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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

PubMedAntioxidants & redox signaling2026-09-07

uPAR Amplifies Macrophage Inflammation via NF-κB Pathway to Promote Fibrotic Transition Following Acute Kidney Injury.

Zheng Shengchun S, Chen Yan Y, Liu Jiaona J, Gong Na N et al.

Persistent inflammation is recognized as a major driver of the acute kidney injury (AKI) to chronic kidney disease (CKD) transition, yet upstream macrophage-activation signals remain incompletely understood. Here, we investigated whether the urokinase receptor (uPAR), traditionally linked to matrix remodeling, functions instead as an inflammatory signaling hub that links kidney injury to chronic fibrotic remodeling. In a unilateral renal ischemia-reperfusion injury model, uPAR was induced during the fibrotic phase of postischemic kidney injury. Functional enhancement- and loss-of-function approaches revealed a striking dichotomy: exogenous urokinase (uPA) aggravated renal dysfunction, inflammation, oxidative stress, and fibrosis, whereas uPAR deletion was protective. Mechanistically, uPA/uPAR signaling amplified macrophage inflammatory responses, enhancing M1 polarization, pro-inflammatory cytokine production, reactive oxygen species generation, and NF-κB activation. Molecular docking, mutational modeling, and co-immunoprecipitation analyses revealed a previously underappreciated association between activated uPAR and toll-like receptor 4 (TLR4)-containing complexes. This interaction enhanced myeloid differentiation primary response gene 88-dependent NF-κB signaling and potentiated macrophage inflammatory amplification rather than initiating inflammation independently. NF-κB blockade abolished the pro-inflammatory effects of uPA/uPAR signaling, establishing the functional importance of this pathway. We demonstrate that uPA-activated uPAR engages TLR4-associated signaling to intensify macrophage-driven inflammation, oxidative stress, and fibrotic remodeling. These findings redefine uPAR as a molecular switch governing maladaptive kidney repair and identify the uPA/uPAR-TLR4 signaling interface as a promising therapeutic target. Our findings suggest that the uPA/uPAR-TLR4 axis is involved in regulating the progression from AKI to fibrosis. Targeting this signaling node may represent a novel strategy to interrupt maladaptive repair and prevent CKD following AKI. Antioxid. Redox Signal. 00, 000-000.

PMID 42704671
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PubMedQuantitative imaging in medicine and surgery2026-09-06

Contrast-enhanced ultrasound-guided precision fibrinolysis for refractory loculated chylothorax after lung transplantation: a case report.

Jiang Tingting T, Chen Wuxi W, Peng Zifeng Z, Qiu Shuyi S et al.

Pleural complications remain a major source of morbidity after lung transplantation, with chylothorax posing particular therapeutic challenges. When complicated by fibrinous septation, effective drainage becomes difficult, often necessitating intrapleural fibrinolytic therapy (IPFT). However, in the early post-transplant period, blind fibrinolysis carries substantial risks, including hemorrhage and disruption of fragile bronchial anastomoses or lymphatic vessels. We report a 31-year-old woman with pulmonary lymphangioleiomyomatosis (PLAM) who developed refractory loculated chylothorax 39 days after bilateral lung transplantation. Initial chemical pleurodesis was ineffective and subsequently induced a honeycomb-like, non-communicating pleural effusion that was not amenable to conventional drainage. To balance the need for septation lysis against the risk of bleeding, contrast-enhanced ultrasound (CEUS) was integrated as a real-time guidance tool. CEUS facilitated the precise differentiation between avascular fibrin septa and vascularized pleural tissue, allowing targeted low-dose urokinase injection into isolated locules. The restoration of inter-locule communication was directly visualized, permitting early termination of fibrinolytic exposure. Subsequent drainage and repeat pleurodesis resulted in full lung re-expansion without recurrence. To our knowledge, this is the first case utilizing CEUS to guide precision fibrinolysis in a lung transplant recipient. This case provides a proof-of-concept that CEUS-guided precision fibrinolysis can transform a traditionally blind and high-risk intervention into a controlled, visualization-driven procedure. By enabling targeted intervention and real-time efficacy assessment, this approach offers a safer salvage strategy for high-risk patients.

PMID 42701514
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PubMedMolecular and cellular endocrinology2026-09-04

Fibroblast growth factor 23 (FGF23): From synthesis to cleavage.

Yuan Shusen S, Wang Qi Q, Meng Chao C, Ji Hongjie H et al.

Fibroblast growth factor 23 (FGF23) maintains phosphate and vitamin D homeostasis. In the kidney, recognition of FGF23 is mediated by fibroblast growth factor receptors (FGFRs), α-Klotho, and heparan sulfate. Structural studies indicate that an FGF23-FGFR-α-Klotho recognition unit recruits a second FGFR with assistance from heparan sulfate to form an asymmetric 1:2:1:1 complex that activates Ras-mitogen-activated protein kinase (MAPK) signaling. Circulating intact FGF23 reflects transcription, post-translational processing, secretion, and clearance. In FGF23-producing cells, polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3)-mediated O-glycosylation at Thr178 protects the cleavage site, whereas phosphorylation of Ser180 by FAM20C, a Golgi-associated secretory pathway kinase, limits this protection. Furin and related proprotein convertases cleave FGF23 within the secretory pathway, although their in vivo contributions remain unresolved. In cell-free experiments, tissue-type and urokinase-type plasminogen activators directly cleave recombinant FGF23; mouse data also implicate the plasminogen activator inhibitor-1 axis, but its quantitative contribution to the human circulating pool is unknown. Receptor availability further shapes signaling. Although osteocytes and osteoblasts are the principal endocrine sources, human skin cells express and secrete FGF23 in vitro. Their response to 1,25-dihydroxyvitamin D3 depends partly on the vitamin D receptor, but whether skin contributes to circulating FGF23 remains undefined. Chronic kidney disease, autosomal dominant hypophosphatemic rickets, hyperphosphatemic familial tumoral calcinosis, X-linked hypophosphatemia, Raine syndrome, and ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) deficiency illustrate the relationships among FGF23 processing, bone-matrix signaling, and pyrophosphate homeostasis. This review integrates these mechanisms and evaluates burosumab, selective FGFR inhibition, C-terminal peptides, small-molecule antagonists, and ENPP1 enzyme replacement according to current evidence.

PMID 42697502
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PubMedAnnals of vascular diseases2026-09-02

Acute Thrombotic Occlusion Induced by an Inferior Vena Cava Filter Implanted 13 Years Earlier, Treated with the Indigo System and Filter Retrieval.

Anzai Hitoshi H, Kajiwara Keigo K, Saito Rikako R, Kato Takehiro T et al.

A patient in his 40s, who had experienced acute deep vein thrombosis (DVT) of his left leg 13 years ago, developed acute DVT of his right leg due to an inferior vena cava filter (IVCF) thrombotic occlusion. A thrombus extended from just below the IVCF to the bilateral femoral veins. Given the limited availability of urokinase and the strict guidelines for the proper use of the Indigo CAT8 in Japan, we first performed catheter-directed thrombolysis with alteplase for 2 days, followed by aspiration with the CAT8 catheter after confirming the absence of an IVC thrombus. Finally, we successfully retrieved this IVCF, implanted 13 years earlier, using the bidirectional technique.

PMID 42682384
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PubMedMedicine2026-09-01

Perioperative severe airway hemorrhage during veno-arterial extracorporeal membrane oxygenation for acute massive pulmonary embolism: A case report.

Cao Kun K, Hai Feng F

According to the 2019 ERS/ESC guidelines, high-risk pulmonary embolism is defined as a case that presents with hemodynamic instability, obstructive shock, or cardiac arrest, and this condition has an extremely high death rate. ECMO can provide temporary circulatory support, acting as a bridge to definitive reperfusion therapy. The patient is a 25-year-old woman who had previously used estrogen-containing oral contraceptives. She sustained trauma to her right lower limb, necessitating prolonged immobilization. One month before her symptoms started, she had a high fever. One hour before she was admitted to the hospital, she fainted and went into cardiac arrest. Ten minutes of cardiopulmonary resuscitation were needed before her spontaneous circulation returned. The electrocardiography test showed an S1Q3T3 pattern. An ultrasonography check confirmed thrombosis in the right popliteal vein. Transthoracic echocardiography found that the right heart was enlarged, and the left ventricle had a D shape. Computed tomography pulmonary angiography showed a saddle embolus right at the bifurcation of the pulmonary artery, which confirmed acute massive pulmonary embolism (MPE). The patient was supported with veno-arterial extracorporeal membrane oxygenation (VA-ECMO), followed by catheter-directed thrombolysis and targeted airway hemostasis. Urokinase was administered through 2 thrombolysis catheters, and anticoagulation was adjusted dynamically according to bleeding and coagulation status. After the procedure, airway bleeding was stopped using targeted hemostasis methods, and the patient was able to come off ECMO successfully after 73 hours of use. In this case, we achieved successful support from VA-ECMO for a patient with acute MPE. Our work shows that even severe bleeding in the airway can be handled safely, and you don't have to stop anticoagulation treatment to do it. This approach ended up with the patient making a full recovery in the end.

PMID 42675758
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PubMedJournal of the American Heart Association2026-08-31

Sex Differences in Treatment Effect of Adjunctive Intra-Arterial Urokinase After Successful Thrombectomy: A Post Hoc Secondary Analysis of the POST-UK Randomized Clinical Trial.

Chen Xuanyu X, Li Linyu L, Li Gaoming G, Zhang Lingyu L et al.

Whether adjunct intra-arterial urokinase has differential effectiveness and safety by sex among patients with acute ischemic stroke who achieve near-complete to complete reperfusion after endovascular thrombectomy (EVT) remains unknown. This post hoc analysis of the POST-UK (Adjunctive Intra-Arterial Urokinase After Successful Endovascular Thrombectomy in Patients With Large-Vessel Occlusion Stroke) multicenter randomized clinical trial included 534 patients with proximal intracranial large-vessel occlusion who achieved near-complete to complete reperfusion after endovascular thrombectomy. Participants were assigned to intra-arterial urokinase or no adjunct intra-arterial thrombolysis. The primary effectiveness outcome was 90-day survival without disability, defined as a modified Rankin Scale score of 0 to 1. Primary safety outcomes were 90-day all-cause death and symptomatic intracranial hemorrhage within 48 hours. Among 534 participants, 223 were female and 311 were male. The treatment-by-sex interaction for the primary outcome was not statistically significant (P for interaction=0.06). In sex-stratified analyses, intra-arterial urokinase showed a potential benefit signal for 90-day survival without disability among female participants (46.7% versus 32.2%; adjusted risk ratio [RR], 1.47 [95% CI, 1.07-2.02]; P=0.02), whereas no statistically significant difference was observed among male participants (44.1% versus 46.6%; adjusted RR, 0.97 [95% CI, 0.77-1.22]; P=0.79). No statistically significant differences in safety outcomes were observed between treatment groups in either sex, including 90-day mortality and symptomatic intracranial hemorrhage. Adjunct intra-arterial urokinase after endovascular thrombectomy showed a potential benefit signal for 90-day disability-free survival among female participants, without statistically significant differences in male participants or hemorrhagic outcomes across sex subgroups. These findings should be considered hypothesis generating and warrant confirmation in future prospective studies. URL: www.chictr.org.cn; Unique Identifier: ChiCTR2200065617.

PMID 42669921
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