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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

PubMedJournal of endovascular therapy : an official journal of the International Society of Endovascular Specialists2026-07-17

A Hybrid Protocol of Emergent Endovascular Intervention With Adjunctive Systemic Thrombolysis for Acute Limb Ischemia: A Single-Center Pilot Study.

Yu LianHui L, Cheng Shih-Tsung ST, Liu Fang F, Liu HsiaoQian H et al.

To evaluate the feasibility and early outcomes of a hybrid pharmacomechanical strategy combining emergent endovascular revascularization with adjunctive systemic thrombolysis for the treatment of acute limb ischemia (ALI). This retrospective single-center pilot study included 20 consecutive patients presenting with ALI within 96 hours of symptom onset who underwent primary endovascular revascularization between 2016 and 2018. Mechanical thrombectomy and angioplasty were performed as first-line interventions. In cases of incomplete reperfusion, adjunctive intravenous systemic urokinase infusion was administered followed by repeat angiographic assessment within 48 to 72 hours. Technical success, limb salvage, complications, and in-hospital mortality were evaluated. Initial mechanical endovascular intervention achieved successful reperfusion in 13 patients (65%). Seven patients with persistent low-flow states received adjunctive systemic thrombolysis, resulting in additional successful reperfusion in 5 cases. The overall technical success rate was therefore 90%. Two patients required fasciotomy for compartment syndrome. One patient developed severe ischemia-reperfusion injury resulting in multiorgan failure and death. Limb salvage was achieved in 18 of 20 patients during the index hospitalization. Mean clinical follow-up was (145.1 ± 182.3) days (median: 65 days). A staged hybrid pharmacomechanical strategy incorporating adjunctive systemic thrombolysis following mechanical endovascular revascularization was associated with a feasible treatment option for selected patients with ALI when initial mechanical intervention results in incomplete reperfusion. Larger studies are required to determine the comparative effectiveness of this approach in contemporary endovascular practice.Clinical ImpactFor patients with acute limb ischemia and suboptimal flow (TIMI 0-1) after initial endovascular mechanical thrombectomy-defined angiographically as TIMI 0 (no antegrade flow beyond the occlusion) or TIMI 1 (minimal penetration of contrast without distal bed filling), analogous to coronary grading-adjunctive systemic thrombolysis was associated with successful salvage in 83% of otherwise refractory cases in this pilot study, raising overall technical success from 65% to 90%. This staged hybrid strategy offers a practical "bail-out" option before resorting to repeat intervention or open surgery. Urokinase was delivered as a peripheral intravenous infusion; although not available in all regions (it has not been Food and Drug Administration-approved in the United States since 2010), the principle may be applied with alternative agents such as tissue plasminogen activator. The innovation lies in its simplicity: a predefined protocol using systemic urokinase without specialized catheter-directed systems. Clinicians should consider this approach in hemodynamically stable patients with persistent low-flow states, potentially reducing the need for immediate reintervention while achieving acceptable limb salvage and mid-term amputation-free survival.

PMID 42466592
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PubMedFrontiers in neuroscience2026-07-16

Inhibiting the uPAR/FPR1 interactions reduces blood-retinal barrier breakdown and improves retinal function in a rat model of diabetes.

Canovai Alessio A, Amato Rosario R, Melecchi Alberto A, De Fenza Maria M et al.

Diabetic retinopathy (DR) is a leading cause of blindness characterized by early neurovascular damage driven by hyperglycemia-induced mechanisms, including inflammation. The system composed of the urokinase-type plasminogen activator (uPA) and its receptor (uPAR) has previously emerged as a potential regulator of the pro-inflammatory events in DR, possibly through the interaction of uPAR with its lateral partners, such as formyl peptide receptors (FPRs). This study explored whether the inhibition of uPAR/FPR1 crosstalk may reduce early neurovascular alterations in DR by targeting inflammation. To this aim, the new FPR1 antagonist N-19004 was tested in a rat model of streptozotocin-induced diabetes. N-19004 was administered subcutaneously for 7 days at 1 month from diabetes onset. Immunofluorescence, RT-qPCR, Western blot and Evans blue perfusion were performed to evaluate the effects of N-19004 on inflammation, reactive gliosis, blood-retinal barrier (BRB) integrity and apoptosis. In addition, electroretinogram (ERG) was used to assess N-19004 efficacy on retinal function. N-19004 inhibited the activation of inflammation-related transcription factors, including nuclear factor kappa-light-chain-enhancer of activated B cells and signal transducer and activator of transcription 3, leading to reduced interleukin-1β and tumor necrosis factor-α expression. The attenuation of inflammatory processes resulted in reduced glial activation, as indicated by lower glial fibrillary acidic protein expression and Müller cell gliosis. The anti-inflammatory activity of N-19004 was accompanied by decreased BRB breakdown, as demonstrated by N-19004-mediated reduction of vascular endothelial growth factor, increased levels of tight junction components and diminished vessel leakage. The amelioration of BRB integrity was associated with reduced activation of caspase 3 and partial preservation of scotopic ERG a- and b-wave amplitudes, thereby improving retinal viability and function in N-19004-treated STZ rats. These results support the possible involvement of uPAR/FPR1 interactions in the regulation of DR-related inflammation and suggest a novel therapeutic target for the management of the early phases of disease.

PMID 42459363
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PubMedAnnals of vascular surgery2026-07-14

Radiological and clinical outcomes of transcatheter thrombolysis via superior mesenteric artery vs percutaneous mechanical thrombectomy in patients with anticoagulation-refractory acute mesenteric venous thrombosis.

Li Wenrui W, Liu Bin B, Feng Hai H

The aim of this study was to evaluate the safety and efficacy of indirect catheter-directed thrombolysis (CDT) via the superior mesenteric artery (SMA) and percutaneous mechanical thrombectomy (PMT) for acute mesenteric venous thrombosis (MVT). From December 2020 to March 2024, the clinical data of patients with acute MVT who received endovascular therapy were retrospectively reviewed. Patients were stratified by the treatment strategy. The primary outcome measure was technical success, which was assessed by thrombolysis grade. Secondary outcomes were complications, time to resume oral intake, dosage of Urokinase used, postischemia intestinal stenosis and mortality. Forty-two consecutive patients were identified. CDT was initiated in 24 patients, and 18 patients received PMT treatment. In PMT group, 13 patients (72.2%) received adjunctive indirect CDT after mechanical thrombectomy. The time of thrombolysis and dosage of Urokinase were both less in PMT group(P<0.05). The bowl rest time is less in PMT group (8 vs 5 days; P<0.05). No difference was found in perioperative complications, mortality and bowel stricture between two groups. More patients in the PMT group had better revascularization with lysis grade of III (0% vs 38.9%, P<0.05) and fully revascularization (0% vs 27.8%, P<0.05). Compared with indirect CDT via SMA, PMT is an effective treatment for anticoagulation-refractory acute MVT without increasing safety risks.

PMID 42442535
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PubMedJournal of controlled release : official journal of the Controlled Release Society2026-07-14

Enhancing insulin sensitivity by reducing adipocyte senescence using uPAR-targeted nanoparticles in high-fat-diet-induced obese mice.

Jung Jin Ki JK, Nguyen Thi Oanh Oanh TOO, Jung Won Chul WC, Nguyen Bao Loc BL et al.

The urokinase-type plasminogen activator receptor (uPAR) is a glycosylphosphatidylinositol-anchored membrane protein that regulates fibrinolysis, cell adhesion, migration, and intracellular signaling. Elevated uPAR expression is linked to numerous pathological conditions, including cancer, inflammation, and metabolic dysfunction. In obesity and aging, increased uPAR levels are associated with chronic inflammation, adipose tissue impairment, and systemic metabolic disturbances. uPAR also modulates adipocyte differentiation and contributes to the progression of inflammatory obesity, while serving as a key regulator of cellular senescence triggered by oncogenic stress, chemotherapy, or aging. These characteristics position uPAR as a compelling therapeutic target for metabolic and age-related diseases. To address this, we developed a nanoparticle-based targeted therapy optimized for senolytic delivery, which enhances accumulation in uPAR-overexpressing cells and improves drug stability. Dasatinib and quercetin, two established senolytic agents, were co-encapsulated into uPAR-targeted hybrid nanoparticles to selectively eliminate senescent cells, reduce inflammation, and restore metabolic homeostasis, presenting a promising therapeutic strategy for obesity- and aging-associated disorders.

PMID 42442548
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-07-13

Identification of an Osteochondral Erosion Process in Gout Driven by Fibrinogen-Integrin Activation and Local MSU Crystallization.

Xu Hanlin H, Bi Simin S, Liu Zhechen Z, Zhou Xiaofeng X et al.

Gout is characterized by monosodium urate (MSU) crystal deposition, recurrent inflammatory flares, and progressive cartilage erosion. However, the reasons for preferential MSU crystal formation at cartilage injury sites and the drivers of cartilage degradation remain unknown. Here, the dynamics of MSU crystal deposition in cartilage were investigated using stimulated Raman scattering microscopy combined with isotope labeling. MSU crystals preferentially accumulated at cartilage injury sites in a crystallization‑frequency‑dependent pattern, and multicycle MSU crystallization promoted deeper deposition in injured cartilage. Proteomics revealed local enrichment of the fibrinogen complex following cartilage injury. In vivo and in vitro validation experiments further showed that fibrinogen gamma chain (FGG) deposition co‑localized with local MSU accumulation, accelerated MSU crystallization, and determined the site preference of deposition in a gout model. FGG and MSU deposition were further linked to integrin‑related adhesion signaling and matrix-degrading programs. Cartilage injury, FGG deposition, and selective MSU crystallization together constitute a vicious cycle in gouty cartilage erosion, which can be interrupted by urokinase treatment or cartilage barrier restoration. In conclusion, cartilage injury promotes local fibrinogen deposition and deeper crystal invasion, thereby forming a self‑amplifying loop that contributes to gout‑associated cartilage erosion. This study also provides new biomarkers and therapeutic targets for gout management.

PMID 42439437
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PubMedPediatric surgery international2026-07-12

Heparin combined with urokinase therapy for the treatment of acute portal vein thrombosis in children.

JinShan Zhang Z, TaiJi Kuang K, Long Li L

Acute portal vein thrombosis (PVT) poses a significant threat to life, with mortality rates ranging from 20% to 50%. However, a clear consensus on the management of acute PVT in children is lacking, and treatment strategies often rely on protocols established for adults. This study summarizes our experience and results in treating acute PVT with heparin combined with urokinase, providing reference data for the diagnosis and treatment of pediatric acute PVT. From November 2017 to February 2026, 5 children (2 males and 3 females) experienced acute PVT after surgery in our hospital. The ages of these children ranged from 2 to 14 years (median: 13 years). Among the 5 patients, one had hereditary spherocytosis (HS), one had total splenic infarction caused by myeloproliferative neoplasms (MPNs), and three had Abernethy malformation. Splenectomy was performed in two patients with HS and MPN, and ligation of the portosystemic shunt was performed in the other three patients with Abernethy malformation. Abdominal ultrasound (US) and enhanced computed tomography (CT) were routinely performed at postoperative days 1-7 to detect PVT. An anticoagulant and thrombolytic treatment protocol involving the combined use of heparin and urokinase is implemented in cases of PVT involving the main portal vein and/or superior mesenteric vein (SMV); in this, intravenous heparin is administered continuously at an initial dosage of 20 U/kg per hour with an increased infusion rate to achieve APTT of 60-85 s, and intravenous urokinase is continuously administered at a dosage of 4400 U/kg per hour for 2-6 h every day. After the stabilization or disappearance of the PVT, oral medications, including aspirin and dipyridamole or rivaroxaban, were used for 6 months. The routine follow-up was performed after 1, 3, and 6 months, and every 6 months thereafter. The acute PVT was detected by US and CT in all patients at postoperative days 1-7 (median: 3 days). The thrombus was located in the main portal vein in 3 patients, in the SMV in 4 patients, in the IMV in 3 patients, and in the splenic vein in 4 patients. PVT occurred simultaneously in three or more branches of the portal vein system in 4 patients. One patient experienced severe abdominal pain caused by PVT, and there were no symptoms, including abdominal pain, hematochezia, nausea, or vomiting in the other 4 patients. When portal vein thrombosis is detected, there is a notable elevation in D-dimer levels. The level of D-dimer was gradually reduced, followed by the reduction of PVT after the anti-coagulation and thrombolysis therapy. The usage of heparin combined with urokinase therapy was successful in all patients; one patient developed CTPV but exhibited no symptoms of portal hypertension, whereas the PVT completely resolved in the remaining four patients between after 19 days to 6 months. There was no bleeding caused by anticoagulation or thrombolysis during therapy. The duration of hospitalization after surgery ranged from 15 to 34 days (median: 20 days). The duration of follow-up ranged from 2 months to 4 years (median: 1 year). There was no recurrence of PVT in all patients. The use of heparin combined with urokinase for the treatment of pediatric PVT is feasible and effective under the premise of ensuring safety. Nevertheless, further verification of its safety and effectiveness is still needed through increased sample size.

PMID 42437407
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