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UR

urokinase (Breokinase / Alphakinase / Thrombolase)

✓ Approved

Mitsubishi Tanabe Pharma Corporation · PLAU

What is urokinase?

urokinase is a therapeutic agent developed by Mitsubishi Tanabe Pharma Corporation. It is approved for therapeutic indications.

Drug Profile

Brand NamesBreokinase, Alphakinase, Thrombolase
CompanyMitsubishi Tanabe Pharma Corporation
Molecular TargetPLAU
StatusApproved
Sources: ClinicalTrials.gov, Mitsubishi Tanabe Pharma Corporation

Mechanism of Action

Molecular Targets

urokinase acts on 1 molecular target:

PLAUplasminogen activator, urokinase (URK, UPA)
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Therapeutic Indications

urokinase is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Respiratory, thoracic and mediastinal disordersPulmonary thrombosis✓ Approved

Related Research Articles

PubMedPloS one2026-07-23

Trends in general practitioner dispensing of thickeners in the NHS England, 2019-24.

McCurtin Arlene A, Collins Lindsey L, Doody Owen O, Kelly Dervla D et al.

Oropharyngeal dysphagia is common and often results in aspiration. Thickeners are widely used to thicken liquids to slow the liquid bolus and prevent aspiration and aspiration pneumonia, despite multiple concerns about their use. To date, there is little data on prescribing/dispensing practices. This study aims to provide the first overview of thickener dispensing practices, serve as foundational material for parties interested in research, practice and policy making, and guide further work in this area. We explored English general practitioner thickener dispensing practices for the five-year period 2019-2024 via the NHS Business Services Authority ePACT2 database and using descriptive statistics and linear regression to analyse the data. We hypothesized that with a large data set, it would be possible to detect trends in dispensing. Between 2019 and 2024, nearly three million thickening items were dispensed in primary care in England at a cost of nearly 90 million sterling. Thickened liquids is primarily an intervention for older people although there was a significant decreasing trend in dispensed thickener items in adult populations. Thickener dispensing has increased in the youngest age group (0-1-years-old). The cost of thickeners to the NHS has risen in the last year under study despite the significant decline in use observed for most age groups. Of dispensed items over the five-year period, the vast majority were gum-based. While the data provided in this study is limited to GP dispensed thickeners in England, it provides researchers, clinicians and policy makers with initial information on dispensing practices. From the available data, a decreasing dispensing trend is seen in the context of rising costs, older people comprise the population who primarily receive thickeners and gum-based products dominate the market. This study raises a number of questions regarding the use of thickeners for people with swallowing problems.

PMID 42490585
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PubMedFrontiers in medicine2026-07-23

Therapeutic effect of modified meridian-guided acupoint pressing on lumbar facet joint osteoarthritis: an integrated microbiomics and metabolomics analysis.

Jiang Yu Y, Qin Wanan W, Wei Li L, Liao Yalian Y et al.

To investigate the therapeutic efficacy of Modified Meridian-Guided Acupoint Pressing (MMGAP) in lumbar facet joint osteoarthritis (LFJ OA) and to explore its underlying mechanisms through integrated microbiomics and metabolomics. Animal model study (urokinase-induced LFJ OA in SD rats) with MMGAP intervention, fecal microbiota transplantation (FMT), and mTORC1 inhibitor (rapamycin) validation. Histological, molecular, 16S rRNA sequencing, and UPLC-MS/MS metabolomic analyses were carried out to assess relevant outcomes. MMGAP significantly reduced inflammatory cell infiltration in lumbar muscles/facet joints, markedly downregulated serum IL-1β and TNF-α (p < 0.05) as well as TRPV1 protein expression by >40% at the mRNA and protein levels. It reshaped gut microbiota (significantly elevated Observed Species, Shannon and Chao1 indices, p < 0.05; distinct β-diversity clustering vs model group) and serum metabolomic profiles, enriching the mTOR signaling pathway. FMT from MMGAP-treated rats recapitulated therapeutic effects, while rapamycin mimicked MMGAP's anti-inflammatory/analgesic actions. MMGAP alleviates LFJ OA through gut microbiota reshaping, serum metabolomic reprogramming, and mTORC1 pathway inhibition. These preclinical findings lay preliminary experimental groundwork supporting the research potential of MMGAP as a non-invasive candidate intervention for degenerative joint diseases.

PMID 42487937
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PubMedJournal of the neurological sciences2026-07-22

Intra-arterial thrombolytics after endovascular thrombectomy for acute ischemic stroke: A network meta-analysis of RCTs.

Elfil Mohamed M, Abbas Abdallah A, Sabet Haneen H, Elmashad Ahmed A et al.

Endovascular thrombectomy (EVT) is the gold standard treatment for acute ischemic stroke (AIS) caused by large vessel occlusion (LVO) in patients meeting certain eligibility criteria. A critical challenge in this regard is the phenomenon of futile recanalization, which can be partially explained by embolism of the distal microcirculation. Thus, a few clinical trials investigated the efficacy and safety profile of intra-arterial thrombolysis (IAT) post successful EVT aiming to improve EVT's clinical outcomes without increasing the risk of hemorrhagic complications. We aim to evaluate the efficacy and safety of adjunctive IAT after successful EVT for AIS-LVO. A systematic review and network meta-analysis (NMA) of randomized controlled trials comparing IAT (Alteplase (ALT), Tenecteplase (TNK), or Urokinase (UK)) versus EVT alone were conducted. Primary outcomes were 90-day modified Rankin Scale (mRS) 0-1, mRS 0-2, and mortality; safety outcomes included any and symptomatic intracranial hemorrhage (any ICH and sICH). Eight trials (2564 patients) were included. EVT + TNK 0.125 mg/kg (RR 1.54, 95% CI 1.07-2.20) and EVT + ALT 0.225 mg/kg (RR 1.51, 95% CI 1.22-1.89) improved excellent outcomes (mRS 0-1) versus EVT alone. No regimen improved mRS 0-2 or mortality. EVT + TNK 0.0625 mg/kg increased the risk of any ICH (RR 1.34, 95% CI 1.08-1.66), but not the risk of sICH. IAT, particularly with ALT 0.225 mg/kg or TNK 0.125 mg/kg, may enhance post-EVT recovery without increasing sICH risk. Larger trials are needed to confirm optimal dosing and patient selection.

PMID 42480380
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PubMedRecent advances in inflammation & allergy drug discovery2026-07-22

IL-17RA/IL-17RC Blockade Restores Fibrinolytic Balance in Bleomycin-induced Acute Lung Injury.

Charavu Rakshitha R, Madambath Jeena Thrikkandiyoor JT, Jain Akarsha B AB, Bhandary Yashodhar P YP

Interleukin-17A (IL-17A) signalling disrupts fibrinolysis and drives inflammation and fibrotic remodelling in acute lung injury (ALI). IL-17A signals through a heterodimeric complex of IL-17RA and IL-17RC, initiating a cascade of immunological responses, including the synthesis of chemokines and inflammatory mediators. This leads to compromised epithelial integrity and barrier dysfunction. To determine the therapeutic potential of IL-17RA and IL-17RC neutralising antibodies on inflammation and the fibrinolytic system in a bleomycin (BLM)-induced ALI model. A549 cells and C57BL/6 mice were used to study the effects of neutralising IL-17RA and IL-17RC. ALI was induced in both models using BLM. A549 cells were subsequently treated with IL-17RA and IL-17RC neutralising antibodies. In mice, ALI was induced via intranasal administration of BLM. Neutralising antibodies against IL-17RA and IL-17RC were administered intranasally. Collected lung tissues and cell pellets were assessed for expression of the fibrinolytic system and inflammation. Our study demonstrates the active involvement of IL-17 receptors, IL-17RA, and IL17RC in ALI. BLM treatment significantly increased PAI-1 expression ~ 3.5-fold, whereas neutralisation of IL-17RA or IL-17RC markedly reduced PAI-1 levels by over 90% compared to the BLM treated group, while restoring the expression of urokinase plasminogen activator (uPA) and its receptor (uPAR) and suppressing pro-inflammatory cytokines TNF-α and IL-6. This study reveals that neutralisation of IL-17RA or IL-17RC in BLM-induced ALI reduced inflammation and restored normal fibrinolytic balance. Our study suggests that IL-17RA and IL-17RC play a major role in inflammation and the regulation of fibrinolysis during ALI. Targeting these receptors can mitigate lung injury and restore normal fibrinolytic activity, highlighting a novel receptor-specific IL-17 blockade as a potential therapeutic strategy to limit lung injury and improve ALI and Acute respiratory distress syndrome (ARDS) outcomes.

PMID 42483914
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PubMedInflammation research : official journal of the European Histamine Research Society ... [et al.]2026-07-19

SERPINE1 in ARDS: an emerging regulator of inflammation-coagulation-fibrinolysis crosstalk.

Gao Nan N, Yang Song S, Zhang Wei-Jian WJ, Lu Hao-Tian HT et al.

This narrative review synthesizes current evidence on the role of SERPINE1/PAI-1 in acute respiratory distress syndrome (ARDS), with particular emphasis on inflammation-coagulation-fibrinolysis crosstalk. Published experimental, translational, genetic, and clinical studies addressing SERPINE1/PAI-1 in ARDS and related critical illnesses were summarized. Not applicable. We summarized evidence on the pathobiological functions, cellular sources, biomarker potential, genetic associations, and therapeutic implications of SERPINE1/PAI-1. SERPINE1 limits tissue-type and urokinase-type plasminogen activator activity, thereby promoting hypofibrinolysis and persistent fibrin deposition in the injured lung. Experimental and clinical evidence further links elevated PAI-1 to inflammatory amplification, endothelial injury, pulmonary microvascular thrombosis, greater disease severity, and adverse outcomes, although the strength of evidence and the degree of causal support vary across these processes. High-expression SERPINE1 variants may also influence clinical outcomes in selected critical illness settings. Pharmacological PAI-1 inhibition is biologically plausible, but its translation to ARDS remains limited by disease heterogeneity, uncertainty regarding treatment timing, and the risk of bleeding. SERPINE1 is a potentially important integrative regulator and biomarker of dysregulated inflammation, coagulation, and fibrinolysis in ARDS. Future studies should clarify its causal, cell-specific, and phenotype-dependent roles to facilitate the development of targeted therapeutic strategies.

PMID 42470461
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PubMedJournal of translational medicine2026-07-19

Hypoxia tumor-associated macrophages facilitate hepatocellular carcinoma metastasis via uPA-uPAR pathway.

Wang Yijun Y, You Xiaomin X, Luo Xiangyuan X, Huang Wenjie W et al.

Hepatocellular carcinoma (HCC) arises within a hypoxic and immunosuppressive tumor microenvironment (TME), where tumor-associated macrophages (TAMs) constitute a major immune population. The impact of hypoxia on TAM functional heterogeneity and their contribution to HCC growth and metastasis remain incompletely understood. We integrated multiple single-cell RNA sequencing datasets and developed a machine learning framework to map cellular hypoxia at single-cell resolution. Hypoxic TAMs (H-TAM) were characterized using transcriptomic and functional assays, including pseudotime trajectory analysis, regulatory network inference, in vitro co-culture, and orthotopic mouse models. Drug sensitivity correlations and in vivo validation were performed to evaluate therapeutic strategies. H-TAM represented the most hypoxic immune population in HCC and exhibited enhanced interactions with malignant hepatocytes. Transcriptomic profiling revealed HIF-1α-dependent hypoxia signaling and upregulation of plasminogen activator, urokinase (uPA, encoded by PLAU). H-TAM-derived uPA engaged its receptor uPAR on HCC cells, promoting epithelial-mesenchymal transition (EMT), migration, invasion, and lung metastasis. In line with this, genetic silencing of the corresponding mouse gene Plau in hypoxia-exposed bone marrow-derived macrophages (H-BMDM) markedly attenuated these pro-tumorigenic effects. Integrative drug sensitivity analysis identified dasatinib as a potential therapeutic agent in HCC with high uPAR expression, and in vivo administration selectively suppressed H-BMDM mediated tumor progression and metastasis while prolonging mouse survival. Hypoxia drives TAM heterogeneity in HCC via an H‑TAM‑intrinsic HIF‑1α-uPA axis that engages uPAR on HCC cells to promote metastasis. uPAR is a potential prognostic biomarker, and dasatinib is a promising therapy to block this axis and improve outcomes.

PMID 42471734
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