Amarin Presents Key Eicosapentaenoic Acid (EPA) Mechanism Data at ESC 2025

Amarin Corporation presented new *in vitro* data at ESC Congress 2025 regarding VASCEPA®/VAZKEPA® (EPA). The research demonstrated EPA’s potential to reduce inflammation in atherosclerotic cardiovascular disease (ASCVD) by modulating the ATP-P2X7 axis and NLRP3 inflammasome in macrophages. Additionally, EPA inhibited lipoprotein(a) [Lp(a)] oxidation, mitigating oxidative stress and pro-inflammatory protein expression in endothelial cells. These findings suggest cardiovascular benefits of EPA may extend beyond triglyceride reduction, potentially offering further risk mitigation.

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Amarin Corporation (NASDAQ:AMRN) unveiled compelling new *in vitro* data at the European Society of Cardiology (ESC) Congress 2025 in Madrid, offering a deeper dive into the mechanistic actions of VASCEPA®/VAZKEPA® (eicosapentaenoic acid/EPA).

The research pinpointed two key findings: first, EPA demonstrated its potential to dial down inflammation in atherosclerotic cardiovascular disease (ASCVD) by tweaking the ATP-P2X7 axis and NLRP3 inflammasome activation within monocyte-derived macrophages. Second, EPA showcased its prowess in inhibiting lipoprotein(a) [Lp(a)] oxidation, thereby softening its impact on oxidative stress and the expression of pro-inflammatory proteins in endothelial cells.

These results hint that the cardiovascular perks of EPA might stretch beyond merely reducing triglyceride levels, potentially unlocking extra avenues for mitigating cardiovascular risk in patients who need it most.

Amarin Corporation (NASDAQ:AMRN) ha presentato nuovi dati in vitro al Congresso della European Society of Cardiology (ESC) 2025 a Madrid, evidenziando importanti approfondimenti meccanicistici su VASCEPA®/VAZKEPA® (acido eicosapentaenoico/EPA).

Lo studio ha riportato due risultati rilevanti: in primo luogo, l’EPA ha mostrato il potenziale di ridurre l’infiammazione nella malattia cardiovascolare aterosclerotica (ASCVD) modulando l’asse ATP-P2X7 e l’attivazione dell’inflammasoma NLRP3 nei macrofagi derivati da monociti. In secondo luogo, l’EPA è stata in grado di inibire l’ossidazione della lipoproteina(a) [Lp(a)] e attenuare i suoi effetti sullo stress ossidativo e sull’espressione di proteine pro-infiammatorie nelle cellule endoteliali.

Questi risultati suggeriscono che i benefici cardiovascolari dell’EPA potrebbero andare oltre la riduzione dei trigliceridi, offrendo potenzialmente meccanismi aggiuntivi per diminuire il rischio cardiovascolare nei pazienti a rischio.

Amarin Corporation (NASDAQ:AMRN) presentó nuevos datos in vitro en el Congreso 2025 de la European Society of Cardiology (ESC) en Madrid, destacando importantes conocimientos mecanicistas sobre VASCEPA®/VAZKEPA® (ácido eicosapentaenoico/EPA).

La investigación reveló dos hallazgos clave: primero, el EPA mostró potencial para reducir la inflamación en la enfermedad cardiovascular aterosclerótica (ASCVD) al modular el eje ATP-P2X7 y la activación del inflamasoma NLRP3 en macrófagos derivados de monocitos. Segundo, el EPA demostró capacidad para inhibir la oxidación de lipoproteína(a) [Lp(a)] y atenuar sus efectos sobre el estrés oxidativo y la expresión de proteínas proinflamatorias en células endoteliales.

Estos hallazgos sugieren que los beneficios cardiovasculares del EPA podrían ir más allá de su conocido efecto reductor de triglicéridos, ofreciendo potencialmente mecanismos adicionales para disminuir el riesgo cardiovascular en pacientes en riesgo.

Amarin Corporation (NASDAQ:AMRN)은 마드리드에서 열린 유럽 심장학회(ESC) 2025 연례회의에서 VASCEPA®/VAZKEPA®(에이코사펜타엔산/EPA)에 대한 새로운 체외(in vitro) 데이터를 발표하며 주요 기전적 통찰을 제시했습니다.

연구는 두 가지 주요 결과를 밝혀냈습니다. 첫째, EPA는 단핵구 유래 대식세포에서 ATP-P2X7 축과 NLRP3 인플라마좀 활성화를 조절함으로써 죽상경화성 심혈관질환(ASCVD)에서 염증을 저감할 가능성을 보였습니다. 둘째, EPA는 지단백질(a)[Lp(a)]의 산화를 억제하고 혈관내피세포에서 산화 스트레스 및 친염증성 단백질 발현에 대한 영향을 완화하는 능력을 나타냈습니다.

이 결과는 EPA의 심혈관 혜택이 알려진 중성지방 감소 효과를 넘어 확장될 수 있으며, 위험군 환자의 심혈관 위험을 낮추기 위한 추가적인 기전을 제공할 수 있음을 시사합니다.

Amarin Corporation (NASDAQ:AMRN) a présenté de nouvelles données in vitro au congrès 2025 de la European Society of Cardiology (ESC) à Madrid, mettant en lumière des mécanismes clés concernant VASCEPA®/VAZKEPA® (acide eicosapentaénoïque/EPA).

La recherche a mis en évidence deux résultats importants : premièrement, l’EPA a montré un potentiel à réduire l’inflammation dans la maladie cardiovasculaire athéroscléreuse (ASCVD) en modulant l’axe ATP-P2X7 et l’activation de l’inflammasome NLRP3 dans les macrophages dérivés des monocytes. Deuxièmement, l’EPA a démontré sa capacité à inhiber l’oxydation de la lipoprotéine(a) [Lp(a)] et à atténuer ses effets sur le stress oxydatif et l’expression de protéines pro-inflammatoires dans les cellules endothéliales.

Ces résultats suggèrent que les bénéfices cardiovasculaires de l’EPA pourraient s’étendre au-delà de sa réduction connue des triglycérides, offrant potentiellement des mécanismes supplémentaires pour diminuer le risque cardiovasculaire chez les patients à risque.

Amarin Corporation (NASDAQ:AMRN) stellte neue in vitro-Daten auf dem Congress der European Society of Cardiology (ESC) 2025 in Madrid vor und hob dabei wichtige mechanistische Erkenntnisse zu VASCEPA®/VAZKEPA® (Eicosapentaensäure/EPA) hervor.

Die Forschung ergab zwei wesentliche Befunde: Erstens zeigte EPA das Potenzial, Entzündungen bei atherosklerotischer Herz-Kreislauf-Erkrankung (ASCVD) zu verringern, indem die ATP-P2X7-Achse und die Aktivierung des NLRP3-Inflammasoms in aus Monozyten abgeleiteten Makrophagen moduliert wurden. Zweitens zeigte EPA die Fähigkeit, die Oxidation von Lipoprotein(a) [Lp(a)] zu hemmen und dessen Auswirkungen auf oxidativen Stress sowie die Expression proinflammatorischer Proteine in Endothelzellen abzuschwächen.

Diese Erkenntnisse deuten darauf hin, dass die kardiovaskulären Vorteile von EPA über die bekannten triglyceridsenkenden Effekte hinausgehen könnten und zusätzliche Mechanismen bieten, um das kardiovaskuläre Risiko bei gefährdeten Patienten zu reduzieren.

Positive Takeaways

  • Research suggests EPA may provide additional cardiovascular benefits beyond triglyceride lowering
  • Data shows EPA’s potential to reduce inflammation in ASCVD patients
  • Evidence demonstrates EPA’s ability to inhibit Lp(a) oxidation

Insights

New lab studies reveal how Amarin’s EPA drug may reduce heart disease through anti-inflammatory effects beyond triglyceride lowering.

The new laboratory data presented at ESC 2025 significantly advances our understanding of VASCEPA®/VAZKEPA®’s mechanisms in cardiovascular protection. The findings demonstrate that eicosapentaenoic acid (EPA) likely works through multiple pathways beyond triglyceride reduction.

The first study shows EPA can modulate the NLRP3 inflammasome pathway in macrophages – a critical driver of atherosclerosis progression. By reducing extracellular ATP release and caspase 1 activation, EPA appears to dampen the inflammatory cascade that contributes to plaque formation and instability. This provides a mechanistic explanation for why VASCEPA shows clinical benefits that exceed what would be expected from triglyceride lowering alone.

The second study reveals EPA’s ability to inhibit lipoprotein(a) [Lp(a)] oxidation, which is particularly notable since elevated Lp(a) is an independent, genetic cardiovascular risk factor that has proven difficult to target therapeutically. The research demonstrates EPA acts as a lipid-centric scavenger that prevents Lp(a) oxidation, potentially explaining why VASCEPA reduced cardiovascular events in patients with elevated Lp(a) in previous clinical trials.

These mechanistic insights suggest EPA works through multiple complementary pathways to reduce vascular inflammation and oxidative stress – key drivers of atherosclerotic cardiovascular disease. While still at the in vitro stage, these findings provide biological plausibility for the cardiovascular outcome benefits observed in clinical trials and may eventually help identify which patient populations might benefit most from EPA therapy.

08/31/2025 – 08:30 AM

— Data Further Advance Understanding of VASCEPA®/VAZKEPA® Potential Mechanisms of Action —

DUBLIN, Ireland and BRIDGEWATER, N.J., Aug. 31, 2025 (GLOBE NEWSWIRE) — Amarin Corporation plc (NASDAQ:AMRN) today highlighted *in vitro* data assessing the effects of EPA on lipoprotein(a) [Lp(a)] oxidation and on cellular stress and inflammatory protein expression in endothelial cells and preliminary data showcasing the potential anti-inflammatory mechanism of icosapent ethyl (IPE) via modulation of nod-like receptor protein-3 (NLRP3) inflammasome by monocyte-derived macrophages (MDMs). The data was presented at the European Society of Cardiology (ESC) Congress 2025 in Madrid, Spain.

“These *in vitro* analyses provide additional insight into the mechanisms of action for VASCEPA/VAZKEPA, including the potential effect of reducing inflammation in atherosclerotic cardiovascular disease (ASCVD) as well as its reported impact on reducing cardiovascular (CV) events in at-risk patients with elevated Lp(a),” said Steven Ketchum, Ph.D., EVP, President of R&D, and Chief Scientific Officer at Amarin. “This data continues to advance understanding around potential underlying mechanisms of action for this molecule.”

The *in vitro* analyses and their key findings are outlined below:

Eicosapentaenoic acid (EPA) modulates inflammasome activation in monocyte-derived macrophages isolated from individuals with and without established atherosclerotic cardiovascular disease (ASCVD)

This analysis evaluated anti-inflammatory mechanisms of action of IPE, a purified form of EPA, that may be associated with cardiovascular risk reduction beyond triglyceride lowering.​

Researchers focused on monocyte-derived macrophages (MDMs), which are thought to contribute to ASCVD progression in part via P2X7 receptor–mediated activation of the NLRP3 inflammasome and impairment of autophagy.​

Key findings suggest that EPA may reduce extracellular ATP release and caspase 1 activation in stimulated MDMs from individuals with and without ASCVD.​ The analysis presents novel preliminary evidence that EPA may protect against inflammation in ASCVD by modulating the ATP–P2X7 axis and downstream NLRP3 activation in MDMs.

“These findings offer compelling preliminary evidence that eicosapentaenoic acid (EPA) may play a protective role against inflammation in atherosclerotic cardiovascular disease. By modulating the ATP–P2X7 axis and downstream NLRP3 inflammasome activation in monocyte-derived macrophages, EPA demonstrates potential mechanisms of cardiovascular risk reduction that extend beyond triglyceride lowering,” said Professor Kelvin Lee, Consultant Interventional Cardiologist and Director of the Cardiovascular Research Program at United Lincolnshire Hospitals NHS Trust (ULHT).

Eicosapentaenoic Acid (EPA) Inhibited Lipoprotein(a) [Lp(a)] Oxidation and its Effects on Expression of Oxidative Stress and Pro-Inflammatory Proteins in Endothelial Cells

Elevated Lp(a) is associated with an increased risk for ASCVD and aortic valve stenosis. Lp(a) is a major carrier of oxidized phospholipids (oxPLs). Atherogenic mechanisms for Lp(a) include increased endothelial dysfunction linked to its oxPL content. ​

This analysis assessed the effects of EPA on attenuation of Lp(a) oxidation and the effects of Lp(a) ± EPA on protein expression in endothelial cells during conditions of oxidative stress. Results showed that EPA attenuated Lp(a) oxidation and its effects on oxidative stress and pro-inflammatory protein expression.​

IPE/EPA was reported to reduce CV events in high-risk patients with elevated Lp(a). Mechanistic insights suggest that EPA inhibits lipoprotein oxidation by a potent lipid-centric scavenging mechanism. By inhibiting Lp(a) oxidation, EPA may reduce its effects on endothelial dysfunction and inflammation.

FAQ

What new data did Amarin (NASDAQ:AMRN) present at ESC 2025?

Amarin presented *in vitro* data showing EPA’s ability to reduce inflammation in ASCVD through modulation of the ATP-P2X7 axis and NLRP3 inflammasome, plus its capacity to inhibit Lp(a) oxidation and reduce inflammatory protein expression.

How does EPA (VASCEPA/VAZKEPA) potentially reduce cardiovascular risk according to the new research?

The research shows EPA may reduce cardiovascular risk through multiple mechanisms: by modulating inflammasome activation in monocyte-derived macrophages, inhibiting Lp(a) oxidation, and reducing endothelial dysfunction and inflammation.

What are the implications of Amarin’s EPA research for ASCVD patients?

The research suggests that EPA may provide protective effects against inflammation in ASCVD patients beyond triglyceride lowering, potentially offering additional cardiovascular benefits through its anti-inflammatory and antioxidant properties.

What did the ESC 2025 data reveal about EPA’s effect on Lipoprotein(a)?

The data showed that EPA can attenuate Lp(a) oxidation and reduce its effects on oxidative stress and pro-inflammatory protein expression in endothelial cells, which may help reduce cardiovascular risk in patients with elevated Lp(a).

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