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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

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)
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Therapeutic Indications

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

Therapeutic AreaConditionPhase
Vascular disordersThrombosis✓ Approved

Related Research Articles

PubMedFrontiers in systems biology2026-11-11

From telomere dysfunction to seno-antigen selection: a conceptual framework and route-specific evidence appraisal for senolytic immunotherapy.

Niazi Sarfaraz K SK

Cellular senescence causally contributes to age-related and chronic diseases, rendering the targeted immune clearance of pathological senescent cells a promising therapeutic avenue. Progress remains limited by heterogeneity across cell lineages, tissues, inducing stressors, and temporal factors. As antigen expression alone does not ensure immune accessibility, functional recognition, or safety for healthy tissues, these aspects warrant thorough evaluation. A conceptual framework is proposed, distinct from a validated or implementable algorithm, for identifying and prioritizing senescence-associated antigens. This framework requires four criteria that a single candidate antigen must meet within the same cellular context: persistent pathological senescence, immune accessibility via a confirmed surface antigen or naturally presented human leukocyte antigen (HLA) peptide, modality-appropriate functional immune recognition, and exclusion from vital healthy or beneficially senescent states. The mechanistic origin, such as telomere dysfunction, serves as an optional stratification axis that defines coherent subsets rather than a universal prerequisite; data lacking matched telomere and antigen information in the same cells remain unverified. The process distinguishes target nomination from product validation: evidence of recognition in a single modality, such as chimeric antigen receptor (CAR) targeting of a surface antigen, does not confirm validation for alternatives like peptide vaccines. Application of the framework to urokinase-type plasminogen activator receptor (uPAR) and glycoprotein nonmetastatic melanoma protein B (GPNMB) indicates that neither candidate currently meets all criteria, and the telomere axis remains untested for both. Given that multivalent vaccination elicits immunity against each component independently, combining candidates that fail individual criteria risks amplifying liabilities rather than ensuring intersectional specificity. This outcome would require an engineered AND-gated recognition system, where the capitalized operators AND, OR, and NOT denote Boolean logic gates rather than emphasis. The framework remains in the validation phase. Each criterion receives an ordinal grade, a non-compensatory decision rule, a route-specific ligand-density window that sets the quantitative condition for recognition and healthy-cell sparing, and a predefined seven-compartment counter-screening panel. Recognition architectures are formally compared, and a pre-registered benchmarking study with specified falsification criteria is outlined as the framework's validation test.

PubMedClinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis2026-11-10

Fibrinolytic Response to Protein C Zymogen and Plasma in Sepsis-Associated Purpura Fulminans: A Case Series of Nine Consecutive Patients.

Meli Andrea A, Marchesi Tiziana T, Silvestri Ivan I, Caccioppola Alessio A et al.

Purpura fulminans (PF) is a rare and life-threatening manifestation of disseminated intravascular coagulation, leading to multiorgan failure. Protein C (PC) zymogen supplementation has a strong pathophysiological rationale, but its effects on the viscoelastic fibrinolytic profile have not been described. We retrospectively analyzed nine patients (six adults, three children) admitted to our intensive care units between 2017 and 2025 with PF associated with septic shock, treated with PC zymogen concentrate and fresh frozen plasma (FFP). In the six adults, PC and fibrinolysis were measured before and a median of 13 hours after the PC loading dose, fibrinolysis with modified viscoelastic hemostatic assays (urokinase-modified thromboelastography [UK-TEG] in three, tissue plasminogen activator test [TPA-test, ClotPro] in three). Median (interquartile range) PC rose from 23 (10-31)% to 102 (63-137)% and Lysis, the percentage of clot lysis at the modified assays, from 15 (0-47)% to 78 (60-100)%. All six patients had fibrinolysis resistance before treatment. Lysis increased in five and returned within the reference interval in one; in the three TPA-test patients, lysis time became measurable after treatment but remained above 300 s. Three patients died and four required surgery for necrotic skin or soft tissue lesions. PC and FFP administration was followed by a partial recovery of the fibrinolytic response, which cannot be attributed to PC alone, since plasma was given at the same time. Modified viscoelastic assays may help monitor the response to PC and plasma therapy.

PubMedCell death and differentiation2026-11-08

DGKE acts as a negative regulator of podocyte migration and injury in glomerular diseases.

Zuo Fuwen F, Wang Mingwei M, Du Junyao J, Wang Xiaofeng X et al.

Podocyte injury is a major determinant of glomerular diseases. Although considerable advances have been made in the understanding of the mechanisms that trigger podocyte injury, effective cell-specific therapies remain clinically unavailable. In particular, recent studies have revealed that podocyte adhesion dysfunction and aberrant migration are pivotal events in the pathogenesis of podocyte loss and injury. Therefore, identifying candidate pathways for therapeutic intervention in podocyte migration has significant clinical importance. Here, we found that diacylglycerol kinase epsilon (DGKE) expression level is reduced in kidney biopsies from patients with glomerular diseases, which correlates with estimated glomerular filtration rate (eGFR). Moreover, urinary migrasome levels, a marker of migration, were significantly elevated in patients and negatively correlated with DGKE levels. Podocyte-specific overexpression of DGKE attenuated podocyte injury and proteinuria in three independent mouse models, adriamycin (ADR)-, puromycin aminonucleoside (PAN)- and streptozotocin plus high-fat diet (STZ/HFD)-induced nephropathy. Mechanistically, DGKE regulates podocyte migration through the urokinase plasminogen activator receptor (uPAR)/β3 integrin axis and its downstream Rac1/Cdc42 signaling cascades. Collectively, our findings provide new insights into the pivotal role of DGKE in maintaining podocyte function and suggest that DGKE may represent a potential therapeutic target for treating patients with glomerular diseases.

PubMedFrontiers in cardiovascular medicine2026-11-06

Correction: Urokinase redux: route, compartment, access, and pharmacological evolution from native urokinase to recombinant prourokinase.

Frontiers Production Office

[This corrects the article DOI: 10.3389/fcvm.2026.1904249.].

PubMedFrontiers in immunology2026-11-06

Soluble urokinase plasminogen activator receptor across the kidney-cardiometabolic continuum: a systematic review.

Wu Qishun Q, Yu Zhiliang Z, Lin Xin X, Yang Ling L et al.

Soluble urokinase plasminogen activator receptor (suPAR), a circulating marker of innate immune activation, has been proposed as a risk biomarker in chronic kidney disease (CKD) and related cardiometabolic conditions, but its clinical utility remains uncertain. We performed a systematic review according to PRISMA 2020 and the Synthesis Without Meta-analysis (SWiM) guideline, searching PubMed, Embase, Web of Science, Scopus, the Cochrane Library, medRxiv, ClinicalTrials.gov, and WHO ICTRP from inception to May 15, 2026. Two reviewers independently screened records, extracted data, and assessed quality using the Newcastle-Ottawa Scale, the JBI checklist, RoB 2, and QUADAS-2; certainty of evidence was rated with the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework. Twenty studies comprising 31,416 participants were included. In adults with preserved kidney function, elevated suPAR predicted incident CKD (adjusted odds ratio (OR) 3.13 for the highest versus lowest quartile, 95% confidence interval (CI) 2.11-4.65) and end-stage kidney disease (ESKD) (adjusted hazard ratio (HR) 1.53 for the highest versus lowest tertile, 95% CI 1.10-2.12), but the gain in discrimination was modest (absolute C-statistic increase 0.027-0.08) and no study performed decision curve analysis (DCA). suPAR did not distinguish focal segmental glomerulosclerosis (FSGS) from other glomerular diseases, and prognostic evidence in FSGS rested on a single moderate-quality study. In pediatric CKD and in metabolic cohorts, suPAR lost independent association after adjustment for baseline kidney function or inflammatory markers. Associations with cardiovascular outcomes were directionally consistent but observational and of low certainty. No study reported sex-stratified analyses. Routine clinical measurement of suPAR is not currently supported; assay harmonization, sex-disaggregated analyses, prospective validation with decision curve analysis, and trials of suPAR-targeted therapy are needed first. https://www.crd.york.ac.uk/PROSPERO/view/CRD420261320503, identifier CRD420261320503.

PubMedClinical journal of the American Society of Nephrology : CJASN2026-11-06

suPAR Is Associated with Progressive Albuminuria in Type 1 Diabetes: Findings from the PERL Trial.

Ismail Anis A, Vasbinder Alexi A, Farhat Theresa T, Bobby Bobby B et al.

Soluble urokinase plasminogen activator receptor (suPAR) is an immune-derived glycoprotein implicated in chronic kidney disease (CKD) and glomerulopathy. suPAR predicts CKD progression, but whether it is associated with longitudinal albuminuria worsening, including in patients without established albuminuria, is untested in diabetic kidney disease (DKD). We examined this in type 1 diabetes using albumin excretion rate (AER) trajectory. Post hoc analysis of 506 participants with a single baseline suPAR measurement from the PERL trial, a 3-year multicenter randomized controlled trial in type 1 diabetes with early-to-moderate DKD. Linear mixed models estimated suPAR's association with AER and iohexol-measured glomerular filtration rate (iGFR) trajectories. Structural equation modeling assessed whether albuminuria level accounted for the association between suPAR and iGFR decline. Mean age was 51 years, 34% female, diabetes duration 35 years, iGFR 68 mL/min/1.73 m2, median AER 44 μg/min, and median suPAR 3.43 ng/mL. Each suPAR doubling was associated with 11.6% per year additional AER increase (P<0.001), with a dose-response across quartiles and robust to sensitivity analyses. Time-lagged analysis confirmed the association with subsequent AER worsening (P=0.004). Among 125 eGFR-decline qualifiers (predominantly normoalbuminuric), higher suPAR was associated with accelerated AER worsening (+13.1%/yr per doubling, P=0.005; +11.7%/yr in the 101 normoalbuminuric), although none crossed the proteinuria threshold. suPAR was also associated with AER category progression (HR 1.61, P=0.002) and ≥40% eGFR loss (HR 1.86, P=0.01). suPAR was not independently associated with GFR slope (total effect P=0.49); its association with lower GFR was accounted for by albuminuria level (indirect effect -0.59 mL/min/yr per doubling, P<0.001). suPAR was independently associated with progressive albuminuria worsening in type 1 diabetes with DKD, including accelerated worsening among normoalbuminuric patients. These associations are consistent with suPAR marking active podocyte injury and support its evaluation for early risk stratification.

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