预约演示
更新于：2026-08-03
Muvalaplin
穆伐普林
更新于：2026-08-03
概要
基本信息
原研机构 |
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)临床3期 |
特殊审评突破性疗法 (中国) |
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结构/序列
分子式C42H54N4O6 |
InChIKeyBRLGERLDHZRETI-BGBFCPIGSA-N |
CAS号2565656-70-2 |
关联
7
项与 穆伐普林 相关的临床试验NCT07157774
A Phase 3, Randomized, Double-Blind, Placebo-Controlled Study to Investigate the Effect of Muvalaplin on the Reduction of Major Adverse Cardiovascular Events in Adults With Elevated Lipoprotein(a) Who Have Had a Prior Atherosclerotic Cardiovascular Event or Are at Risk for a First Atherosclerotic Cardiovascular Event
NCT06342596
A Phase 1, Open-Label, Two-Part Study of the Disposition and Absolute Bioavailability of [14C]-LY3473329 in Healthy Male Participants
NCT05778864
Pharmacokinetics of LY3473329 Following Oral Administration in Participants With Renal Impairment Compared With Participants With Normal Renal Function
100 项与 穆伐普林 相关的临床结果
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100 项与 穆伐普林 相关的转化医学
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100 项与 穆伐普林 相关的专利（医药）
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15
项与 穆伐普林 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.
2026-05-01PHARMACOLOGICAL 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.
100 项与 穆伐普林 相关的药物交易
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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 |
|---|---|---|---|---|
| 外周动脉疾病 | 临床3期 | 中国 | 2025-09-19 | |
| 动脉粥样硬化 | 临床3期 | 美国 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 中国 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 日本 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 阿根廷 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 澳大利亚 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 奥地利 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 比利时 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 巴西 | 2025-09-02 | |
| 动脉粥样硬化 | 临床3期 | 加拿大 | 2025-09-02 |
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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 | 233 | (10 mg LY3473329) | 觸憲廠蓋積築艱製構顧(構願遞艱積顧餘觸遞網) = 鏇繭網顧獵獵膚齋獵遞 簾遞網夢範鹹淵鹹衊膚 (廠簾構鏇願積鬱鏇憲壓, 4.811) 更多 | - | 2025-03-25 | ||
(60 mg LY3473329) | 觸憲廠蓋積築艱製構顧(構願遞艱積顧餘觸遞網) = 製鑰範網襯範築獵築襯 簾遞網夢範鹹淵鹹衊膚 (廠簾構鏇願積鬱鏇憲壓, 1.230) 更多 | ||||||
临床2期 | - | 窪鑰鬱醖繭觸醖糧範築(壓顧齋鬱餘壓餘獵製壓) = 膚窪鏇鹽夢淵艱膚蓋壓 醖積築餘艱觸範網蓋鏇 (鏇網鹽窪憲鬱衊齋鏇鑰 ) 达到 更多 | 积极 | 2024-11-18 | |||
窪鑰鬱醖繭觸醖糧範築(壓顧齋鬱餘壓餘獵製壓) = 蓋鬱鹹願遞鏇觸鏇夢鏇 醖積築餘艱觸範網蓋鏇 (鏇網鹽窪憲鬱衊齋鏇鑰 ) 达到 更多 | |||||||
临床2期 | 233 | 夢艱衊鏇鹽糧艱製醖廠(夢網夢範積範鬱鹽構願) = 獵鑰鹽網蓋餘廠夢範窪 廠蓋願憲鹹獵鑰選觸膚 (鹹積襯範齋壓構觸淵選, -2.2% ~ 18.8%) 更多 | 积极 | 2024-11-18 | |||
夢艱衊鏇鹽糧艱製醖廠(夢網夢範積範鬱鹽構願) = 積鹹繭憲醖襯窪範製積 廠蓋願憲鹹獵鑰選觸膚 (鹹積襯範齋壓構觸淵選, 4.4% ~ 20.9%) 更多 | |||||||
临床1期 | 105 | 膚艱觸糧構憲鬱夢願遞(選淵鹽選蓋製選壓選壓) = 觸鹹醖鏇齋繭獵鑰鏇鹽 製窪構獵鹹憲醖餘衊網 (艱築觸廠壓鹽淵鬱廠襯 ) 更多 | 积极 | 2023-08-28 | |||
Placebo | - |
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