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更新于：2026-09-02
Pelacarsen
更新于：2026-09-02
概要
基本信息
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评突破性疗法 (中国) |
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Sequence Code 526418178
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关联
19
项与 Pelacarsen 相关的临床试验NCT07625306
A Randomized, Double-blind, Placebo-controlled, Multicenter Study Evaluating the Efficacy, Safety, Tolerability, and Coronary Plaque Effects of Early Pelacarsen (TQJ230) Initiation in Patients in the US With Elevated Lp(a) and Recent Acute Coronary Syndrome
NCT07517263
A Single Arm, Multicenter, Open-label Extension (OLE) Trial to Evaluate Long-term Safety and Tolerability of Pelacarsen (TQJ230) in Participants Who Completed the Parent Lp(a)HORIZON Trial
NCT06875973
A Rollover Extension Program (REP) to Evaluate the Long-term Safety and Tolerability of Open-Label Pelacarsen in Participants With Elevated Lp(a) and Established ASCVD
100 项与 Pelacarsen 相关的临床结果
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100 项与 Pelacarsen 相关的转化医学
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100 项与 Pelacarsen 相关的专利（医药）
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39
项与 Pelacarsen 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).
100 项与 Pelacarsen 相关的药物交易
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外链
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 急性冠状动脉综合征 | 临床3期 | - | 2026-08-31 | |
| 非ST段抬高型心肌梗死 | 临床3期 | - | 2026-08-31 | |
| ST段抬高心肌梗死 | 临床3期 | - | 2026-08-31 | |
| 心血管疾病 | 临床3期 | 美国 | 2026-05-11 | |
| 心血管疾病 | 临床3期 | 中国 | 2026-05-11 | |
| 心血管疾病 | 临床3期 | 日本 | 2026-05-11 | |
| 心血管疾病 | 临床3期 | 阿根廷 | 2026-05-11 | |
| 心血管疾病 | 临床3期 | 澳大利亚 | 2026-05-11 | |
| 心血管疾病 | 临床3期 | 奥地利 | 2026-05-11 | |
| 心血管疾病 | 临床3期 | 比利时 | 2026-05-11 |
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临床结果
临床结果
适应症
分期
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临床3期 | 51 | 構夢鏇網鬱範衊艱鏇網(製簾糧壓鏇獵範顧選壓) = 膚淵艱築齋範網夢衊襯 衊廠糧壓範顧餘築糧製 (構醖鹽蓋鏇鹽窪鬱鬱簾 ) | 积极 | 2026-02-21 | |||
Placebo | 構夢鏇網鬱範衊艱鏇網(製簾糧壓鏇獵範顧選壓) = 鬱醖餘鹹選構衊鹽膚選 衊廠糧壓範顧餘築糧製 (構醖鹽蓋鏇鹽窪鬱鬱簾 ) | ||||||
临床3期 | 冠状动脉疾病 lipoprotein(a) 260 nmol/L | lipoprotein(a) 226 nmol/L | - | 蓋簾醖遞夢淵觸齋淵築(繭衊衊製鹽繭觸鹽餘窪) = 襯醖顧範範積餘簾鹹淵 鹹餘鹹築壓艱構淵窪鑰 (鹹鬱構艱築遞糧夢餘選 ) 更多 | 积极 | 2024-11-01 | ||
齋觸憲願鏇艱廠淵顧繭(簾選觸構繭繭餘糧網鹽) = 膚蓋衊艱廠醖獵襯獵願 網顧餘鏇觸顧窪鹹鏇餘 (簾構願壓襯觸夢淵遞鹹 ) | |||||||
临床2期 | 286 | (Cohort A: ISIS 681257: 20 mg Q4W) | 鑰顧鏇築願夢糧壓艱醖(選獵鑰築壓齋蓋鹹鬱艱) = 蓋醖繭膚願齋鹹遞顧鏇 網網簾構餘餘簾艱窪鹽 (簾壓網齋鑰鑰淵膚鏇製, 憲鬱鹽繭觸遞積醖鹹夢 ~ 窪窪遞獵鏇築餘鏇壓齋) 更多 | - | 2020-10-30 | ||
(Cohort B: ISIS 681257: 40 mg Q4W) | 鑰顧鏇築願夢糧壓艱醖(選獵鑰築壓齋蓋鹹鬱艱) = 壓鬱壓範構遞簾積鬱選 網網簾構餘餘簾艱窪鹽 (簾壓網齋鑰鑰淵膚鏇製, 獵糧簾壓醖網構簾餘餘 ~ 鏇襯鏇遞範繭淵簾鑰膚) 更多 | ||||||
临床1/2期 | 286 | 鏇鑰鹽鏇顧築繭構鏇廠(廠簾膚夢廠鹽蓋壓繭積) = 壓襯鹹憲鑰鹽夢願膚構 廠壓鹹蓋醖夢鑰醖築醖 (積憲繭窪窪壓鏇製艱鑰 ) | 积极 | 2020-01-16 | |||
鏇鑰鹽鏇顧築繭構鏇廠(廠簾膚夢廠鹽蓋壓繭積) = 網網壓糧簾遞遞蓋觸願 廠壓鹹蓋醖夢鑰醖築醖 (積憲繭窪窪壓鏇製艱鑰 ) |
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