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elastase (elastase / Elaszym)

✓ Approved

Eisai Co., Ltd. · 治疗药物

什么是 elastase？

elastase 是一种治疗药物，由Eisai Co., Ltd.研发。该药已获批，用于治疗相关适应症。

药物档案

商品名elastase, Elaszym
公司Eisai Co., Ltd.
状态Approved
来源： ClinicalTrials.gov, Eisai Co., Ltd.

治疗适应症

elastase 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersArteriosclerosis✓ Approved

相关研究文献

PubMedJournal of inflammation research2026-07-26

Therapeutic Efficacy of Sivelestat Sodium in ARDS Following Aortic Dissection: A Pilot Physiological Trial with Exploratory Transcriptomic Analysis.

Wang Hanyu H, Kong Dekai D, Li Lingfeng L, Zhang Jiaxin J et al.

To evaluate the physiological and clinical effects of sivelestat, a selective neutrophil elastase inhibitor, in patients with aortic dissection-associated acute respiratory distress syndrome (ARDS), and to explore its potential mechanisms using transcriptomic analysis. This single-center, randomized, placebo-controlled pilot trial enrolled adult patients who developed ARDS with systemic inflammatory response syndrome after aortic dissection surgery. Participants were randomized 1:1 to receive continuous intravenous sivelestat (0.2 mg/kg/h) or placebo for 5 days. The primary outcome was the PaO2/FiO2 ratio on Day 5. Secondary outcomes included Sequential Organ Failure Assessment (SOFA) score, requirement and duration of invasive mechanical ventilation, and ICU length of stay. Inflammatory biomarkers were measured on Days 1, 3, and 5. Peripheral blood RNA sequencing was performed on Day 5. Ten patients were enrolled (sivelestat n=5; placebo n=5). By Day 5, the sivelestat group showed significantly higher PaO2/FiO2 (317.2 ± 115.8 vs 168.6 ± 79.4 mmHg; p=0.046), lower SOFA scores (5.8 ± 1.3 vs 9.0 ± 1.9; p=0.014), lower CRP levels on Days 3 and 5 (both p=0.005), and shorter ICU stay (6.0 ± 2.5 vs 13.0 ± 3.6 days; p=0.009). RNA sequencing identified 518 differentially expressed genes, with six hub genes (BPI, ELANE, CEBPE, MPO, CTSG, and DEFA3) enriched in neutrophil protease-related inflammatory pathways. In this hypothesis-generating pilot study, early sivelestat was associated with preliminary signals of improved oxygenation, reduced systemic inflammation, and shorter ICU stay. Exploratory transcriptomics identified six hub genes (BPI, ELANE, CEBPE, MPO, CTSG, DEFA3) implicating neutrophil protease-centered pathways. These findings support the need for larger, biomarker-integrated multicenter trials to confirm efficacy and define responsive subgroups.

PMID 42502580
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PubMedJHLT open2026-07-25

Eliminating circulating donor passenger leukocytes during clinical ex vivo lung perfusion does not attenuate inflammation.

Hu M A MA, Zhang Z L ZL, Hoffmann R F RF, Gan C T CT et al.

During Ex Vivo Lung Perfusion (EVLP), it is standard practice to incorporate a leukocyte filter to remove donor passenger leukocytes and attenuate their inflammatory effects. The widely used leukocyte filter, LeukoGuard 6, seems to be ineffective in reducing circulating leukocytes during EVLP. Therefore, we performed contemporary leukocyte filtration using BioR 02 plus leukocyte filters to reduce these leukocytes and investigate whether inflammation could be reduced. EVLP was performed for a minimum of 180 min with 15 bilateral donor lungs. Perfusate samples were taken from the in- and outlet of the leukocyte filter, which was subsequently clamped after 60 min. Contemporary parallel leukocyte filtration was performed in 9 EVLPs (intervention group) and in 6 EVLPs without (control group). After EVLP, 6/6 donor lungs were transplanted in the control group and 6/9 in the intervention group. Leukocytes increased significantly from 30 to 180 min in the standard group compared with the intervention group. During EVLP IL-1, IL-6, IL-8, TNF-α, neutrophil elastase, CD-14, syndecan-1, hyaluronan and VCAM-1, levels were not significantly different between the groups at 90 and 180 min. Post-transplant, primary graft dysfunction (PGD) and 1-month survival were similar. The intervention group showed significantly lower circulating donor passenger leukocytes. However, this did not lead to attenuated inflammatory cytokines, leukocyte activation, glycocalyx shedding or endothelial activation. Clinical outcomes were similar between groups. Further research is needed to determine the exact effect of these donor passenger leukocytes.

PMID 42499652
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PubMedOncology research2026-07-25

miR-320d Is Associated with Reduced Nasopharyngeal Carcinoma Progression, Potentially through the NF-κB/IL-8 Axis-Mediated Inhibition of Neutrophil Extracellular Trap Formation.

Liu Liu L, Liu Jie J, Ning Shuangchen S, Wang Jin J et al.

Objectives: Nasopharyngeal carcinoma (NPC) is an aggressive head and neck malignancy in which post-treatment recurrence and distant metastasis remain major contributors to poor clinical outcomes. Although microRNAs are important post-transcriptional regulators of tumor progression, the role of miR-320d in NPC remains incompletely understood. This study evaluated the biological role of miR-320d and explored whether it is involved in regulating neutrophil extracellular trap (NET) formation through the nuclear factor kappa-B (NF-κB)/interleukin-8 (IL-8) signaling axis. Methods: miR-320d was overexpressed in NPC cell lines S18 and 5-8F, and cell viability, migration, and invasion were evaluated. Integrated transcriptomic and proteomic analyses were performed to identify miR-320d-regulated genes, proteins, and pathways. Western blotting, immunohistochemistry, and immunofluorescence analyses were used to validate NET-associated proteins, including glycoprotein Ib platelet subunit alpha (GP1BA), histone deacetylase 10 (HDAC10), and fibrinogen gamma chain (FGG), as well as the expression of NET formation markers, including peptidyl arginine deiminase 4 (PADI4), myeloperoxidase (MPO), and neutrophil elastase (NE); and key components of the NF-κB/IL-8 axis. Results: miR-320d overexpression significantly inhibited the viability, migration, and invasion of both S18 and 5-8F cells. Multi-omics analyses indicated that miR-320d-regulated molecules were mainly enriched in NET-related pathways. Consistently, miR-320d reduced the expression of GP1BA, HDAC10, FGG, PADI4, MPO, and NE. Mechanistically, miR-320d suppressed NF-κB signaling, as shown by decreased phosphorylated NF-κB (p-NF-κB) and total NF-κB levels, and reduced IL-8 secretion in NPC cells. Conclusion: miR-320d may suppress NPC progression, at least in part, by attenuating NF-κB/IL-8-associated NET formation. These findings suggest that the miR-320d/NF-κB/IL-8/NET regulatory axis may participate in NPC progression and may warrant further translational investigation.

PMID 42500573
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PubMedKidney international2026-07-25

IL-33 as a component of neutrophil extracellular traps mediates contrast-induced acute kidney injury by promoting ferroptosis in tubular epithelial cells.

Ma Mengqing M, Zhang Hao H, Deng Weijuan W, Du Xia X et al.

Contrast-induced acute kidney injury (CIAKI) is a leading cause of hospital-acquired kidney dysfunction, yet its immune-mediated pathogenic mechanisms remain poorly defined. Neutrophil extracellular traps (NETs) have been implicated in acute kidney injury. However, whether contrast agents directly induce NETs formation and whether NETs drive tubular ferroptosis through IL-33 has not been investigated. A prospective cohort of 330 patients undergoing coronary angiography was enrolled, with serial measurement of circulating NETs markers (myeloperoxidase, neutrophil elastase) and IL-33 at pre-contrast, two- and 12-hour time points. A murine CIAKI model was established in wild-type, peptidyl arginine deaminase 4 (PAD4) -knockout, and IL-33-knockout mice, and single-cell transcriptomic profiling of CIAKI kidneys was performed. In vitro, the serine/threonine kinase IKKα- and β-catenin-overexpressing and knockdown HK-2 cells were stimulated with iodixanol-induced NETs to evaluate how NETs regulate ferroptosis through IL-33-mediated modulation of IKKα and β-catenin. CIAKI occurred in 12.1% (40/330) of patients. Circulating NETs markers and IL-33 were significantly elevated at two and 12 hours post-contrast in CIAKI compared with non-CIAKI patients. Single-cell transcriptomics identified neutrophils as the predominant source of IL-33 in CIAKI kidneys and revealed enrichment of NET formation and ferroptosis pathways. In vivo, PAD4 and IL-33 deficiency each significantly attenuated NETs and ferroptosis in CIAKI mice. Mechanistically, IL-33-enriched NETs suppressed IKKα expression, disrupted IKKα-β-catenin interaction, and impaired β-catenin nuclear translocation, thereby de-repressing long chain acyl CoA synthetase 4 transcription and amplifying ferroptotic injury. Restoration of IKKα stabilized β-catenin and attenuated NET-induced ferroptosis. Our study demonstrates that IL-33-enriched NETs promote renal tubular ferroptosis in CIAKI by suppressing IKKα and impairing β-catenin nuclear translocation. These findings identify the NETs-IL-33-IKKα-β-catenin pathway as a novel and therapeutically actionable mechanism underlying CIAKI, providing potential targets for its diagnosis and treatment.

PMID 42498057
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PubMedThe Turkish journal of pediatrics2026-07-24

A rare cause of congenital diarrhea: a homozygous AGR2 frameshift variant in an infant.

Arslan Melike M, Keçeci Hayriye Nermin HN, Ergani Anna Carina AC, Ömeroğlu Ethem E et al.

Congenital diarrheal disorders and enteropathies (CODE) are rare genetic conditions presenting with severe diarrhea and growth failure beginning in infancy. Biallelic variants in the anterior gradient 2 (AGR2) gene have recently been associated with a cystic fibrosis-like disorder characterized by multisystem involvement, including gastrointestinal and respiratory manifestations. We report a male infant born to consanguineous parents, who presented with severe congenital secretory diarrhea starting in the neonatal period, failure to thrive, dehydration, and metabolic acidosis. The diarrhea was refractory to bowel rest, suggesting a secretory mechanism. Stool studies, fecal elastase, sweat chloride testing, and CFTR gene analysis were normal. Endoscopic evaluation revealed antral gastritis, bulbitis, and duodenitis, with duodenal biopsies showing villous flattening. The patient developed recurrent hyponatremia requiring prolonged oral sodium supplementation and experienced a single episode of bronchiolitis, which may represent either a possible early respiratory manifestation or a coincidental common infantile infection. Whole exome sequencing identified a homozygous frameshift variant in the AGR2 gene (c.247_250del; p.His83ValfsTer4), and parental testing confirmed autosomal recessive inheritance. This case expands the clinical spectrum of AGR2-related disease by highlighting a predominantly gastrointestinal presentation with severe congenital secretory diarrhea, failure to thrive, electrolyte imbalance, and a possible early respiratory manifestation. Given the rarity of this condition, AGR2 deficiency may be considered in selected infants presenting with severe congenital diarrhea and failure to thrive, particularly in the setting of consanguinity, even in the absence of definite pulmonary involvement.

PMID 42497436
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PubMedClinica chimica acta; international journal of clinical chemistry2026-07-23

Reduced fecal GP2 levels in ulcerative colitis associate with inflammatory activity and microbial composition.

Uchitel Yoav Y, Roggenbuck Dirk D, Leibovitzh Haim H, Cohen Nathaniel Aviv NA et al.

Loss of tolerance to GP2, an antimicrobial immune-modulating component of intestinal cells and receptor on microfold cells, is associated with disease severity in Crohn's disease (CD). However, the role of GP2 in inflammatory bowel diseases remains poorly understood. This study aimed to evaluate fecal GP2 levels in patients with ulcerative colitis (UC) and CD and to examine associations with disease activity, response to biologic therapy, and microbial features. We conducted a retrospective study of adults with UC, CD, and healthy controls recruited at a tertiary IBD clinic. Fecal GP2 levels and serum anti-GP2 antibodies were measured using ELISA and correlated with disease activity, inflammatory biomarkers (CRP, fecal calprotectin and elastase activity), and microbiome assessed by 16S rRNA amplicon sequencing. The study included 87 patients with CD, 58 with UC, and 31 healthy controls. Fecal GP2 levels were significantly lower in UC, particularly in active UC, compared with CD or controls (P ≤ 0.05). In CD, fecal GP2 levels did not differ significantly from controls across activity strata but correlated with elastase activity. Further, fecal GP2 levels increased following induction therapy among clinical responders and were associated with gut microbial diversity. No correlation was observed between serum anti-GP2 and fecal GP2 levels, or serum anti-GP2 and responsiveness to induction therapy. Fecal GP2 concentrations are reduced in UC, particularly during active disease, but are preserved in CD. This suggests a disease-specific pattern in UC, potentially reflecting altered microbial interactions or increased luminal protein degradation.

PMID 42486317
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