do not reach recommended LDL-C targets, especially those who cannot take statins.
Inclisiran and alirocumab reduce LDL-C through different mechanisms. Inclisiran decreases the production of PCSK9 in the liver, while alirocumab binds circulating PCSK9 in the blood. Combining these therapies may lead to a greater reduction in LDL-C levels.
In this randomized, open-label clinical trial, approximately 60 patients in secondary prevention will be assigned to one of three groups: inclisiran alone, alirocumab alone, or a combination of both treatments. Patients will be followed for 9 months with regular clinical and laboratory assessments.
The main goal of the study is to determine whether combination therapy leads to greater LDL-C reduction compared to each treatment alone. Secondary objectives include assessing the proportion of patients achieving target LDL-C levels and evaluating treatment safety and tolerability.

开始日期2026-05-18

申办/合作机构

UMC Ljubljana

100 项与阿利西尤单抗相关的临床结果

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100 项与阿利西尤单抗相关的转化医学

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100 项与阿利西尤单抗相关的专利（医药）

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624

项与阿利西尤单抗相关的文献（医药）

2026-07-01·AMERICAN HEART JOURNAL

Rationale, design, and baseline characteristicss of the effect of PCSK9 inhibition on cardiovascular risk in treated HIV infection: EPIC-HIV randomized clinical trial

Article

作者: Sereti, Irini ; Kawai, Kosuke ; Schaffer, Veronica ; Ma, Yifei ; Li, Danny ; Deeks, Steven G ; Tawakol, Ahmed ; Durstenfeld, Matthew S ; Hsue, Priscilla Y ; Levkova-Clark, Marta ; Lu, Michael T ; Abohashem, Shady

RATIONALE:

People with HIV (PWH) are at increased risk of cardiovascular disease. Moderate lipid lowering with statins has been demonstrated to reduce cardiovascular risk among PWH. Accordingly, evaluation of more potent lipid-lowering strategies for prevention is needed, especially for PWH at higher risk. Prior research suggests that proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors safely lower low-density lipoprotein cholesterol by 60% among people with HIV, but the impact of PCSK9 inhibitors on arterial inflammation, endothelial function, coronary plaque, or markers of immune dysfunction among PWH remains unknown.

METHODS:

The effect of PCSK9 inhibition on cardiovascular risk in treated HIV infection study is a randomized, placebo-controlled, and double-blinded clinical trial. Adults at least 40 years old with treated and virally suppressed HIV and at least one cardiovascular risk factor (primary prevention) or a prior cardiovascular event (secondary prevention) are randomized in a 2:1 ratio to alirocumab or a matching placebo injected subcutaneously. ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography, coronary computed tomographic angiography, and flow-mediated dilation of the brachial artery are conducted at baseline and after 1 year of treatment. The primary study outcome is the change in arterial inflammation assessed using the target-to-background ratio of the most diseased arterial segment on positron emission tomography/computed tomography from baseline to 1 year, and key secondary endpoints will include the change in noncalcified coronary plaque on coronary computed tomographic angiography, change in endothelial function, and safety according to the intention-to-treat principle.

ENROLLMENT:

One hundred eighteen participants were randomized. The mean age was 59.5 years, and 6% were female.

CONCLUSIONS:

The effect of PCSK9 inhibition on cardiovascular risk in treated HIV infection study will provide evidence regarding the mechanisms by which potent lipid lowering with PCSK9 inhibitors may alter the pathogenesis of atherosclerosis among PWH.

TRIAL REGISTRATION:

https://clinicaltrials.gov/study/NCT03207945.

2026-06-01·Journal of Clinical Lipidology

Lipoprotein(a) reduction with inclisiran, alirocumab, evolocumab, enlicitide, and lerodalcibep: A systematic review and meta-analysis of randomized controlled trials

Review

作者: Mulligan, Martin D ; Vishwakarma, Rishabh ; Gandhi, Rahul S ; Bhattacharya, Romit

BACKGROUND AND AIMS:

Lipoprotein(a) [Lp(a)] is a causal contributor to atherosclerotic cardiovascular disease (ASCVD). While no therapies are currently approved solely for lowering Lp(a), subgroup analyses suggest that individuals with elevated Lp(a) may gain added benefit from intensive lipid-lowering strategies. No prior meta-analysis has compared evolocumab, alirocumab, inclisiran, lerodalcibep, and enlicitide in their Lp(a)-lowering efficacy. We aimed to determine whether proprotein convertase subtilisin/kexin type 9 (PCSK9) targeted therapies differ significantly in Lp(a) reduction, or whether agent selection can be guided primarily by other factors such as dosing frequency, cost, and patient preference.

SOURCES OF MATERIAL:

We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) reporting percent change in Lp(a) following treatment with the 5 PCSK9-targeted agents. A random-effects model calculated pooled estimates of percentage Lp(a) change, and mixed-effects meta-regression assessed differences between agents.

ABSTRACT OF FINDINGS:

Thirty-one RCTs were included. PCSK9 inhibitors and inclisiran reduced Lp(a) by a pooled mean of -25.76% vs control (95% CI -29.54 to -21.99; P < .0001). Meta-regression revealed no significant differences between agents (alirocumab vs evolocumab: +3.3%, 95% CI -1.40 to 8.07, P = .16; inclisiran vs evolocumab: +4.9%, 95% CI -2.31 to 12.16, P = .18; inclisiran vs alirocumab: +1.6%, 95% CI -5.38 to 8.55, P = .65). Lerodalcibep and enlicitide demonstrated similar approximate 25% reductions; however, insufficient trial numbers precluded a powered head-to-head comparison.

CONCLUSIONS:

No statistically significant differences in Lp(a) reduction were observed between currently available PCSK9-targeting medications. Agent selection may reasonably be based on non-efficacy factors, including administration frequency, cost, and patient preference.

2026-05-05·Journal of the American Heart Association

Comparative Efficacy of Statins Versus PCSK9 Inhibitors in Coronary Heart Disease Treatment

Article

作者: Li, Yi ; Zhou, Xiang ; Ren, Yuxin ; Xie, Jiaying ; Xiang, Boyang ; Yu, Linchan

Background:

Combining PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors with statins significantly lowers low‐density lipoprotein cholesterol and reduces cardiovascular events in patients with coronary heart disease versus statins alone. However, it remains unclear which monotherapy offers greater cardiovascular benefit.

Methods:

This prospective non‐randomized real‐world observational cohort study enrolled coronary heart disease inpatients from July 2020 to March 2024. Patients received either alirocumab (75 mg/2 weeks) or statins (atorvastatin 20 mg/day or rosuvastatin 10 mg/day). The primary outcome was a composite of cardiovascular death, myocardial infarction, stroke, heart failure hospitalization, or coronary revascularization. Cox proportional hazards models and restricted mean survival time analyses were used.

Results:

Among 1165 analyzed patients, 215 received PCSK9 inhibitors and 950 received statins. After 1 month, low‐density lipoprotein cholesterol reduction was greater in the PCSK9 inhibitor group (from 2.57 to 0.75 mmol/L) than in the statin group (from 2.29 to 1.40 mmol/L; P <0.001). However, this difference was not significant at 12 months (1.44 versus 1.52 mmol/L; P =0.058). Multivariate Cox regression analysis revealed an adjusted hazard ratio of 0.74 (95% confidence interval, 0.49–1.12; P =0.152) for the primary outcome with statins versus PCSK9 inhibitors. The restricted mean survival time was 26.11 months for the PCSK9 inhibitor group and 26.48 months for the statin group. The results were consistent across key subgroups. No serious adverse events occurred during the follow‐up.

Conclusions:

PCSK9 inhibitor monotherapy showed no statistically significant difference from statin monotherapy in long‐term lipid‐lowering efficacy or cardiovascular risk reduction, suggesting it may be an effective alternative for secondary prevention in coronary heart disease.

810

项与阿利西尤单抗相关的新闻（医药）

2026-06-30

·药闻康策

这8种药7月1日起退出医保报销！

☝ 点击上方一键预约 ☝ 最新最热的医药健康新闻政策 ☝ ☝ 点击查看峰会活动议程 ☝ ☝ 根据国家医保局与人力资源社会保障部联合印发的《国家基本医疗保险、工伤保险和生育保险药品目录（2025年）》，8种协议期内未成功续约的谈判药品，将于2026年7月1日起正式退出医保统筹基金支付。6月30日24:00是过渡期的最后一天。这8种药品具体包括：贝那鲁肽注射液、达诺瑞韦钠片、盐酸拉维达韦片、阿利西尤单抗注射液、度维利塞胶囊、八氟丙烷脂质微球注射液、甘露特钠胶囊、林普利塞片，覆盖糖尿病、丙肝、高血脂、淋巴瘤、阿尔茨海默病等多个治疗领域。为什么要退出医保？核心原因：续约没谈拢。国谈药品的协议期一般为5年，协议到期后需重新谈判续约。这8种药多为2020—2022年首批国谈品种，5年协议期满进入续约环节时，企业报价未能达到医保局的预期。具体来看，主要有三种情况：一是企业主动放弃续约，如贝那鲁肽注射液，目录内已有司美格鲁肽等同类型药品可替代；二是药企停止推广或药品退市，如阿利西尤单抗注射液，已有多款国产同类药纳入医保，价格仅为其1/3；三是注册审批未通过或临床价值不足被调出，如甘露特钠胶囊已正式停产。需要强调的是，药品调出不等于无药可用。医保目录内已有疗效和性价比更优的替代药品，正在使用相关药物的患者可在医生指导下平稳换药，少数存在个体差异的患者也可自费购买仍在市场流通的原药，不必过度焦虑。来源：药客行药闻康策新媒体矩阵微信公众号点击下方一键关注【免责声明】 1.“药闻康策”部分文章信息来源于网络转载是出于传递更多信息之目的，并不意味着赞同其观点或证实其内容的真实性。如对内容有疑议，请及时与我司联系。2.“药闻康策”致力于提供合理、准确、完整的资讯信息，但不保证信息的合理性、准确性和完整性，且不对因信息的不合理、不准确或遗漏导致的任何损失或损害承担责任。3.“药闻康策”所有信息仅供参考，不做任何商业交易或医疗服务的根据，如自行使用“药闻康策”内容发生偏差，我司不承担任何责任，包括但不限于法律责任，赔偿责任。欢迎转发分享、点赞、点在看

2026-06-29

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从“对症”到“修正”| 吴永健教授：ASCVD脂代谢紊乱疾病修正治疗的现在与未来

编者按：动脉粥样硬化性心血管疾病（ASCVD）是造成我国居民死亡的首要慢病诱因之一，临床数据显示国内经皮冠状动脉介入治疗（PCI）年手术量已突破250万例，临床主要依靠支架植入等对症治疗手段，缺少从发病本源阻断动脉粥样硬化进展的疾病修正理念。在此临床背景下，第二十二届北大糖尿病论坛紧扣疾病修正治疗（DMT）核心主题，打破内分泌学科壁垒，联动多学科专家开展跨界研讨，探寻从源头干预代谢与血管病变的全新路径。会议特邀国家心血管病中心、中国医学科学院阜外医院吴永健教授进行专题授课，立足三十余年心血管临床实践与多项循证研究结果，从ASCVD治疗理念变迁、PCSK9抑制剂的DMT突破性价值、Lp(a)前沿靶点探索等维度，系统梳理脂代谢紊乱DMT从理论走向临床落地的发展脉络。一、理念跨越：ASCVD治疗从对症缓解迈入疾病修正新时代上世纪中叶，临床对动脉粥样硬化的病理机制认知尚浅，治疗聚焦缓解胸痛、胸闷等不适症状，单纯依靠对症处理无法阻止病变持续进展。随着Framingham心脏研究、4S研究等多项里程碑式循证结果问世，明确低密度脂蛋白胆固醇（LDL-C）是驱动动脉粥样硬化发生发展的核心危险因素之一[1,2]。以此为理论基础，ASCVD的DMT理念正式建立：该治疗策略靶向脂代谢紊乱、血管内皮损伤、血管慢性炎症等核心病理机制开展干预，从病因层面实现粥样斑块的稳定甚至逆转，阻断疾病自然进展轨迹，最终降低心肌梗死、缺血性卒中、心血管死亡等严重不良终点事件的发生风险。临床主要通过三项标准评估DMT疗效[3-4]：极高危患者需长期将LDL-C控制在1.4 mmol/L以下；借助血管内超声、光学相干断层扫描（OCT）等影像技术证实斑块缩小或稳定性改善；经长期大样本研究证实方案可显著降低心血管硬终点事件。大量循证证据已明确，LDL-C水平与ASCVD的发生、进展及不良事件风险呈明确相关性[5,6]，积极管控LDL-C也因此成为落实ASCVD疾病修正治疗的核心抓手。他汀类药物作为指南推荐的一线降脂药，应用广泛，但仍存在不可忽视的治疗局限。一项巴西单中心回顾性研究显示，即便使用高强度他汀类药物治疗，急性心肌梗死患者LDL-C＜50 mg/dl达标率仅7.48%[7]。而HPS2-THRIVE研究则证实，我国ASCVD患者强化他汀治疗后肝酶升高、肌病发生率显著高于欧洲人群，限制了强化降脂方案的应用[8]。即便血脂达标，患者仍存在较高残余心血管风险[9-11]，他汀类药物的降脂天花板与残余风险问题，成为阻碍DMT全面落地的关键因素，临床亟需新型药物实现治疗突破。二、靶向破局：PCSK9抑制剂，实现ASCVD疾病修正的里程碑药物面对他汀治疗的临床瓶颈，PCSK9抑制剂凭借独特的作用机制，突破传统降脂药物的局限，成为全面契合DMT三大核心目标的新型治疗药物。该类药物的作用通路与他汀存在本质差异：他汀通过抑制胆固醇合成间接上调低密度脂蛋白（LDL）受体表达，而PCSK9抑制剂可直接保护LDL受体，避免受体被降解，使其重新循环至肝细胞表面，进而实现强效降脂效果，二者作用机制互补，联用可产生“1+1>2”的协同效应[12]。PCSK9抑制剂主要包括单克隆抗体类、小干扰RNA（siRNA）类，另有小分子/肽类及基因编辑疗法目前仍处于前期探索阶段。✓1.单抗类药物：开启PCSK9抑制剂临床应用时代PCSK9单抗通过直接结合并中和循环中的PCSK9蛋白，保护LDL受体免受降解，从而实现强效降脂。多项关键临床研究证实了该类药物的疗效与安全性：FOURIER研究：纳入27 564例ASCVD患者，在他汀治疗基础上联用依洛尤单抗，主要复合终点（心血管死亡、心肌梗死、卒中、不稳定心绞痛住院或冠脉血运重建）风险降低15%，关键次要终点（心血管死亡、心肌梗死或卒中）风险降低20%[13]。ODYSSEY OUTCOMES研究：纳入18 924例近期发生ACS的患者，应用阿利西尤单抗治疗使主要复合终点（冠心病死亡、非致死性心肌梗死、缺血性卒中或不稳定心绞痛住院）风险降低15%，且基线Lp(a)较高的患者获益更显著[14]。托莱西单抗注册研究亚组分析：作为首个国产原研PCSK9单抗，治疗12周后患者LDL-C较基线降幅达68.63%，同时有84.83%的患者实现LDL-C＜1.4 mmol/L且降幅≥50%的严苛治疗目标[15]。除了降低事件风险，PCSK9抑制剂在斑块逆转方面也展现出明确效果：GLAGOV研究：纳入968例冠心病患者，随访78周显示，他汀联合依洛尤单抗可使冠状动脉斑块体积百分比（PAV）下降0.95%，而安慰剂组斑块体积百分比小幅上升0.05%[16]（组间差异-1.0%，95%CI：-1.8%~-0.64%，P<0.001）。PACMAN-AMI研究：纳入300例急性心肌梗死患者，经PCSK9抑制剂治疗52周后，患者斑块体积百分比明显下降，纤维帽厚度增加、脂质核心缩小，标志着斑块稳定性显著提升[17]。✓2.siRNA类药物：实现血脂超长效管理的重要突破Inclisiran是靶向PCSK9的siRNA类药物，经皮下注射进入肝细胞后，可通过RNA干扰技术降解PCSK9的信使RNA，从源头抑制PCSK9蛋白合成。ORION系列Ⅲ期研究（ORION-9/10/11）证实，该药物全年仅需皮下注射两次，给药第540天，患者LDL-C降幅仍可达51%；在给药90天至540天区间内，LDL-C平均降幅维持在48%[18,19]。超长效的给药模式，大幅改善了慢病患者长期治疗的用药依从性。✓3.基因编辑疗法：面向未来的根本性干预探索2025年Nature Medicine刊发的一项临床前研究，为降脂治疗提供了全新方向。研究团队设计了一种非DNA切割型表观遗传编辑工具，借助dCas9蛋白靶向PCSK9基因启动子区域，通过诱导DNA甲基化沉默基因表达。动物实验显示，单次给药可在28天内将血浆PCSK9水平降低98%，疗效持续时长超过1年，且甲基化修饰可逆向调控，有效规避了DNA断裂带来的安全风险[20]。该技术目前虽处于临床前研究阶段，但有望实现“单次治疗、长期获益”的终极降脂目标。基于丰富的循证证据，国内外权威指南已明确PCSK9抑制剂为极高危ASCVD患者的核心联合治疗药物，尤其针对急性冠脉综合征患者，推荐在入院后尽早启动他汀+PCSK9抑制剂的联合降脂方案，以实现LDL-C早期快速达标，从源头干预疾病进程。三、新靶点Lp(a)：进一步降低残余风险的关键方向在LDL-C之外，脂蛋白(a)[Lp(a)]正成为研究的新焦点。Lp(a)的结构类似LDL，但颗粒更小、氧化性更强，且其载脂蛋白a与纤溶酶原具有同源性，因此兼具致动脉粥样硬化和促血栓形成双重风险，提示其危害可能不亚于LDL-C。研究数据显示，Lp(a)颗粒的致病强度是LDL颗粒的6.6倍，Lp(a)-apoB增加20 nmol/L与LDL-apoB增加132 nmol/L具有相同的ASCVD风险[21]。即便将LDL-C降得再低，也难以抵消Lp(a)升高带来的ASCVD风险[22]。然而，既往针对Lp(a)的干预手段十分有限，传统他汀类药物不仅无法有效降低Lp(a)，甚至可能造成其水平轻度升高。针对这一临床困境，国内外多部权威指南统一建议，所有人群一生中至少完成一次Lp(a)检测，以识别ASCVD高危患者。目前，多款靶向Lp(a)的创新药物已进入临床后期研究阶段：以Pelacarsen、Olpasiran和Zerlasiran为代表的药物，通过靶向Apo(a) mRNA可显著降低Lp(a)水平（降幅可达35%~98%），部分关键Ⅲ期研究预计将于2026年完成，有望为Lp(a)升高相关ASCVD风险提供新的治疗选择。值得关注的是，国产原研药物托莱西单抗在现有PCSK9抑制剂中，降低Lp(a)的效果表现优异，为临床同步管控LDL-C与Lp(a)提供了理想选择。总结纵观ASCVD脂代谢紊乱的诊疗演进，治疗思路已正式迈入以阻断疾病进展为目标的疾病修正新时代。经典研究奠定了LDL-C干预的理论根基，也让他汀类药物的临床瓶颈愈发凸显。PCSK9抑制剂系列药物成为重要治疗选择，结合长效制剂、基因编辑等前沿技术，层层突破传统治疗壁垒，真正践行了DMT的核心目标。而Lp(a)这一高风险靶点的探索与新药研发，则指向了残余心血管风险的破解方向。多靶点、多机制、多剂型的创新格局逐步形成，持续推动心血管疾病治疗向病因干预、全程管理迈进，为实现心血管事件早防早治、改善患者长期预后筑牢根基。专家简介吴永健教授中国医学科学院阜外医院北京协和医学院长聘教授、博士研究生导师中国医学科学院阜外医院心血管内科主任医师，冠心病中心主任、结构性心脏病中心副主任、冠心病二病区病区主任，阜外医院学术委员会常委主要从事冠心病和老年瓣膜性心脏病介入治疗及其相关研究科技部重点专项首席专家教育部科学技术进步奖一等奖第一完成人、中华医学奖二等奖第一完成人、北京市科技进步奖一等奖第一完成人曾任中华医学会心血管病分会青年委员会副主任委员，中国医师协会心血管病分会常委、结构性心脏病学组组长现任中华医学会心血管病分会常委、介入心脏病学组组长，北京医学会心血管病分会副主任委员中国康复学会心脏介入与康复分会主委、世界中医药协会联合会心脏康复分会主委欧洲心脏病学会委员（FESC）、美国血管造影与介入学会委员（FSCAI）、美国心脏病学院委员（FACC）荣誉称号：首届首都金牌好医生、第二届国家名医、第三届白求恩提名奖获得者，北京市有突出贡献的专家、西城百名英才参考文献：上下滑动可查看1.KANNEL WB, DAWBER TR, KAGAN A, et al. Ann Intern Med. 1961 Jul;55:33-50.2.Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994 Nov 19;344(8934):1383-9.3.Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017 Aug 21;38(32):2459-2472.4.Gourdy P, Schiele F, Halimi JM, et al. Atherosclerotic cardiovascular disease risk stratification and management in type 2 diabetes: review of recent evidence-based guidelines. Front Cardiovasc Med. 2023 Sep 26;10:1227769.5.Boekholdt SM, Hovingh GK, Mora S, et al. Very low levels of atherogenic lipoproteins and the risk for cardiovascular events: a meta-analysis of statin trials. J Am Coll Cardiol. 2014 Aug 5;64(5):485-94.6.Cholesterol Treatment Trialists’ (CTT) Collaboration; Baigent C, Blackwell L, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010 Nov 13;376(9753):1670-81.7.Nicolau JS, et al. Achievement of LDL-C targets after acute myocardial infarction in a public healthcare center in Brazil. 2025 ESC Congress.8.HPS2-THRIVE Collaborative Group. HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment. Eur Heart J. 2013 May;34(17):1279-91.9.Chapman MJ, Redfern JS, McGovern ME, et al. Niacin and fibrates in atherogenic dyslipidemia: pharmacotherapy to reduce cardiovascular risk. Pharmacol Ther. 2010 Jun;126(3):314-45.10.Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004 Apr 8;350(15):1495-504.11.LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005 Apr 7;352(14):1425-35.12.冯艳荣，刘育宇，郝磊，等. PCSK9 抑制药的研究进展 [J]. 中国医院药学杂志，2025, 45 (9): 1059-1064.13.Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. N Engl J Med. 2017 May 4;376(18):1713-1722.14.Schwartz GG, Steg PG, Szarek M, et al. Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome. N Engl J Med. 2018 Nov 29;379(22):2097-2107.15.Qi L, Shen H, Chai M, et al. Efficacy and safety of Tafolecimab in Chinese patients with type 2 diabetes and hypercholesterolemia: a post-hoc analysis of pooled data from three phase 3 trials. Cardiovasc Diabetol. 2025 Jul 3;24(1):264.16.Nicholls SJ, Puri R, Anderson T, et al. Effect of Evolocumab on Progression of Coronary Disease in Statin-Treated Patients: The GLAGOV Randomized Clinical Trial. JAMA. 2016 Dec 13;316(22):2373-2384.17.Zanchin C, Koskinas KC, Ueki Y, et al. Effects of the PCSK9 antibody alirocumab on coronary atherosclerosis in patients with acute myocardial infarction: a serial, multivessel, intravascular ultrasound, near-infrared spectroscopy and optical coherence tomography imaging study-Rationale and design of the PACMAN-AMI trial. Am Heart J. 2021 Aug;238:33-44.18.Raal FJ, Kallend D, Ray KK, T, et al. Inclisiran for the Treatment of Heterozygous Familial Hypercholesterolemia. N Engl J Med. 2020 Apr 16;382(16):1520-1530.19.Ray KK, Wright RS, Kallend D, et al. Two Phase 3 Trials of Inclisiran in Patients with Elevated LDL Cholesterol. N Engl J Med. 2020 Apr 16;382(16):1507-1519.20.Tremblay F, Xiong Q, Shah SS, et al. A potent epigenetic editor targeting human PCSK9 for durable reduction of low-density lipoprotein cholesterol levels. Nat Med. 2025 Apr;31(4):1329-1338.21.Tsimikas S, Bittner V. Particle Number and Characteristics of Lipoprotein(a), LDL, and apoB: Perspectives on Contributions to ASCVD. J Am Coll Cardiol. 2024 Jan 23;83(3):396-400.22.Bhatia HS, Wandel S, Willeit P, et al. Independence of Lipoprotein(a) and Low-Density Lipoprotein Cholesterol-Mediated Cardiovascular Risk: A Participant-Level Meta-Analysis. Circulation. 2025 Jan 28;151(4):312-321.声明：本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。（来源：《心肾代谢时讯》编辑部）

2026-06-29

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降脂针，已卖白菜价

国内市场，白热化的不止是减重药，还有降脂药。 6月25日，NMPA已正式受理莱达西贝普的生物制品上市许可申请，这是中国第五款国产第三代PCSK9抑制剂，由美国公司LIB Therapeutics研发，国内商业化由云顶新耀负责。重磅，又一款降脂新药，国内申报上市降血脂药是一个相当庞大的似乎长，我国血脂异常人群规模已经超过4亿，成人血脂异常患病率超过35%，每三人中就有一人血脂异常。目前主流的降脂药物是他汀类和贝特类，尤其是他汀类药物，是高血脂治疗的基石，诞生了多款“神药”。但再神的药都会有不可避免的缺陷。他汀类易发生不耐受，包括肝功能异常、肌肉相关并发症、新发糖尿病风险等，一旦发生不耐受，就需要找寻替代用药，此外单独使用他汀达不达标情况，需要联合其他降脂药使用。 PCSK9抑制剂就是其中之一，可单用或与他汀联用，属于新一代降血脂药。目前PCSK9抑制剂都是皮下注射剂，市场被统一称为“降脂针”，曾经的降脂针是高不可攀的代名词，动辄千元一针。 2018年国内首款PCSK9抑制剂获批上市，是来自安进的依洛尤单抗（商品名：瑞百安），一年后赛诺菲的阿利西尤单抗（商品名：波立达）上市，前者依洛尤单抗上市后售价为1298元/支，年治疗费用超3万，后者售价1982元/支，年治疗费用超5万，相当昂贵。然而经过2021年国家医保谈判，两款降脂针已经大降价，依洛尤单抗降到了283元/支，阿利西尤单抗降到了306元/支，降幅都接近80%，年治疗费用均降到了万元以下。有趣的是，这两款降脂针降价后，呈现出了两种截然不同的结果，依洛尤单抗销售额在2021年后开始飞速增长，2025年全终端医院销售额超25亿，较24年几乎翻倍。图源：摩熵医药而赛诺菲的阿利西尤单抗，销售额一直被限制在10亿以下，不温不火。 2025年7月，赛诺菲直接宣布阿利西尤单抗退出了中国市场，原因是原材料供应紧张以及竞争加剧。赛诺菲的阿利西尤单抗退出后，不仅给了老对手安进机会，也给了其他PCSK9抑制剂机会。国产最早的降脂针来自信达生物的托莱西单抗2024年纳入国谈目录，2025年正式可实行医保报销后，托莱西单抗一年就达到了5亿的销售额，简直是奇迹。目前，我国已经获批上市的国产PCSK9抑制剂包括信达生物的托莱西单抗、康方生物的伊努西单抗、君实生物的昂戈瑞西单抗以及恒瑞医药的瑞卡西单抗，云顶新耀刚刚报产的是国内第五款。到了2025年，康融、博创、恒瑞的降脂针一起进入了国谈目录，2026年正式实行，而国谈后呈现出的结果就是降脂针越来越便宜，已经到了百元级别。但这些单抗的长效性仍然不及英克司兰，英克司兰通过小干扰RNA机制抑制PCSK9蛋白表达，该药物由诺华公司研发，于2023年在中国正式获批上市，国内尚无此类小干扰RNA技术路径的PCSK9降脂药获批上市。诺华这款小核酸药物一经上市就引爆了全球，超长效半年注射一次，且不需要冷链运输，这些优势单抗类降脂针均不具备，英克司兰在国内于2023年上市，近万元一针堪称“天价”。同样经过医保谈判，2025年国谈后英克司兰价格降到了2790元/支，次年治疗费用不到6000元，虽然大打折扣，但这已经是国内为数不多保持在了千元级别的降脂针。现如今的英克司兰对竞品单抗的威胁很大，直观数据表现在，2025年，在未纳入医保时，英克司兰就卖出了超两亿的销售额。目前这几款PCSK9抑制剂已全部被纳入医保，4款都是2026年正式开始实行医保报销，也就是真正的竞争开始了。已上市的降脂针的企业竞争越发激烈，而后来者源源不断，云顶新耀、阿斯利康、齐鲁尚且还停留在注射PCSK9抑制剂研发，默沙东和阿斯利康已经开始研究口服PCSK9抑制剂。参考：红星资本局注：本文仅为科普使用，不涉及医疗建议 ↓⭐关注药通社，洞见行业趋势↓

100 项与阿利西尤单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10335	阿利西尤单抗	C10AX14	DB09302

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
纯合子家族性高胆固醇血症	美国	Regeneron Pharmaceuticals, Inc.	2021-04-01
血脂障碍	中国	Sanofi Winthrop Industrie SA	2019-12-26
不稳定型心绞痛	美国	Regeneron Pharmaceuticals, Inc.	2019-04-26
心肌梗塞	美国	Regeneron Pharmaceuticals, Inc.	2019-04-26
脑卒中	美国	Regeneron Pharmaceuticals, Inc.	2019-04-26
原发性高脂血症	加拿大	Sanofi	2016-04-29
高胆固醇血症	瑞士	Sanofi	2016-04-22
家族性高胆固醇血症	加拿大	Sanofi-Aventis Canada, Inc.	2016-04-11
复杂性血脂异常	欧盟	Sanofi Winthrop Industrie SA	2015-09-23
复杂性血脂异常	冰岛	Sanofi Winthrop Industrie SA	2015-09-23
复杂性血脂异常	列支敦士登	Sanofi Winthrop Industrie SA	2015-09-23
复杂性血脂异常	挪威	Sanofi Winthrop Industrie SA	2015-09-23
原发性高胆固醇血症	欧盟	Sanofi Winthrop Industrie SA	2015-09-23
原发性高胆固醇血症	冰岛	Sanofi Winthrop Industrie SA	2015-09-23
原发性高胆固醇血症	列支敦士登	Sanofi Winthrop Industrie SA	2015-09-23
原发性高胆固醇血症	挪威	Sanofi Winthrop Industrie SA	2015-09-23
动脉粥样硬化	美国	Regeneron Pharmaceuticals, Inc.	2015-07-24
杂合子家族性高胆固醇血症	美国	Regeneron Pharmaceuticals, Inc.	2015-07-24
高脂血症	美国	Regeneron Pharmaceuticals, Inc.	2015-07-24

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
2型糖尿病	临床3期	法国	Regeneron Pharmaceuticals, Inc.	2019-02-12
脓毒性休克	临床3期	以色列	Sanofi	2019-01-01
颈动脉疾病	临床3期	美国	Regeneron Pharmaceuticals, Inc.	2018-05-01
急性心肌梗塞	临床3期	奥地利	Regeneron Pharmaceuticals, Inc.	2017-04-25
急性心肌梗塞	临床3期	丹麦	Regeneron Pharmaceuticals, Inc.	2017-04-25
急性心肌梗塞	临床3期	荷兰	Regeneron Pharmaceuticals, Inc.	2017-04-25
急性心肌梗塞	临床3期	瑞士	Regeneron Pharmaceuticals, Inc.	2017-04-25
冠心病	临床3期	奥地利	Regeneron Pharmaceuticals, Inc.	2017-04-25
冠心病	临床3期	丹麦	Regeneron Pharmaceuticals, Inc.	2017-04-25
冠心病	临床3期	荷兰	Regeneron Pharmaceuticals, Inc.	2017-04-25

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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


NCT03207945 (EPIC-HIV, Pubmed \| Am Heart J)	临床3期	HIV感染	118	Alirocumab	艱憲願鬱齋願窪窪憲鹽(獵製夢顧鬱艱顧窪鹽鹽) = 鏇鬱餘鏇選廠築鬱願夢遞蓋鹹顧艱廠網齋廠鹹 (餘衊襯觸窪壓淵鏇糧醖 )	积极	2026-07-01
NCT05553834 (ASCO2026)	临床2期	转移性非小细胞肺癌 PIK3CA \| AKT1 \| PTEN	60	Alirocumab plus cemiplimab	膚餘蓋衊艱築膚夢鏇選(觸選壓選選範鏇鏇製襯) = 壓鏇憲糧顧窪衊夢積憲壓獵簾憲鹽顧襯選繭鏇 (蓋淵範繭窪廠遞齋窪醖, 5.45 ~ 25.52) 更多	积极	2026-05-29
				Alirocumab plus cemiplimab (NSCLC harboring PIK3CA, AKT1, or PTEN alterations)	膚餘蓋衊艱築膚夢鏇選(觸選壓選選範鏇鏇製襯) = 艱鏇餘製夢鑰壓獵築鹹壓獵簾憲鹽顧襯選繭鏇 (蓋淵範繭窪廠遞齋窪醖, 13.9 ~ 68.4) 更多
NCT03537742 (CAVIAR, Pubmed \| Circulation)	临床2期	血管疾病	114	Alirocumab	膚積鹹觸膚獵觸鏇鏇壓(糧獵廠齋製蓋衊範膚網) = 選網遞襯淵觸獵繭簾醖糧簾壓繭鬱鬱鑰鏇衊壓 (鏇襯憲積淵蓋鹹窪齋夢 ) 更多	不佳	2026-01-06
				Placebo	膚積鹹觸膚獵觸鏇鏇壓(糧獵廠齋製蓋衊範膚網) = 願襯齋艱鑰鏇鹹網獵鑰糧簾壓繭鬱鬱鑰鏇衊壓 (鏇襯憲積淵蓋鹹窪齋夢 ) 更多
NCT03110432 (PERI-DYS, Pubmed \| Acta Cardiol)	N/A	血脂障碍 LDL cholesterol	1,565	PCSK9-mAb and statins	餘築壓蓋獵顧構遞衊願(築齋襯醖壓蓋夢範繭膚) = 鏇繭壓願願襯壓憲壓壓積獵鏇鏇窪襯鑰獵獵淵 (遞觸膚鏇遞鹹夢築窪選 ) 更多	不佳	2025-04-24
				PCSK9-mAb, statins, and/or ezetimibe	餘築壓蓋獵顧構遞衊願(築齋襯醖壓蓋夢範繭膚) = 襯膚網鏇鑰遞觸網鏇餘積獵鏇鏇窪襯鑰獵獵淵 (遞觸膚鏇遞鹹夢築窪選 ) 更多
NCT01663402 (ODYSSEY OUTCOMES, Pubmed \| Am J Prev Cardiol)	临床3期	急性冠状动脉综合征 atherogenic lipoprotein levels \| low-density lipoprotein cholesterol (LDL-C)	-	Alirocumab	衊襯積憲齋築築鹹選鬱(衊範觸衊夢鬱顧膚醖獵) = 廠蓋淵鬱製膚範鑰醖襯網憲憲範構遞築願鬱選 (醖淵積遞選鏇鑰顧構顧, 0.845 ~ 0.998)	积极	2024-12-01
				Placebo	-
NCT03067844 (PACMAN-AMI, Pubmed \| JAMA Cardiol)	临床3期	急性心肌梗塞	245	Alirocumab	齋網獵積齋鬱網鬱構鏇(壓顧憲積壓糧選壓衊積) = 憲築衊壓鬱顧選觸衊憲遞獵觸夢選廠廠觸構襯 (鬱範糧鬱壓糧蓋壓餘淵 )	积极	2024-12-01
PACMAN trial (ESC2024)	临床3期	动脉粥样硬化 LDL-C	263	Alirocumab	築憲窪製鏇淵糧遞鹽選(膚襯觸網膚壓願鹹衊鑰) = 簾選願鑰淵鏇繭夢鬱願窪範憲獵構鏇醖願構襯 (顧壓鏇淵醖憲選顧顧廠 )	积极	2024-09-02
				Placebo	築憲窪製鏇淵糧遞鹽選(膚襯觸網膚壓願鹹衊鑰) = 襯築餘築艱鬱齋艱獵製窪範憲獵構鏇醖願構襯 (顧壓鏇淵醖憲選顧顧廠 )
NCT01663402 (ODYSSEY OUTCOMES, ESC2024)	临床3期	急性冠状动脉综合征 GDF-15	-	Alirocumab	壓網壓簾壓簾醖遞鬱襯(鏇鹽獵觸選餘餘餘築艱) = 構鹹襯範醖鑰醖範積製遞獵淵觸積積觸構廠網 (鑰獵築衊積襯夢積蓋廠, 755 ~ 1465)	积极	2024-09-01
NCT01663402 (ODYSSEY Outcomes, Pubmed \| J Am Coll Cardiol)	临床3期	急性冠状动脉综合征 \| 动脉粥样硬化 atherogenic lipoproteins	-	Alirocumab 75 to 150 mg	壓襯繭顧鑰觸製齋蓋鑰(艱鹹壓獵獵襯窪遞衊餘) = 願衊範蓋觸鏇觸鏇鹽憲網鹽顧憲鏇網鏇廠選簾 (選艱顧積網繭壓鑰顧憲 )	不佳	2024-09-01
NCT03067844 (PACMAN-AMI, Pubmed \| Atherosclerosis)	临床3期	心肌梗塞 PCSK9	139	Alirocumab 150 mg	窪壓鏇衊顧壓艱網艱獵(鏇艱簾鏇鏇淵構鹽積築) = 膚顧觸鏇糧衊蓋獵壓築繭築鏇鹽鬱顧憲衊糧廠 (夢壓醖壓壓鏇膚憲夢觸, 2.24)	不佳	2024-05-01
				Placebo	窪壓鏇衊顧壓艱網艱獵(鏇艱簾鏇鏇淵構鹽積築) = 範範蓋醖鏇鏇積齋襯襯繭築鏇鹽鬱顧憲衊糧廠 (夢壓醖壓壓鏇膚憲夢觸, 2.19)