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

PubMedEuropean journal of obstetrics & gynecology and reproductive biology: X2026-08-04

Cord blood procalcitonin and soluble urokinase-type plasminogen activator receptor in predicting histological chorioamnionitis - A pilot study.

Jalkanen Kati K, Tammela Outi O, Virtanen Anita A, Aittoniemi Janne J et al.

Chorioamnionitis, caused by microbial invasion of amniotic cavity or sterile inflammation, can lead to prematurity and cytokine storm of fetus known as fetal inflammatory response syndrome (FIRS). Histological chorioamnionitis (HCA) on fetal side of placenta is a surrogate to FIRS. Cord blood (CB) reflects intrauterine inflammation. Our aim was to evaluate if more novel biomarkers procalcitonin (PCT) and soluble urokinase- type Plasminogen Activator Receptor (suPAR) were useful for identifying fetuses/neonates with high risk for FIRS/HCA. Twenty two women with a clinically confirmed preterm premature rupture of membranes (PPROM) or a suspicion of chorioamnionitis without PPROM (uterine tenderness, maternal fever ≥38°C, leukocytosis, fetal tachycardia ≥160 beats/minute) were enrolled at gestational weeks 23+0-34+6. Interleukin-6 (IL-6), PCT and suPAR were measured in cord blood samples obtained immediately after birth. The fetal side HCA was used as a surrogate for FIRS. The cord blood concentration of IL-6 was significantly higher (p = 0.01) and had the best predictability for fetal side HCA (AUC 0.96, p = 0.03). Cord blood concentrations of PCT tended to be higher (p = 0.05), and to show significance for predicting fetal-side HCA (AUC 0.91, p = 0.07). No significant findings were found for suPAR. Cord blood IL-6 had the best ability to predict fetal side HCA. Cord blood PCT may be a promising biomarker. There were no significant findings for cord blood suPAR, suggesting its limited value as a biomarker in this context.

PMID 42549044
阅读全文 →
PubMedBMC cardiovascular disorders2026-08-04

Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair.

Schlegl Johannes J, Bannehr Marwin M, Lichtenauer Michael M, Kücken Tanja T et al.

Risk stratification after transcatheter tricuspid edge-to-edge repair (T-TEER) remains challenging, particularly in patients with advanced right-sided heart failure and systemic disease burden. Biomarkers reflecting inflammation, stress response and multiorgan dysfunction may provide additional prognostic information in this setting. This prospective single-centre cohort study included 84 consecutive patients undergoing T-TEER for severe tricuspid regurgitation using the TriClip or PASCAL system. Baseline concentrations of growth differentiation factor-15 (GDF-15), soluble urokinase plasminogen activator receptor (suPAR), and NT-proBNP were measured prior to intervention. The primary endpoint was all-cause mortality at 12 months. Secondary endpoints included cardiovascular rehospitalisation and a combined cardiovascular endpoint. Prognostic performance was assessed using receiver operating characteristic and tertile-based Kaplan-Meier analyses. Owing to the limited number of events, all analyses were considered exploratory. During 12-month follow-up, all-cause mortality occurred in 10 patients (11.9%), while cardiovascular rehospitalisation was observed in 29 patients (34.5%). GDF-15 demonstrated good discriminative performance for all-cause mortality (AUC 0.823, 95% CI 0.714-0.932, p = 0.001), whereas suPAR showed moderate prognostic discrimination (AUC 0.742, 95% CI 0.605-0.878, p = 0.013). In contrast, NT-proBNP showed no significant discrimination for all-cause mortality (AUC 0.535, 95% CI 0.362-0.709, p = 0.720). Higher tertiles of both GDF-15 and suPAR were associated with reduced overall and rehospitalisation-free survival. Baseline GDF-15 and suPAR were associated with adverse outcomes after T-TEER and demonstrated greater prognostic discrimination than NT-proBNP in this exploratory cohort. These exploratory findings support further investigation of systemic stress and inflammation biomarkers for risk stratification in patients with severe tricuspid regurgitation.

PMID 42547888
阅读全文 →
PubMedHeart rhythm2026-08-01

Protein Mediators Linking Autoimmune Diseases and Incident Atrial Fibrillation: Insights from the UK Biobank.

Huang Jingwen J, Liu Chang C, Merchant Faisal M FM, Alonso Alvaro A et al.

Emerging evidence suggests autoimmune diseases (AIDs) are associated with atrial fibrillation (AF) through systemic inflammation. However, causal mechanisms and potential protein mediators remain unexplored. To identify proteins mediating the link between AIDs and incident AF using high-dimensional mediation analysis. This study used UK Biobank data with proteomic profiling (Olink platform). Participants without prevalent AF were grouped into musculoskeletal (MSK), vasculitis, gastrointestinal (GI), neurologic, and rheumatic fever subsets. Fine-Gray models identified AID-AF associations, treating non-cardiovascular death as a competing risk. Two separate Proteome-wide association studies (PWAS) identified proteins linked to AIDs and incident AF, respectively. All models adjusted for age, sex, lipids, BMI, smoking, hypertension, diabetes, coronary artery disease, peripheral vascular disease, stroke, and heart failure. Proteins associated with both AIDs and AF were selected for high-dimensional mediation analysis (HIMA). Among 419,888 participants (median age 58 years, 45.7% male) followed for a median 14.4 years, MSK, vasculitis, GI, and rheumatic fever AIDs significantly increased incident AF risk (HR 1.17, 1.39, 1.17, and 1.46, respectively; P<0.001), but not neurologic AID (P=0.13). In 44,872 participants with proteomic data, HIMA of 232 proteins identified 60 unique mediators, with adrenomedullin, soluble urokinase plasminogen activator receptor, and insulin-like growth factor binding protein 2 shared across multiple AID groups. The identification of protein biomarkers that may help elucidate potential pathways between AID and AF provides mechanistic insights into immune-related atrial remodeling and suggests possible therapeutic targets for AF prevention and risk stratification in AID patients.

PMID 42537973
阅读全文 →
PubMedJournal of Cancer2026-07-29

Long-Term Empagliflozin Treatment (50 Days) Attenuates Protease Activity, Migration, and Stemness-Associated Phenotypes in BFTC-909 Renal Pelvis Transitional Cell Carcinoma Cells.

Lee Yi-Hsun YH, Chen Pei-Ni PN, Hsieh Yi-Hsien YH, Chu Yi-Cheng YC et al.

Empagliflozin is a sodium-glucose cotransporter 2 inhibitor widely prescribed for the treatment of type 2 diabetes mellitus. It promotes urinary glucose excretion by inhibiting renal glucose reabsorption. Although empagliflozin has been widely used in clinical practice, its effects and underlying mechanisms related to metastasis, cytokine secretion, and stemness-associated phenotypes in renal pelvis transitional cell carcinoma (TCC) remain poorly understood. In this study, we investigated the long-term (50 days) effects of empagliflozin (5 μM) on BFTC-909 human renal pelvis TCC cells. Prolonged empagliflozin treatment suppressed the migration of tumor cells and the proteolytic activities of matrix metalloproteinase-2 and urokinase-type plasminogen activator. In addition, empagliflozin markedly reduced the viability and self-renewal capacity of BFTC-909 cells. Analysis of conditioned media revealed that long-term empagliflozin exposure significantly reduced the secretion of interleukin-1Ra, interleukin-8, granulocyte colony-stimulating factor, and vascular endothelial growth factor. Together, these findings suggest that empagliflozin suppresses the protease activity, tumor invasiveness, and stemness-associated phenotypes of renal pelvis TCC cells. Overall, this study indicates that long-term empagliflozin treatment reduces the metastatic potential of BFTC-909 renal pelvis TCC cells and highlights the need for additional in vivo and clinical investigations.

PMID 42524255
阅读全文 →
PubMedFrontiers in pharmacology2026-07-28

Sodium bicarbonate combined with urokinase for the prevention and management of hemodialysis central venous catheter dysfunction.

Lin Lin L, Hu Lin-Jie LJ, Geng Jia-Fei JF, Zhang Ying Y et al.

Central venous catheter (CVC) dysfunction remains a common problem in maintenance hemodialysis and may impair prescribed blood flow and dialysis adequacy. This study aimed to evaluate whether a sodium bicarbonate-urokinase lock within a standardized dwell-and-aspiration protocol was associated with improved catheter patency and safety outcomes compared with a saline-urokinase lock. This retrospective study included 220 clinically stable adults undergoing maintenance hemodialysis with an indwelling CVC between December 2023 and March 2024. Patients were grouped according to the predefined catheter-locking schedule used in routine practice: sodium bicarbonate plus urokinase group (n = 115) and 0.9% sodium chloride plus urokinase group (n = 105). Urokinase was prepared at 10,000 U/mL, instilled at 1.1-1.2 times the catheter lumen volume, dwelled for 30 min, and followed by standardized negative-pressure aspiration. Outcomes included catheter dysfunction, event rates, dialysis performance, procedural response, recurrence, catheter exchange, and safety events. Multivariable logistic regression was used to adjust for clinically relevant covariates. Catheter dysfunction occurred in 20.9% of patients in the sodium bicarbonate-urokinase group and 34.3% in the saline-urokinase group (P = 0.026). Dysfunction event rates were 4.35 versus 8.30 per 1,000 catheter-days, respectively (incidence rate ratio = 0.52, P = 0.002). After covariate adjustment, the sodium bicarbonate-urokinase regimen was associated with lower odds of dysfunction (adjusted odds ratio = 0.49, 95% confidence interval: 0.26-0.90; P = 0.024). Single-procedure patency restoration was more frequent (85.7% vs. 65.6%; P = 0.033), while repeat intervention and catheter exchange/reinsertion were less frequent. Bleeding events and laboratory safety indicators were comparable. Catheter-related bloodstream infection was infrequent but observed less often in the sodium bicarbonate-urokinase group (0.9% vs. 6.7%; P = 0.029). Sodium bicarbonate combined with urokinase within a standardized dwell-and-aspiration protocol may be associated with lower observed rates of CVC dysfunction, fewer dysfunction-related events, a higher observed rate of single-procedure patency restoration, and a comparable safety profile. Infection-related findings should be interpreted cautiously because of the small number of events and should be considered hypothesis-generating.

PMID 42518352
阅读全文 →
PubMedBrain communications2026-07-28

Identification of a robust multitarget protein panel for Parkinson's disease via absolute quantification and large-scale external replication.

Lee Ho-Won HW, Choi Youngtae Y, Lee Shinrye S, Kim Jung-Eun JE et al.

This study aimed to identify and validate a robust, generalizable panel of plasma protein biomarkers to improve diagnostic precision in Parkinson's disease. We analysed plasma samples from 12 patients with [18F]-FP-CIT PET-confirmed Parkinson's disease and 15 healthy controls using the Olink Target 96 Inflammation Panel to identify differentially expressed proteins. Candidate biomarkers were subsequently validated through absolute quantification using Luminex and Olink Flex platforms in an independent cohort of 46 patients with Parkinson's disease and 33 amyloid-negative and cognitively normal control participants. To assess generalizability, the findings were replicated across multiple heterogeneous populations using large-scale datasets from the UK Biobank and Global Neurodegeneration Proteomics Consortium (GNPC) cohorts. Markers of neurodegeneration [neurofilament light chain (NfL)] and Alzheimer's disease [phosphorylated tau (pTau181), amyloid β [Aβ]42, Aβ40] co-pathology were measured using the single molecule array platform. Our analyses revealed elevated levels of interleukin (IL)-10 and IL-17C and reduced levels of urokinase plasminogen activator (uPA) and neurotrophin-3 (NTF3) in patients with Parkinson's disease. These findings were confirmed in the validation cohort. Multitarget models demonstrated superior diagnostic performance over individual markers, with the combination of IL-17C and uPA achieving the highest discrimination (area under the curve = 0.780). External validation in the UK Biobank and GNPC datasets confirmed consistent directional changes of three candidates (IL-17C, NTF3 and uPA), reinforcing the biological relevance of these markers. Notably, while NfL levels were significantly elevated in Parkinson's disease, no significant differences were observed for pTau181 levels or Aβ42/Aβ40 ratios. These findings identify a specific plasma protein panel, particularly the combination of IL-17C and uPA, as a robust and generalizable diagnostic signature that captures fundamental pathophysiological aspects of Parkinson's disease and enhances diagnostic precision alongside established biomarkers.

PMID 42516760
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