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更新于：2026-07-06
Zerlasiran
更新于：2026-07-06
概要
基本信息
非在研机构- |
权益机构- |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
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Sequence Code 452929085
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Sequence Code 452929086
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关联
2
项与 Zerlasiran 相关的临床试验NCT05537571
A Multi-centre, Randomised, Double-blind, Placebo-controlled, Phase 2 Study to Investigate Efficacy, Safety and Tolerability of SLN360 in Participants With Elevated Lipoprotein(a) at High Risk of Atherosclerotic Cardiovascular Disease Events
NCT04606602
A Randomised, Double-blind, Placebo Controlled, First-in-human Study to Investigate the Safety, Tolerability, Pharmacokinetic and Pharmacodynamic Response of SLN360 in Subjects With Elevated Lipoprotein(a)
100 项与 Zerlasiran 相关的临床结果
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100 项与 Zerlasiran 相关的转化医学
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100 项与 Zerlasiran 相关的专利（医药）
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22
项与 Zerlasiran 相关的文献（医药）2026-06-01CARDIOVASCULAR DRUGS AND THERAPY
Lipoprotein(a) in Cardiovascular Diseases and Emerging Therapeutic Strategies
Review
作者: Smith, Emily Lauren Schenk ; Selico-Dunn, Alexandra C ; Al-Horani, Rami A
Abstract:
Purpose:
Lipoprotein(a) [Lp(a)] is increasingly recognized as a genetically determined, independent risk factor for atherosclerotic cardiovascular disease (ASCVD). This review examines the structure, pathophysiology, and epidemiology of Lp(a), with a focus on its contribution to ASCVD and related conditions such as aortic valve stenosis and peripheral artery disease. The main research question addresses how Lp(a) influences cardiovascular risk and how emerging therapies may modify this risk.
Methods:
This review synthesizes published evidence describing the biological characteristics of Lp(a), its mechanistic roles in disease, and its epidemiologic associations with cardiovascular outcomes. It also evaluates current and investigational therapeutic approaches by examining clinical trial data for agents targeting Lp(a).
Results:
Lp(a) contributes to residual cardiovascular risk through proatherogenic, proinflammatory, and prothrombotic mechanisms. Current evidence highlights its involvement in ASCVD, aortic valve stenosis, and peripheral artery disease. Clinical studies of antisense oligonucleotides, small interfering RNAs, oral small molecules, and CRISPR-based gene editing, including pelacarsen, olpasiran, zerlasiran, lepodisiran, muvalaplin, and obicetrapib, demonstrate promising efficacy and safety. These agents show potential to significantly reduce Lp(a) levels and influence future cardiovascular prevention strategies.
Conclusion:
As novel therapies advance and clinical guidelines evolve, Lp(a) is emerging as a central determinant in personalized cardiovascular care. The increasing emphasis on Lp(a) testing underscores its importance in risk stratification and future therapeutic decisionmaking.
2026-06-01PROGRESS IN LIPID RESEARCH
Structure-guided dissection of the genetic variations within human LPA locus and its role in the development of cardiovascular diseases
Review
作者: Tonevitsky, Alexander ; Jeiran, Kianoush ; Stepanova, Anna ; Baranova, Ancha ; Shkurnikov, Maxim ; Antipenko, Ivan
Lipoprotein (a) [Lp(a)] is a highly heterogeneous lipoprotein particle promoting panvascular disease. Structurally, it consists of an LDL-like core covalently bound to apolipoprotein (a) [apo(a)]. Molecular determinants linking various genetic variants of apo(a) constituent of Lp(a) to vascular pathology remain incompletely defined. We have built a model allowing dissection which variations in LPA gene are functional, and which are mere associates of these functional variations. Copy number changes in kringle IV type 2 (KIV-2), together with a spectrum of single nucleotide polymorphisms (SNPs), regulate apo(a) size, expression, and function. These variants can be broadly categorized into Lp(a)-increasing, Lp(a)-lowering, and null alleles, with distinct prevalence across populations. Notably, risk alleles such as rs10455872 and rs3798220 account for substantial variance in circulating Lp(a) and confer elevated susceptibility to coronary artery disease, whereas splice-altering and nonsense alleles markedly reduce Lp(a) concentrations. The therapeutic implications of modifying circulating Lp(a) levels are profound. While conventional lipid-lowering therapies exert little influence on Lp(a), antisense oligonucleotides (pelacarsen) and small interfering RNA agents (olpasiran, SLN360) achieve robust Lp(a) reductions. Integrating genetic insights with structural modeling provides a framework to disentangle functional from proxy associations within LPA and neutralize the cardiovascular hazard conferred by elevated levels of Lp(a).
2026-05-01PHARMACOLOGICAL RESEARCH
Comparative efficacy and safety of novel Lp(a)-lowering therapies for ASCVD prevention: A network meta-analysis
Review
作者: Wang, Xing-Jin ; Li, Yi ; Hu, Jia-Qiang ; Xu, Ying ; Li, Jin-Wei ; Liu, Song ; Wu, An-Xin ; Zhao, Chen
Elevated lipoprotein(a) [Lp(a)] is a genetically determined and independent risk factor for atherosclerotic cardiovascular disease (ASCVD) that is largely resistant to conventional lipid-lowering therapies. Novel Lp(a)-targeted agents, including small interfering RNA (siRNA), antisense oligonucleotides (ASO), and the oral small-molecule inhibitor muvalaplin, have shown potent efficacy in early trials. We conducted a systematic review and network meta-analysis to comprehensively compare their efficacy and safety. A total of 25 randomized controlled trials (RCTs) involving 7715 participants were included, evaluating six siRNA agents, four ASO agents, and one small-molecule inhibitor. The primary outcome was percentage change from baseline in Lp(a). Secondary outcomes included absolute change in Lp(a), percentage changes in apolipoprotein B (apoB) and low-density lipoprotein cholesterol (LDL-C), and adverse events. SiRNA therapies achieved the greatest Lp(a) reductions (olpasiran: mean difference [MD] -92.1%, 95% CI -100.1 to -84.0%; zerlasiran: -80.6%, 95% CI -87.7 to -73.5%), followed by muvalaplin (-76.8%, 95% CI -90.3 to -63.2%) and ASO therapy (pelacarsen: -54.2%, 95% CI -72.2 to -36.2%; all P < 0.001). Most agents achieved absolute Lp(a) reductions exceeding 105 nmol/L, suggesting clinically meaningful benefit. Baseline Lp(a) levels significantly modified treatment response (P < 0.001), and concomitant proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor use further enhanced LDL-C reduction (P = 0.024). All therapies were well tolerated, with injection-site reactions most frequent for injectables, while muvalaplin was well tolerated. These findings indicate that targeted Lp(a)-lowering therapies substantially reduce circulating Lp(a), with siRNA showing the greatest potency and muvalaplin offering a convenient oral alternative for personalized ASCVD risk reduction.
144
项与 Zerlasiran 相关的新闻（医药）2026-07-01
siRNA核酸药物
100 项与 Zerlasiran 相关的药物交易
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 心血管疾病 | 临床3期 | 英国 | - | |
| 动脉粥样硬化 | 临床2期 | 澳大利亚 | 2022-12-13 | |
| 动脉粥样硬化 | 临床2期 | 捷克 | 2022-12-13 | |
| 动脉粥样硬化 | 临床2期 | 丹麦 | 2022-12-13 | |
| 动脉粥样硬化 | 临床2期 | 荷兰 | 2022-12-13 | |
| 动脉粥样硬化 | 临床2期 | 斯洛伐克 | 2022-12-13 | |
| 动脉粥样硬化 | 临床2期 | 南非 | 2022-12-13 | |
| 动脉粥样硬化 | 临床2期 | 英国 | 2022-12-13 | |
| 高脂蛋白血症 | 临床1期 | 美国 | 2020-11-18 | |
| 高脂蛋白血症 | 临床1期 | 美国 | 2020-11-18 |
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临床结果
临床结果
适应症
分期
评价
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临床2期 | 180 | (SLN360 300 mg Q16W) | 鹽獵網齋餘遞憲壓繭淵(鹽鹹齋繭獵構繭鹹獵範) = 鬱襯製願製蓋壓鑰願獵 憲簾鏇範膚鬱顧觸夢築 (淵夢鹽壓醖淵餘襯遞膚, 1.99) 更多 | - | 2025-07-01 | ||
(SLN360 300 mg Q24W) | 鹽獵網齋餘遞憲壓繭淵(鹽鹹齋繭獵構繭鹹獵範) = 鬱鏇艱構艱鹽鹽廠壓遞 憲簾鏇範膚鬱顧觸夢築 (淵夢鹽壓醖淵餘襯遞膚, 1.94) 更多 | ||||||
临床2期 | 动脉粥样硬化 lipoprotein(a) concentration | 178 | Zerlasiran 450 mg every 24 weeks for 2 doses | 衊鏇膚膚構憲顧鏇鹹鏇(餘製繭蓋顧夢糧鹹膚遞) = 觸鹽觸獵壓襯製製顧廠 齋簾選廠膚衊襯壓鑰選 (醖積願鬱鬱醖衊簾淵憲, −90.9 ~ −80.3) 更多 | 积极 | 2024-11-18 | |
Zerlasiran 300 mg every 16 weeks for 3 doses | 衊鏇膚膚構憲顧鏇鹹鏇(餘製繭蓋顧夢糧鹹膚遞) = 膚鬱範築膚繭廠夢積構 齋簾選廠膚衊襯壓鑰選 (醖積願鬱鬱醖衊簾淵憲, −88.2 ~ −77.4) 更多 | ||||||
临床2期 | 178 | 鏇壓窪願窪獵壓艱繭築(鹽獵醖淵製鏇築鹽餘鏇) = 鏇鑰範廠顧蓋積廠夢繭 廠鑰簾製獵窪鏇鬱憲窪 (醖鹹網鹹網艱鑰繭築醖 ) 达到 | 积极 | 2024-06-20 | |||
Placebo | - | ||||||
临床1期 | - | Zerlasiran 300 mg (a single subcutaneous dose) | 夢積獵鑰選壓淵獵膚鹹(襯壓構繭鬱淵齋積膚製) = There were no serious adverse events. 獵夢鹹襯蓋觸築窪壓構 (顧窪鹽鑰鏇鏇窪窪鹽鏇 ) | 积极 | 2024-04-08 | ||
Zerlasiran 600 mg (a single subcutaneous dose) | |||||||
临床2期 | 178 | 糧鑰糧膚壓鑰憲鬱淵範(選繭願鏇齋觸齋憲齋壓) = 衊窪蓋鑰齋淵簾餘鑰網 構窪淵網糧積醖網築積 (獵衊鏇獵願廠壓餘網艱 ) | 积极 | 2024-03-13 | |||
Placebo | - | ||||||
临床1期 | 36 | 鬱醖鏇選構鹽鏇鑰製餘(鹽製壓鹹鏇醖齋鑰積繭) = 膚選衊選觸鏇鑰廠憲製 築願蓋觸壓淵繭淵餘積 (膚齋膚廠顧齋繭憲顧願 ) 更多 | 积极 | 2023-11-01 | |||
Placebo | - | ||||||
临床1期 | Lp(a) | 32 | Placebo | 窪憲築鹹選觸艱積願積(憲蓋網鏇觸襯淵鹽糧願) = One participant experienced 2 serious adverse event episodes: admission to the hospital for headache following SARS-CoV-2 vaccination and later for complications of cholecystitis, both of which were judged to be unrelated to study drug. 獵鏇製鬱衊襯夢簾築獵 (襯齋鬱遞鏇顧顧鑰齋艱 ) | 积极 | 2022-05-03 | |
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