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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

PubMedCardiovascular engineering and technology2026-08-05

Evaluation of Human Stem Cell Conditioned Medium and Culture Conditions on Alleviating Elastase-Compromised Human Aortic Smooth Muscle Cell Function.

Baldwin Christofer S CS, Gustavison Nickolas N, Almodovar Jorge J, Iyer Shilpa S et al.

Cardiovascular health depends critically on the integrity of the vascular extracellular matrix (ECM) and the behavior of vascular smooth muscle cells (VSMCs), both of which can be adversely affected in vascular diseases. This study quantitatively evaluates the therapeutic potential of conditioned medium (CM) derived from bone marrow (BM-MSCs) and adipose-derived stem cells (ADSCs) in an elastase-injured human aortic smooth muscle cell (HASMC) model. We systematically varied seeding densities (2000, 5000, and 10,000 cells/cm2) and serum conditions to optimize the SC-SMC secretome for vascular repair. Our results indicate that neither BM-SMC nor AD-SMC CM significantly enhanced lysyl oxidase (LOX) activity. In fact, serum-supplemented BM-SMC CM significantly suppressed LOX activity at seeding densities of 2000 cells/cm2 (p = 0.0378) and 10,000 cells/cm2 (p = 0.0080) compared to injured untreated controls. High-density AD-SMC CM (10,000 cells/cm2) also resulted in a significant decrease in elastin levels (p < 0.05). In addition, serum presence was critical for maintaining the reparative phenotype. Serum-free (SF) conditions for both cell sources led to widespread, statistically significant reductions (p < 0.0001) in key repair and inflammatory biomarkers, including PDGF-AA, Leptin, Lipocalin-2, Osteopontin, RBP4, MMP-1, and IL-6. IL-11 emerged as a primary discriminatory biomarker, showing significant differences between BM and AD treatments at high seeding densities, with both sources causing a significant decrease (p < 0.0001) compared to injured untreated controls. These findings demonstrate that seeding density and serum conditions are critical variables that quantitatively modulate the efficacy of SC-SMC-CM. The study highlights that BM-SMC-derived CM offers a more stable platform for elastin maintenance under serum-free conditions, providing a foundation for developing tailored, cell-free regenerative therapies for cardiovascular disease.

PMID 42552507
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PubMedFrontiers in immunology2026-08-05

J2R/F4L deleted oncolytic vaccinia virus synergizes with tumor specific killer (ELANE) promotes antitumor immunity with superior safety.

Huang Yu Y, Wang Liming L, Mei Shan S, Zhao Fei F et al.

Oncolytic virotherapy (OVT) represents a promising approach for cancer treatment, employing oncolytic viruses (OVs) that selectively infect and lyse tumor cells while promoting an antitumor immune microenvironment. Vaccinia virus (VACV) serves as an attractive oncolytic vector due to its favorable safety profile, ease of genetic modification, and inherent tumor selectivity. To enhance both safety and tumor-targeting capability, we constructed a recombinant vaccinia virus, VV-dTF/EE, by deleting the viral J2R and F4L genes and inserting the human neutrophil elastase (ELANE) gene, which exhibits tumor-killing activity. Mechanistic studies evaluated with virus replication selectivity, cell apoptosis, genomic damage, immunogenic cell death, alongside analysis of the immune microenvironment. Efficacy was tested in multiple tumor cell models in vitro and lung cancer models in vivo. In tumor cell lines and mouse tumor models, VV-dTF/EE demonstrated tumor-restricted replication, potent oncolytic effects, and induction of immunogenic cell death. Furthermore, VV-dTF/EE augmented VACV-induced antitumor immunity by increasing CD8+ T cell infiltration and suppressing M2-like macrophage polarization. This VV-dTF/EE revealed tumor-selective replication and killing ability while modifying the tumor immune microenvironment to elicit immunogenic cell death. Our findings highlight a novel strategy for safe and effective tumor immunotherapy through dual-gene deletion and ELANE expression in an oncolytic vaccinia platform.

PMID 42553337
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PubMedEuropean journal of clinical nutrition2026-08-05

Digestive enzyme replacement in very preterm infants: a prospective observational study.

Keidel Sina S, Wellmann Sven S, Michel Holger H, Bührer Christoph C

Very preterm infants may display poor postnatal growth despite receiving recommended enteral intakes. This has been linked to transient exocrine pancreatic insufficiency, indicated by low fecal pancreatic elastase-1 (FPE-1) concentrations. We aimed to determine whether growth velocity may be improved by exogenous digestive enzyme replacement. In this bicentric prospective observational study, changes in growth velocity were assessed in very preterm infants (<32 weeks gestational age, <1500 g birth weight) with low FPE-1 concentrations (<200 µg/g). Infants received 350 U lipase from Rhizopus oryzae and 5.4 U protease from Aspergillus oryzae with every meal via gavage; the dosage was doubled once infants reached 1000 g. Average daily weight gain relative to body weight was compared during the 14 days preceding initiation of digestive enzyme replacement and during the first 14 days thereafter. In 71 infants (median [interquartile range] birth weight 700 [570-980] g, gestational age 25.4 [24.4-28.4] weeks) born between March 1, 2022, and December 31, 2023, daily weight gain increased from 14.7 [7.3-19.7] to 19.5 [15.7-24.0] g/kg/d (p < 0.001), relative daily weight gain per kg protein fed from 4.0 [2.0-5.9] to 5.4 [4.4-6.5] g/kg (p < 0.001), and relative daily weight gain per kcal fed from 0.11 [0.06-0.16] to 0.15 [0.13-0.19] g/kcal/d (p < 0.001). Effects were non-significant in infants fed raw milk but marked in those who received pasteurized mother's own milk or donor milk. Administration of exogenous digestive enzymes was associated with increased weight gain in very preterm infants with transient exocrine pancreatic insufficiency.

PMID 42552366
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PubMedHypertension (Dallas, Tex. : 1979)2026-08-03

Roles of Sirtuin-1 in the Prevention of Intracranial Aneurysm Rupture in Mice.

Sato Hiroki H, Ikedo Taichi T, Take Yushiro Y, Kimura Tetsuro T et al.

SIRT1 (sirtuin-1) regulates various cellular and metabolic processes in the vasculature. SIRT1 is an NAD+-dependent deacetylase that deacetylates transcription factors that control vascular inflammation and remodeling. Given that pathways regulated by SIRT1 are implicated in the pathophysiology of intracranial aneurysms, we hypothesized that activation and overexpression of SIRT1 prevent aneurysm rupture by suppressing vascular inflammation. Intracranial aneurysms were induced in mice by systemic hypertension and a single intracisternal injection of elastase. We analyzed the expression of SIRT1 in human and mouse aneurysms. We investigated the role of SIRT1 in aneurysm rupture using genetic overexpression of SIRT1 and cell-specific deletion in the endothelial, vascular smooth muscle, and myeloid lineages. We administered a SIRT1 activator and a SIRT1 inhibitor to assess the rupture rate and mRNA expression in cerebral arteries. SIRT1 expression was significantly lower in intracranial aneurysm tissues than in control cerebral arteries in mice, with a similar trend in human aneurysms. Global overexpression of SIRT1 significantly decreased the rupture rate. Endothelial SIRT1 deletion increased the rupture rate, with no effect observed in other cell types. Inhibition of SIRT1 increased the rupture rate, whereas SIRT1 activation reduced the rupture rate and suppressed mRNA expression of proinflammatory cytokines in cerebral arteries. Our findings support a protective role of SIRT1 against intracranial aneurysm rupture in mice, with endothelial SIRT1 playing an important role in aneurysm stabilization. Pharmacological SIRT1 activation reduced aneurysm rupture and was associated with reduced vascular inflammation, providing a preclinical rationale for further investigation of SIRT1-related pathways.

PMID 42544484
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PubMedZhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica2026-08-03

[Research progress on targeted regulation of inflammation-related signaling pathways by TCM for prevention and treatment of acute exacerbation of chronic obstructive pulmonary disease].

Li Ya Y, Huang Hao-Xuan HX, Zhao Gui-Xiang GX, Wang Long-Yu LY et al.

Acute exacerbation of chronic obstructive pulmonary disease(AECOPD) constitutes the acute deterioration phase of chronic obstructive pulmonary disease(COPD), typified by an abrupt intensification of respiratory symptomatology, encompassing exacerbated dyspnea, heightened cough severity, augmented sputum volume, and pronounced respiratory insufficiency. Systemic inflammatory cascades serve as a cardinal etiological driver of AECOPD, emanating from multifaceted host-pathogen interactions involving viral, bacterial, or polymicrobial infections, superimposed upon environmental modulators that collectively precipitate accelerated pathological progression. These contributory elements markedly escalate the inflammatory milieu within the small airways, surmounting endogenous anti-inflammatory safeguards, thereby precipitating airway epithelial barrier disruption, microvascular dilation, edema, and prolific immune cell infiltration, which in turn perpetuate an inflammatory amplification loop. Such mechanisms converge to synergistically impair pulmonary function and extend durations of inpatient care. Current therapeutic paradigms for AECOPD predominantly incorporate bronchodilators, anti-inflammatory pharmacotherapies, supplemental oxygen administration, and mechanical ventilatory support. Notwithstanding these interventions, persistent limitations include the adverse sequelae of protracted systemic glucocorticoid therapy, escalating antimicrobial resistance profiles, and ventilator-associated morbidities. Ergo, there exists an imperative to investigate novel therapeutic modalities that confer enhanced safety and efficacy. TCM proffers salient therapeutic merits via its multi-target and multi-pathway pharmacodynamics, facilitating regulation of pivotal signaling pathways, including the Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB), NF-κB/NOD-like receptor pyrin domain containing 3(NLRP3), phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt), Janus kinase(JAK)/signal transducer and activator of transcription(STAT), and neutrophil elastase(NE)/mucin 5AC(MUC5AC) pathways. Through such regulatory interventions, TCM efficaciously attenuates inflammatory response, ameliorates symptomatic burden, and diminishes the incidence of AECOPD. The present investigation endeavors to delineate systematically the extant advancements in TCM-mediated regulation of inflammation-related signaling pathways within the context of AECOPD, thereby furnishing a robust theoretical framework and empirical guidance for optimized clinical interventions and pharmaceutical innovations in AECOPD management.

PMID 42543271
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PubMedZhongguo shi yan xue ye xue za zhi2026-08-03

[The Impact of Nutritional Intervention on Complications and Prognosis of Hematopoietic Stem Cell Transplantation Patients].

Zheng Gui-Ju GJ, Yue Meng-Yuan MY, Lin Guo-Qiang GQ, Si Ye-Jun YJ et al.

To investigate the effects of nutritional supportive therapy on hematopoietic stem cell transplantation (HSCT) patients and to analyze its relationship with post-transplant hematopoietic reconstitution, acute graft-versus-host disease (aGVHD). The clinical data of 76 HSCT patients in our hospital were collected from November 2020 to November 2023, included 46 cases in the nutritional intervention group and 30 in the non-intervention group. After assessing the nutritional status of the intervention group, the five-step therapy principle was followed to implement refined nutritional support treatment, the total daily energy requirement by the patients was calculated based on 25-30 kcal/(kg·d) from the first day of pretreatment to 90 days post-transplantation, followed up until March 2024. The nutritional indices and clinical outcomes of both groups pre-transplant and at 30, 60, and 90 days post-transplant was observed. At 30 days and 60 days after transplantation, the total protein level in the intervention group was higher than before transplantation (P<0.05). At 30 days, 60 days, and 90 days after transplan-tation, the triglyceride levels in both groups were higher than before transplantation (P<0.05). At 30 days and 90 days after transplantation, the HDL-C level in the intervention group was lower than before transplantation (P<0.05). At 60 days after transplantation, the BMI level in the intervention group was higher than that in the non-intervention group (P<0.05). At 30, 60, and 90 days after transplantation, the albumin level in the intervention group was higher than that in the non-intervention group (P<0.05). At 30 days after transplantation, the prealbumin level in the intervention group was higher than that in the non-intervention group (P<0.05). At 30 days and 60 days after transplantation, the total protein level in the intervention group was higher than that in the non-intervention group (P<0.05). At 60 days after transplantation, the low density lipoprotein cholesterol (LDL-C) and triglyceride levels in the intervention group were lower than those in the non-intervention group (P<0.05). At 30 days after transplantation, the HDL-C level in the intervention group was lower than that in the non-intervention group (P<0.05). Time of hematopoietic recons-truction after transplantation: the days for granulocyte reconstitution in the intervention group were earlier than those in the non-intervention group (P<0.05), while there was no statistically significant difference in the number of days for megakaryocyte reconstitution between the two groups (P＞0.05). At 30 days after transplantation, the level of soluble growth stimulus expression gene 2 protein (sST2) in the intervention group was significantly lower than that in the non-intervention group (P<0.05). The level of soluble interleukin-2 receptor (sCD25) in the intervention group at 60 days after transplantation was lower than that at 30 days after transplantation (P<0.05). At different time points after transplantation, there was no statistically significant differences between the two groups in regenerative lslet derived protein 3 alpha (REG3α), soluble tumor necrosis factor receptor 1 (sTNFR1), and elastase inhibitory factor (Elafin) (P＞0.05). The implementation of nutritional support therapy not only ameliorates malnutrition and hastens granulopoiesis, but also mitigates the risk of aGVHD and improves the prognosis of patients undergoing hematopoietic stem cell transplantation.

PMID 42544681
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