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urokinase

✓ Approved

Bharat Serums and Vaccines Limited · FSHR · Small Molecule

What is urokinase?

urokinase is a small molecule developed by Bharat Serums and Vaccines Limited. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyBharat Serums and Vaccines Limited
Drug ClassSmall Molecule, Polyclonal Antibodies, Recombinant Proteins, Polypeptide, Antibody
Molecular TargetFSHR, LHCGR, PLAU, PLG
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Bharat Serums and Vaccines Limited

Mechanism of Action

Molecular Targets

urokinase acts on 4 molecular targets:

FSHRfollicle stimulating hormone receptor (FSHRO, ODG1)
LHCGRluteinizing hormone/choriogonadotropin receptor (ULG5, LH/CGR)
PLAUplasminogen activator, urokinase (URK, UPA)
PLGplasminogen (HAE4)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Vascular disordersThrombosis✓ Approved

Related Research Articles

PubMedFrontiers in immunology2026-09-18

Decreased expression of immune activator WARS1 and other pro-inflammatory mediators in type 1-like macrophages as an associated mode of action in response to fucoidan from marine brown algae.

Ostermann Jasmin J, Gemoll Timo T, Schnüttgen Tabea T, Tischhöfer Marie-Theres MT et al.

Macrophages are key regulators of innate and adaptive immune responses through antigen presentation and the production of inflammatory mediators and growth factors. Imbalances in the activation and inhibition of pro-inflammatory type 1-like macrophages (M1) and anti-inflammatory type 2-like macrophages (M2) are closely associated with various autoimmune and chronic inflammatory diseases, underscoring the need for targeted therapeutic approaches. Numerous studies have shown that sulfated polysaccharides from marine algae, especially fucoidans from brown algae, exhibit a wide range of anti-inflammatory activities. This study aims to investigate the anti-inflammatory mode of action of algae-derived fucoidans in monocyte-derived macrophages and to identify the key regulatory proteins and inflammatory mediators involved. We applied data-independent mass spectrometry to comprehensively evaluate protein profiles of monocyte-derived M1/M2-like macrophages under the influence of sulfated polysaccharides from different algae species, namely fucoidans from the brown algae Saccharina latissima, Fucus evanescens, and Laminaria digitata, as well as the sulfated xylogalactan from the red alga Delesseria sanguinea. Furthermore, a series of gradually depolymerized fractions of the fucoidan from Saccharina latissima was investigated to elucidate the impact of molecular weight (MW) on protein expression levels and cytokine secretion patterns using membrane-based cytokine arrays and ELISA measurements. Among the tested sulfated polysaccharides, especially the fucoidan from Saccharina latissima showed anti-inflammatory effects. They significantly reduced expression levels of pro-inflammatory tryptophanyl-tRNA synthetase (WARS1), the cytokines interferon gamma-induced protein 10 (IP-10, syn. CXCL10) and macrophage migration inhibitory factor (MIF), as well as urokinase-type plasminogen activator receptor (uPAR) in pro-inflammatory M1-like macrophages, whereby their effects turned out to be independent of the MW. Our study provides novel insights into the anti-inflammatory mode of action of fucoidan from Saccharina latissimima on monocyte-derived macrophages. Further in vitro and in vivo studies are required to better understand the underlying molecular pathways, the associated mechanism and to evaluate potential medical applications.

PMID 42756851
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PubMedClinics (Sao Paulo, Brazil)2026-09-18

Comparison of the short-term and long-term effects of AngioJet and AcoStream mechanical catheter thrombolysis on acute iliofemoral vein thrombosis.

Yang Yaobo Y, Dong Xuan X, Zhao Yilin Y, Chen Sipan S

To compare the short-term and long-term clinical efficacy and safety of AngioJet and AcoStream thrombectomy devices in the treatment of acute iliofemoral venous thrombosis. We conducted a 4-year retrospective case ‒ control study. A total of 243 patients with acute iliofemoral deep vein thrombosis underwent endovascular interventional therapy in our hospital. According to different operation methods, patients were divided into two groups: Group A (AngioJet mechanical thrombectomy system) and Group B (AcoStream mechanical thrombectomy system). The clinical basic data and short-term postoperative efficacy of the two groups were compared. After 36-months of follow-up, the recurrence rate and long-term efficacy of post-thrombotic syndrome were compared between the two groups. The Kaplan-Meier survival method was used to analyze the proportion of Post-Thrombotic Syndrome (PTS). The thrombus aspiration time in the AngioJet group (4.62 ± 0.12 min) was shorter than that in the AcoStream group (5.87 ± 0.09 min) (p = 0.001); the intraoperative blood loss (264.12 ± 5.46 mL) was less than that in the AcoStream group (307.62 ± 4.52 mL) (p < 0.001); the hemoglobin difference (15.57 ± 0.72 g/L) was less than that in the AcoStream group (24.58 ± 0.86 g/L) (p < 0.001); the D - D decrease rate (0.85 ± 0.03 mg/L/D) was faster than that in the AcoStream group (0.75 ± 0.03 mg/L/D) (p = 0.03); the dosage of urokinase (147.39 ± 0.71) million units was more than that in the AcoStream group (125.33 ± 1.01) million. Units (p < 0.001). The swelling reduction rates of the thigh and calf at 24-hours after surgery were (0.61 ± 0.01%) vs. (0.56 ± 0.01%) and (0.63 ± 0.01%) vs. (0.66 ± 0.01%), respectively, with statistically significant differences between the two groups (p < 0.05). The incidence of postoperative hematuria in the AngioJet group (91.9%) was higher than that in the AcoStream group (0.0%) (p < 0.001). After 36-months of follow-up, the thrombus recurrence rate in the AngioJet group (8.9%) was compared with that in the AcoStream group (2.5%) (p < 0.05), and the incidence of postoperative PTS in the two groups was (34.95%) vs. (21.67%) (p = 0.016). Compared with the AcoStream system, the AngioJet system has a higher efficiency of thrombus clearance, but the incidence of hematuria and the recurrence rate are slightly higher. Of course, both have their advantages and disadvantages, and the appropriate surgical method should be selected according to the individual conditions of patients.

PMID 42759096
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PubMedCalcified tissue international2026-09-11

SERPINE1/PAI-1 in Skeletal Degeneration: A Proposed Context-Dependent Framework for Bone Remodeling Regulation.

Liu Hang H, Yao Dengbo D, Wang Yu Y, Kong Qingquan Q

SERPINE1 encodes plasminogen activator inhibitor-1 (PAI-1), a key inhibitor of tissue-type and urokinase-type plasminogen activators. Beyond fibrinolysis, PAI-1 participates in extracellular matrix remodeling, cellular senescence, inflammatory amplification, fibrosis-like repair, metabolic stress responses, and bone-cell coupling. These processes are central to osteoporosis, osteoarthritis, and intervertebral disc degeneration, yet the role of SERPINE1/PAI-1 in skeletal tissues is highly context dependent. In osteoporosis, excessive PAI-1 activity is mainly associated with impaired osteogenesis, osteoblast-lineage senescence, defective repair, and bone loss. In osteoarthritis, PAI-1 shows a context-dependent role: persistent elevation may promote chondrocyte senescence and maladaptive matrix remodeling, whereas experimental loss-of-function studies suggest that PAI-1 may protect cartilage in specific settings by restraining excessive plasmin-MMP-mediated degradation. In intervertebral disc degeneration, emerging evidence links SERPINE1 expression and PAI-1 activity to nucleus pulposus cell senescence, fibrosis-like extracellular matrix remodeling, oxidative/metabolic stress, and matrix dysregulation. This review synthesizes current evidence and proposes a testable conceptual framework in which SERPINE1/PAI-1 may function as a stress-responsive remodeling rheostat rather than as a uniformly pathogenic or protective factor. From a translational perspective, SERPINE1/PAI-1 is unlikely to serve as a stand-alone diagnostic biomarker or a target for uniform systemic inhibition. Instead, its clinical value may lie in molecular stratification, identification of disease-stage- and compartment-specific endotypes, and locally targeted modulation of pathogenic downstream programs. Future studies should integrate spatial multi-omics, time-resolved disease models, human cohort validation, and tissue-specific delivery strategies to determine when SERPINE1/PAI-1 is therapeutically actionable in skeletal degeneration.

PMID 42726129
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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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