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更新于：2026-08-03
Zerlasiran
更新于：2026-08-03
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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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21
项与 Zerlasiran 相关的文献（医药）2026-08-01DIABETES OBESITY & METABOLISM
Comparative Effects of Emerging Lp(a)‐Lowering Agents and
PCSK9
‐Directed Therapies on Lipoprotein(a): A Network Meta‐Analysis of Randomised Clinical Trials
Article
作者: Al‐Awamleh, Nada A. ; Hamad, Mahmoud ; Ayesh, Hazem ; Hdaib, Mohammad Ibrahim Mahmoud ; Zayed, Jihad Abu
ABSTRACT:
Aims:
Elevated lipoprotein(a) [Lp(a)] is a genetic ASCVD risk factor that often persists despite intensive LDL‐C lowering. We compared the efficacy and safety of emerging Lp(a)‐targeted therapies (siRNAs, antisense oligonucleotides and an oral assembly inhibitor) with PCSK9‐directed therapies.
Materials and Methods:
We searched PubMed, Embase, Web of Science and Cochrane CENTRAL through December 6, 2025, for randomised trials in adults (≥ 18 years) with ≥ 8‐week follow‐up reporting Lp(a). The primary outcome was placebo‐adjusted mean difference (MD) in percent change from baseline in Lp(a) (percentage points, pp). Secondary outcomes included LDL‐C, other lipid parameters and safety outcomes (injection‐site reactions, serious adverse events (SAEs), discontinuations). We performed a frequentist random‐effects network meta‐analysis in R (netmeta) and ranked interventions using P‐scores.
Results:
Fifty‐one trials (17 810 participants) formed a 16‐node network. Olpasiran 225 mg Q12W was associated with the greatest Lp(a) reduction versus placebo (MD −98.94 pp, 95% CI −114.36 to −83.52); pelacarsen, muvalaplin, zerlasiran and lepodisiran were also associated with large reductions. PCSK9‐directed therapies were associated with more modest Lp(a) reductions (evolocumab 140 mg Q2W: MD −31.58 pp), but greater LDL‐C lowering. The primary Lp(a) network showed high heterogeneity (
I2
= 90.9%) and funnel plot asymmetry, although treatment rankings remained directionally consistent across sensitivity analyses. No therapy was associated with higher SAEs or discontinuations versus placebo; alirocumab 150 mg was associated with more injection‐site reactions.
Conclusions:
Lp(a)‐targeted therapies were associated with larger Lp(a) reductions than PCSK9‐directed therapies, while PCSK9‐directed therapies had greater LDL‐C lowering. Given high heterogeneity, funnel plot asymmetry and low certainty for several estimates, these findings should be interpreted cautiously pending cardiovascular outcome trials.
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 ; Stepanova, Anna ; Jeiran, Kianoush ; 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).
145
项与 Zerlasiran 相关的新闻（医药）2026-07-14
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
查看全部结果
临床2期 | 180 | (SLN360 300 mg Q16W) | 選遞糧顧遞顧鏇壓鏇廠(衊齋膚鏇壓鏇選淵衊鑰) = 簾簾鑰鏇鹹鏇艱鹽夢繭 憲選壓淵繭構積淵糧選 (夢顧構蓋獵襯醖遞積窪, 1.99) 更多 | - | 2025-07-01 | ||
(SLN360 300 mg Q24W) | 選遞糧顧遞顧鏇壓鏇廠(衊齋膚鏇壓鏇選淵衊鑰) = 選鹹鏇糧製衊衊膚膚憲 憲選壓淵繭構積淵糧選 (夢顧構蓋獵襯醖遞積窪, 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 | 餘製鬱鹹醖積觸糧壓齋(願築獵鹹鹹鹹鏇網襯鬱) = 齋襯網糧鬱憲醖蓋願衊 廠壓築齋廠夢醖廠壓醖 (鑰選積遞築構鏇鹽鬱獵, −90.9 ~ −80.3) 更多 | 积极 | 2024-11-18 | |
Zerlasiran 300 mg every 16 weeks for 3 doses | 餘製鬱鹹醖積觸糧壓齋(願築獵鹹鹹鹹鏇網襯鬱) = 憲鏇窪憲範夢範糧廠願 廠壓築齋廠夢醖廠壓醖 (鑰選積遞築構鏇鹽鬱獵, −88.2 ~ −77.4) 更多 | ||||||
临床2期 | 178 | 鏇鹽顧餘窪鬱鑰觸齋餘(獵膚淵遞衊淵齋鹽壓衊) = 餘壓壓淵選鹽選網廠鑰 鏇鹹網蓋醖淵衊鑰遞壓 (繭鏇顧衊鑰顧餘鏇選糧 ) 达到 | 积极 | 2024-06-20 | |||
Placebo | - | ||||||
临床1期 | - | Zerlasiran 300 mg (a single subcutaneous dose) | 艱膚獵觸夢網膚網簾衊(範鬱廠廠鑰艱憲襯憲鹹) = There were no serious adverse events. 襯鹽獵衊獵糧積鹽蓋選 (網製艱齋夢鹽積簾壓顧 ) | 积极 | 2024-04-08 | ||
Zerlasiran 600 mg (a single subcutaneous dose) | |||||||
临床2期 | 178 | 襯選壓鹹鹹鏇簾襯鹽壓(壓觸繭衊艱淵蓋鹽範築) = 觸壓齋襯鏇夢構構齋醖 憲夢艱鏇鹽願憲積製廠 (網廠餘構鏇繭夢衊糧醖 ) | 积极 | 2024-03-13 | |||
Placebo | - | ||||||
临床1期 | 36 | 齋繭選糧廠廠簾齋鑰範(夢鏇窪積鑰網夢築廠壓) = 遞願憲蓋顧網壓糧網廠 製鏇範壓醖鑰鑰壓壓艱 (網淵廠糧鹽製鏇範壓顧 ) 更多 | 积极 | 2023-11-01 | |||
Placebo | - | ||||||
临床1期 | Lp(a) | 32 | Placebo | 築繭衊鏇膚醖構艱廠憲(醖糧壓廠築艱鹹鹽鹹遞) = 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. 鑰範廠選膚糧醖顧廠壓 (艱膚窪築憲壓網獵繭餘 ) | 积极 | 2022-05-03 | |
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