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urokinase (Breokinase / Alphakinase / Thrombolase)

✓ Approved

Mitsubishi Tanabe Pharma Corporation · PLAU

什么是 urokinase？

urokinase 是一种治疗药物，由Mitsubishi Tanabe Pharma Corporation研发。该药已获批，用于治疗相关适应症。

药物档案

商品名Breokinase, Alphakinase, Thrombolase
公司Mitsubishi Tanabe Pharma Corporation
分子靶点PLAU
状态Approved
来源： ClinicalTrials.gov, Mitsubishi Tanabe Pharma Corporation

作用机制

分子靶点

urokinase 作用于 1 个分子靶点：

PLAUplasminogen activator, urokinase (URK, UPA)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

urokinase 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
Respiratory, thoracic and mediastinal disordersPulmonary thrombosis✓ Approved

相关研究文献

PubMedFood chemistry2026-08-07

Peptides NAVPITPTLNR and EKVNELSK suppress urokinase-type plasminogen activator-mediated plasmin system activation associated with age gelation in direct ultra-high-temperature skim milk.

Gong Han H, Liu Xiaohan X, Hu Yifan Y, Wang Pengjie P et al.

Age gelation remains a challenge limiting the shelf-life and stability of direct ultra-high-temperature (dUHT) milk. This study investigated the effects of dUHT treatments (142 °C/147 °C for 0.25/3/6 s) on protein stability and gelation behavior by evaluating particle size, casein hydrolysis, plasmin (PL) and plasminogen (PLG)-derived activities and gel microstructure. Gel-derived peptides were identified, and their interactions with urokinase-type plasminogen activator (u-PA) were assessed. Treatments at 142 °C for 3 s or 147 °C for 6 s induced gel formation after prolonged storage associated with moderate proteolysis and aggregation. Conversely, 0.25 s treatments caused rapid clarification due to high PL activity. Treatment at 142 °C for 6 s maintained colloidal stability with minimal protein degradation. NAVPITPTLNR and EKVNELSK were identified as u-PA inhibitors, suppressing PLG-to-PL conversion. These findings provide evidence that casein-derived peptides may participate in the regulation of PL system in dUHT milk, although their practical effects require further validation in real milk matrices.

PMID 42561863
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PubMedFrontiers in medicine2026-08-07

Pediatric pyopneumothorax caused by Prevotella oris successfully diagnosed via mNGS: a case report and literature review.

Yan Zhihui Z, Qian Xiaona X, Liu Yixuan Y, Tian Liyuan L

Empyema and pyopneumothorax are severe complications of pediatric community-acquired pneumonia. While typically caused by aerobic bacteria, anaerobic infections, particularly those involving Prevotella oris (P. oris), are exceedingly rare in children. This study aims to explore the clinical characteristics, diagnostic challenges, and therapeutic strategies for pediatric pyopneumothorax caused by P. oris, thereby enhancing clinical awareness of this uncommon opportunistic pathogen. We retrospectively analyzed the clinical data of a 10-year-old male admitted to the Hebei Children's Hospital in October 2025, presenting with acute chest pain and a history of tooth extraction 1 week prior to symptom onset. Radiological imaging revealed bilateral pneumonia with bilateral pleural effusions (predominantly on the left side). Pleural fluid analysis was consistent with an empyema. Traditional bacterial cultures of blood and pleural fluid yielded negative results. However, probe-based targeted metagenomic next-generation sequencing (mNGS) of the pleural fluid identified P. oris with a high relative abundance (81.86%), alongside other minor oral commensals. Based on the molecular diagnosis and the patient's ongoing clinical deterioration, cefoperazone-sulbactam was selected to strengthen coverage against anaerobic Gram-negative organisms, while linezolid was temporarily added to cover potential Gram-positive pleural co-infection during the acute deterioration phase. This was combined with closed thoracic drainage and intrapleural urokinase instillation for fibrinolysis, leading to a complete clinical recovery. Prevotella oris is a rare but significant pathogen in pediatric empyema. A high index of suspicion should be maintained for anaerobic infections in children presenting with a history of dental procedures, abnormal immune parameters or possible immunological vulnerability, or poor response to empirical antibiotics. Traditional cultures are often inadequate; therefore, mNGS serves as a crucial tool for the early detection and precise treatment of difficult-to-culture anaerobes.

PMID 42564864
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PubMedEuropean journal of obstetrics & gynecology and reproductive biology: X2026-08-04

Cord blood procalcitonin and soluble urokinase-type plasminogen activator receptor in predicting histological chorioamnionitis - A pilot study.

Jalkanen Kati K, Tammela Outi O, Virtanen Anita A, Aittoniemi Janne J et al.

Chorioamnionitis, caused by microbial invasion of amniotic cavity or sterile inflammation, can lead to prematurity and cytokine storm of fetus known as fetal inflammatory response syndrome (FIRS). Histological chorioamnionitis (HCA) on fetal side of placenta is a surrogate to FIRS. Cord blood (CB) reflects intrauterine inflammation. Our aim was to evaluate if more novel biomarkers procalcitonin (PCT) and soluble urokinase- type Plasminogen Activator Receptor (suPAR) were useful for identifying fetuses/neonates with high risk for FIRS/HCA. Twenty two women with a clinically confirmed preterm premature rupture of membranes (PPROM) or a suspicion of chorioamnionitis without PPROM (uterine tenderness, maternal fever ≥38°C, leukocytosis, fetal tachycardia ≥160 beats/minute) were enrolled at gestational weeks 23+0-34+6. Interleukin-6 (IL-6), PCT and suPAR were measured in cord blood samples obtained immediately after birth. The fetal side HCA was used as a surrogate for FIRS. The cord blood concentration of IL-6 was significantly higher (p = 0.01) and had the best predictability for fetal side HCA (AUC 0.96, p = 0.03). Cord blood concentrations of PCT tended to be higher (p = 0.05), and to show significance for predicting fetal-side HCA (AUC 0.91, p = 0.07). No significant findings were found for suPAR. Cord blood IL-6 had the best ability to predict fetal side HCA. Cord blood PCT may be a promising biomarker. There were no significant findings for cord blood suPAR, suggesting its limited value as a biomarker in this context.

PMID 42549044
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PubMedBMC cardiovascular disorders2026-08-04

Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair.

Schlegl Johannes J, Bannehr Marwin M, Lichtenauer Michael M, Kücken Tanja T et al.

Risk stratification after transcatheter tricuspid edge-to-edge repair (T-TEER) remains challenging, particularly in patients with advanced right-sided heart failure and systemic disease burden. Biomarkers reflecting inflammation, stress response and multiorgan dysfunction may provide additional prognostic information in this setting. This prospective single-centre cohort study included 84 consecutive patients undergoing T-TEER for severe tricuspid regurgitation using the TriClip or PASCAL system. Baseline concentrations of growth differentiation factor-15 (GDF-15), soluble urokinase plasminogen activator receptor (suPAR), and NT-proBNP were measured prior to intervention. The primary endpoint was all-cause mortality at 12 months. Secondary endpoints included cardiovascular rehospitalisation and a combined cardiovascular endpoint. Prognostic performance was assessed using receiver operating characteristic and tertile-based Kaplan-Meier analyses. Owing to the limited number of events, all analyses were considered exploratory. During 12-month follow-up, all-cause mortality occurred in 10 patients (11.9%), while cardiovascular rehospitalisation was observed in 29 patients (34.5%). GDF-15 demonstrated good discriminative performance for all-cause mortality (AUC 0.823, 95% CI 0.714-0.932, p = 0.001), whereas suPAR showed moderate prognostic discrimination (AUC 0.742, 95% CI 0.605-0.878, p = 0.013). In contrast, NT-proBNP showed no significant discrimination for all-cause mortality (AUC 0.535, 95% CI 0.362-0.709, p = 0.720). Higher tertiles of both GDF-15 and suPAR were associated with reduced overall and rehospitalisation-free survival. Baseline GDF-15 and suPAR were associated with adverse outcomes after T-TEER and demonstrated greater prognostic discrimination than NT-proBNP in this exploratory cohort. These exploratory findings support further investigation of systemic stress and inflammation biomarkers for risk stratification in patients with severe tricuspid regurgitation.

PMID 42547888
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PubMedHeart rhythm2026-08-01

Protein Mediators Linking Autoimmune Diseases and Incident Atrial Fibrillation: Insights from the UK Biobank.

Huang Jingwen J, Liu Chang C, Merchant Faisal M FM, Alonso Alvaro A et al.

Emerging evidence suggests autoimmune diseases (AIDs) are associated with atrial fibrillation (AF) through systemic inflammation. However, causal mechanisms and potential protein mediators remain unexplored. To identify proteins mediating the link between AIDs and incident AF using high-dimensional mediation analysis. This study used UK Biobank data with proteomic profiling (Olink platform). Participants without prevalent AF were grouped into musculoskeletal (MSK), vasculitis, gastrointestinal (GI), neurologic, and rheumatic fever subsets. Fine-Gray models identified AID-AF associations, treating non-cardiovascular death as a competing risk. Two separate Proteome-wide association studies (PWAS) identified proteins linked to AIDs and incident AF, respectively. All models adjusted for age, sex, lipids, BMI, smoking, hypertension, diabetes, coronary artery disease, peripheral vascular disease, stroke, and heart failure. Proteins associated with both AIDs and AF were selected for high-dimensional mediation analysis (HIMA). Among 419,888 participants (median age 58 years, 45.7% male) followed for a median 14.4 years, MSK, vasculitis, GI, and rheumatic fever AIDs significantly increased incident AF risk (HR 1.17, 1.39, 1.17, and 1.46, respectively; P<0.001), but not neurologic AID (P=0.13). In 44,872 participants with proteomic data, HIMA of 232 proteins identified 60 unique mediators, with adrenomedullin, soluble urokinase plasminogen activator receptor, and insulin-like growth factor binding protein 2 shared across multiple AID groups. The identification of protein biomarkers that may help elucidate potential pathways between AID and AF provides mechanistic insights into immune-related atrial remodeling and suggests possible therapeutic targets for AF prevention and risk stratification in AID patients.

PMID 42537973
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PubMedJournal of Cancer2026-07-29

Long-Term Empagliflozin Treatment (50 Days) Attenuates Protease Activity, Migration, and Stemness-Associated Phenotypes in BFTC-909 Renal Pelvis Transitional Cell Carcinoma Cells.

Lee Yi-Hsun YH, Chen Pei-Ni PN, Hsieh Yi-Hsien YH, Chu Yi-Cheng YC et al.

Empagliflozin is a sodium-glucose cotransporter 2 inhibitor widely prescribed for the treatment of type 2 diabetes mellitus. It promotes urinary glucose excretion by inhibiting renal glucose reabsorption. Although empagliflozin has been widely used in clinical practice, its effects and underlying mechanisms related to metastasis, cytokine secretion, and stemness-associated phenotypes in renal pelvis transitional cell carcinoma (TCC) remain poorly understood. In this study, we investigated the long-term (50 days) effects of empagliflozin (5 μM) on BFTC-909 human renal pelvis TCC cells. Prolonged empagliflozin treatment suppressed the migration of tumor cells and the proteolytic activities of matrix metalloproteinase-2 and urokinase-type plasminogen activator. In addition, empagliflozin markedly reduced the viability and self-renewal capacity of BFTC-909 cells. Analysis of conditioned media revealed that long-term empagliflozin exposure significantly reduced the secretion of interleukin-1Ra, interleukin-8, granulocyte colony-stimulating factor, and vascular endothelial growth factor. Together, these findings suggest that empagliflozin suppresses the protease activity, tumor invasiveness, and stemness-associated phenotypes of renal pelvis TCC cells. Overall, this study indicates that long-term empagliflozin treatment reduces the metastatic potential of BFTC-909 renal pelvis TCC cells and highlights the need for additional in vivo and clinical investigations.

PMID 42524255
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