若生智能
Drug Database
UR

urokinase

✓ Approved

Bharat Serums and Vaccines Limited · FSHR · 小分子

什么是 urokinase？

urokinase 是一种小分子，由Bharat Serums and Vaccines Limited研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

公司Bharat Serums and Vaccines Limited
药物类别小分子, 多克隆抗体, 重组蛋白, 多肽类, 抗体
分子靶点FSHR, LHCGR, PLAU, PLG
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Bharat Serums and Vaccines Limited

作用机制

分子靶点

urokinase 作用于 4 个分子靶点：

FSHRfollicle stimulating hormone receptor (FSHRO, ODG1)
LHCGRluteinizing hormone/choriogonadotropin receptor (ULG5, LH/CGR)
PLAUplasminogen activator, urokinase (URK, UPA)
PLGplasminogen (HAE4)
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
Vascular disordersThrombosis✓ Approved

相关研究文献

PubMedJournal of materials chemistry. B2026-07-27

Mild hyperthermia near-infrared-triggered urokinase release from CREKA-modified PLGA-PEG nanoparticles targeted to deep vein thrombosis.

Wu Junxian J, Ban Rui R, Xiao Qingyang Q, Shan Xiaoqian X

Owing to the short half-life, poor targeting ability, and high bleeding risk of conventional thrombolytic drugs, the treatment of deep vein thrombosis (DVT) remains challenging. In this study, a photothermal-responsive drug delivery platform was developed by combining the thrombolytic activity of urokinase (UK), the photothermal conversion property of copper sulfide (CuS) nanoparticles, and the fibrin-targeting ability of the peptide CREKA (Cys-Arg-Glu-Lys-Ala). The obtained UK@CuS@PLGA-PEG-CREKA (UK@CuS@PP-CREKA) nanoparticles have a particle size of 196.53 ± 10.99 nm and a zeta potential of -2.36 ± 0.83 mV, with good colloidal stability and prolonged circulation characteristics. Under 808 nm near-infrared (NIR) irradiation, the system achieves a photothermal conversion efficiency of 57.5% and a thrombolytic efficiency of 63.66%, which is much higher than that of free UK, with NIR-controlled release behavior. In a murine DVT model, the system increases the drug accumulation at the thrombus site 3.2-fold compared to the non-targeted control, and blood flow is restored within 5 h post-injection without causing detectable bleeding or systemic toxicity. Histopathological analysis further shows reduced P-selectin expression, indicating attenuated thrombus-associated inflammation, and no pathological damage to the major organs (heart, liver, spleen, lungs, kidneys). In summary, this targeted photothermal-controlled release strategy offers a promising approach for the treatment of DVT.

PMID 42507029
阅读全文 →
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
阅读全文 →
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
阅读全文 →
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
阅读全文 →
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
阅读全文 →
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
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多urokinase