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ethyl icosapentate (MND2119 / MND 2119 / icosapent, Mochida)

✓ Approved

Sumitomo Pharma Co., Ltd. · 小分子 · 小分子

什么是 ethyl icosapentate？

ethyl icosapentate 是一种小分子，由Sumitomo Pharma Co., Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名MND2119, MND 2119, icosapent, Mochida
公司Sumitomo Pharma Co., Ltd.
药物类别小分子
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Sumitomo Pharma Co., Ltd.

治疗适应症

ethyl icosapentate 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHyperlipidaemia✓ Approved
Metabolism and nutrition disordersHypertriglyceridaemiaPhase III

相关研究文献

PubMedCarbohydrate polymers2026-06-13

Leaf vein-inspired ethyl cellulose mediated dual-network design for enhanced energy storage in PVDF-based all-organic polymer dielectrics.

Yang Linsheng L, Lu Hongwei H, Li Bengang B, Yang Shijia S et al.

High dielectric loss and relaxation loss restrict the applications of ferroelectric crystalline polymers such as polyvinylidene fluoride (PVDF) in modern electronic systems. Inspired by the supporting structure of leaf veins, flexible all-organic dielectric films were fabricated by incorporating hexafluorobutyl acrylate (HFBA) and ethyl cellulose (EC) into PVDF via solution casting and in-situ ultraviolet (UV) polymerization. Three-dimensional (3D) molecular interpenetrating network from HFBA polymerization and the hydrogen-bond crosslinking network from EC synergistically optimize the film microstructure. The confinement of PVDF chain motion and the trapping of charge carriers effectively reduce dielectric loss and leakage current density. The dielectric loss decreases from 0.0623 for PVDF to 0.0171, and the leakage current density drops from 4.45 × 10-6 A/cm2 to 3.21 × 10-7 A/cm2, over one order of magnitude lower. A maximum energy storage density of 7.74 J/cm3 is achieved, 2.31 times that of pure PVDF (3.35 J/cm3). This work provides a promising strategy for the scalable preparation and application of high-performance flexible dielectrics.

PMID 42285662
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PubMedJournal of the science of food and agriculture2026-06-13

Enhancement of biological activity and volatile organic compounds of sunflower bee pollen via mixed Lactobacillus fermentation.

Ma Tianchen T, An Xin X, Jin Kai K, Zheng Oujie O et al.

Lactobacillus fermentation represents an efficient approach for enhancing the nutritional, bioactive, and sensory properties of bee pollen. However, the biological activities and volatile organic compounds (VOCs) of Lactobacillus-fermented sunflower bee pollen (FSBP) remain unclear. In this study, we employed mixed fermentation with Lactiplantibacillus plantarum and Lacticaseibacillus casei, optimizing the process using single factor and orthogonal experiments. We then characterized the physicochemical properties, biological activities, and VOCs of unfermented sunflower bee pollen (USBP) and FSBP. Compared to USBP, FSBP exhibited 9.68% and 54.57% increases in total phenolic and flavonoid contents. Additionally, FSBP exhibited 26.08% and 17.59% increases in α-glucosidase inhibitory activity (GIA) and tyrosinase inhibitory activity. Notably, antioxidant and anti-inflammatory activities were significantly improved in FSBP. Headspace-solid-phase microextraction-gas chromatography-mass spectrometry analysis identified 52 VOCs. The orthogonal partial least squares discriminant analysis (OPLS-DA) revealed 16 key VOC markers distinguishing USBP and FSBP, including (1S)-(-)-α-pinene, camphene, α-pinene, ethyl butanoate, ethyl caprate, cis-chrysanthenol, butanoic acid, pentanoic acid, octanoic acid, hexanoic acid, isobutyl methyl ketone, acetophenone, nonanal, tridecane, selina-5,11-diene, and p-cymene. In summary, Lactobacillus fermentation not only improves bioactivity but also modulates flavor, making bee pollen more suitable for food applications. © 2026 Society of Chemical Industry.

PMID 42285775
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PubMedChemico-biological interactions2026-06-13

A Microfluidic Human Blood-Brain Barrier Model Reveals Neurovascular Toxicity and Barrier Disruption Induced by E-Cigarette Additives.

Yin Changfeng C, Li Xiao X, Yu Feiju F, Wang Xuran X et al.

The increasing popularity of e-cigarettes raises concerns about their neurotoxic potential. Exposure to flavoring additives may compromise the blood-brain barrier (BBB); however, their effects and underlying mechanisms remain poorly understood, largely due to the lack of physiologically relevant in in vitro models. Here, we developed a dynamic microfluidic BBB co-culture model (CPAC-Co) incorporating human brain endothelial cells and astrocytes under physiological shear stress. CPAC-Co model showed superior barrier integrity, efflux activity, and drug-permeability prediction over conventional models. Using this validated platform, we evaluated seven widely used e-cigarette additives (ethanol, menthol, WS-23, lactic acid, benzoic acid, ethyl maltol, and methylcyclopentenolone). Ethanol, ethyl maltol, and methylcyclopentenolone markedly increased nicotine permeability and reduced transepithelial electrical resistance, indicating BBB disruption. These changes were accompanied by endothelial apoptosis, downregulation of tight-junction genes, and activation of oxidative/nitrosative stress and inflammatory responses. Transcriptomics further revealed upregulation of inflammation- and stress-related pathways, including NF-κB and NOD-like receptor signaling. Our study not only establishes CPAC-Co as a robust, physiologically relevant model for neurovascular toxicity screening but also provides experimental evidence for the safety evaluation of e-cigarette additives, underscoring the need to integrate their central nervous system potential risks into regulatory policies.

PMID 42285244
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PubMedChinese journal of natural medicines2026-06-13

Quzhou Fructus Aurantii extract alleviates metabolic dysfunction-associated steatohepatitis by activating the PPARα signaling pathway.

Wu Lianhao L, Zhu Wenwen W, Zhang Shuohan S, Chen Ranran R et al.

Metabolic dysfunction-associated steatohepatitis (MASH) is a chronic metabolic disease that severely affects human health. Quzhou Fructus Aurantii ethyl acetate extract (QFAEE) is a mixture rich in diverse natural flavonoids that exhibits multiple pharmacological properties, including significant anti-inflammatory and antioxidant activities. However, the anti-MASH effects of QFAEE and the underlying mechanisms remain unknown. This study aimed to investigate the therapeutic effects of QFAEE on MASH and the related mechanisms. The therapeutic effects of QFAEE on hepatic steatosis, inflammatory responses, oxidative stress and apoptotic activity were systematically evaluated in both in vivo and in vitro models of metabolic stress. QFAEE administration significantly reduced hepatic lipid accumulation, inflammatory cell infiltration and liver injury in HFHC diet-fed mice. Combined RNA sequencing and network pharmacology analyses revealed that QFAEE exerted its anti-MASH effects through modulation of the PPAR signaling pathway. QFAEE ameliorated MASH by activating PPARα and subsequently upregulating CPT1A, which promoted mitochondrial and peroxisomal β-oxidation. Notably, PPARα inhibition promoted hepatic lipid accumulation, inflammation and oxidative stress in hepatocytes, all of which were significantly attenuated by QFAEE treatment. These findings suggest that QFAEE prevents metabolic stress-induced MASH progression by activating PPARα signaling.

PMID 42285690
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PubMedTranslational research : the journal of laboratory and clinical medicine2026-06-13

A novel spontaneous rat model of chronic kidney disease with mitochondrial dysfunction driven by thioredoxin insufficiency.

Ohmori Iori K IK, Ouchida Mamoru M, Hada Yoshiko Y, Uchida Haruhito A HA et al.

Chronic kidney disease (CKD) is a global health burden with high prevalence and poor prognosis. Although oxidative stress and mitochondrial dysfunction have been implicated in its pathogenesis, in vivo causal evidence remains limited. Thioredoxin (Trx), encoded by Txn1, is a redox-active protein that plays a central role in controlling oxidative stress and maintaining intracellular redox homeostasis. To address this gap, we investigated the lifelong phenotypes of Txn1-F54L mutant rats harboring approximately one-third of the normal Trx activity. These rats were generated via N-ethyl-N-nitrosourea mutagenesis and validated by clustered regularly interspaced palindromic repeat (CRISPR)/CRISPR-associated protein 9 genome editing. Comprehensive analyses included biochemical testing, histopathology, immunohistochemistry, transmission electron microscopy, RNA-sequencing, western blotting, and cytokine profiling. Txn1-F54L mutant rats spontaneously developed progressive CKD, with median survival times of 110-119 days for homozygotes and 303-346 days for heterozygotes. Their clinical features-elevated blood urea nitrogen, hypoalbuminemia, hypercholesterolemia, hypertension, and arterial medial sclerosis-closely resembled those of human CKD. Histopathological evaluation revealed extensive tubular injury, interstitial fibrosis, and glomerulosclerosis. Transcriptomic profiling identified 3,418 differentially expressed genes significantly enriched in immune activation and fibrosis pathways. Mitochondrial dysfunction was prominent in proximal tubules, accompanied by oxidative stress accumulation and concurrent activation of regulated cell death pathways (apoptosis, necroptosis, and pyroptosis). Elevated serum levels of interleukin-1β, interleukin-6, and interferon-γ indicated systemic inflammation. Our findings demonstrate that lifelong Trx deficiency induces oxidative stress-mediated mitochondrial dysfunction and regulated cell death, leading to inflammation and progressive CKD. This study establishes the Txn1 mutant rat as a valuable spontaneous CKD model, providing translational insights and a platform for developing therapeutic strategies targeting oxidative stress-induced pathways.

PMID 42285432
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PubMedPlants (Basel, Switzerland)2026-06-12

Phytochemical Profiling of Sticta caulescens De Not.: Green Extraction and Multiscale Chemotaxonomic Analysis.

Cifuentes-Araya Nicolás N, Valdivia Diego D, Pertino Mariano Walter MW, Marroquín-Guerra Daniela D et al.

The aim of this research was to identify the wealth of secondary metabolites in the Chilean lichen Sticta caulescens, applying green chemistry approaches and comparing the following two extraction methods: (a) conventional maceration with methanol, and (b) microwave-assisted extraction (MAE) using ethyl lactate as a solvent. In addition, chemoinformatic and chemotaxonomic studies were conducted on S. caulescens and other species of the genus Sticta, which have been reported in previous studies. A UHPLC/ESI-MS/MS analysis allowed for the identification of 32 metabolites obtained from maceration and 33 from MAE, considering carbohydrates, aromatic compounds, acids, depsides, depsidones, dibenzofurans, lipids, anthraquinones, and triterpenes. Maceration using methanol yielded a slightly higher extract percentage than with ethyl lactate (6.3% versus 5.0%), while MAE extracted an almost identical spectrum of metabolites using ethyl lactate,-though including one compound detected only under MAE conditions. This highlighted both the method efficiency and selectivity. This study also incorporates a comprehensive chemoinformatic and chemotaxonomic analysis of secondary metabolites across 12 Sticta species. A computational comparison (Morgan fingerprints, Jaccard similarity, hierarchical clustering, Murcko scaffolds) demonstrated that S. caulescens is one of the most chemically diverse species, closely related to S. cordillerana, and forming part of a major chemotaxonomic lineage, which is characterized by high scaffold richness and shared aromatic/depsidone biosynthetic pathways.

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