北京若生智能科技有限公司
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TH

thrombin (ThrombiRAAS)

✓ Approved

Shanghai RAAS Blood Products Co., Ltd. · F2 · 细胞治疗

什么是 thrombin？

thrombin 是一种细胞治疗，由Shanghai RAAS Blood Products Co., Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名ThrombiRAAS
公司Shanghai RAAS Blood Products Co., Ltd.
药物类别细胞治疗
分子靶点F2
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Shanghai RAAS Blood Products Co., Ltd.

作用机制

分子靶点

thrombin 作用于 1 个分子靶点：

F2coagulation factor II, thrombin (THPH1, PT)
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

thrombin 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersExtravasation blood✓ Approved
Vascular disordersHaemorrhage✓ Approved

相关研究文献

PubMedRenal failure2026-09-10

Kidney injury associated with direct oral anticoagulants: a comparative study of direct thrombin inhibitors and factor Xa inhibitors based on literature and database analysis.

Chen Songhua S, Shi Can C, Li Xiang X, Wang Xia X et al.

While direct oral anticoagulants (DOACs) are widely used, limited real-world studies have explored kidney injury linked to DOACs, particularly differences between direct thrombin inhibitors (DTIs) and factor Xa inhibitors (FXaIs). We conducted a comprehensive analysis of kidney injury cases from the FDA Adverse Event Reporting System (FAERS, 2008-2024) and systematically reviewed published case reports, comparing DTIs (dabigatran) with FXaIs (rivaroxaban, apixaban, edoxaban). Among 8,116 reports of suspected DOAC-associated kidney injury, 1,784 were linked to DTIs and 6,332 to FXaIs. Significant reporting rates were observed for DTIs [reporting odds ratio (ROR) = 2.081, 95% CI: 1.979-2.189; proportional reporting ratio (PRR) = 2.044, CI: 1.947-2.147)] and FXaIs (ROR = 1.483, 95% CI: 1.444-1.523; PRR = 1.472, CI: 1.434-1.510). Notably, substantial intra-class variation existed among FXaIs, with edoxaban showing the highest risk signal (ROR = 4.453, 95% CI: 4.021-4.932; PRR = 4.212, 95% CI: 3.831-4.632). Multivariable logistic regression analysis confirmed that significantly lower kidney injury reporting disproportionality signals with FXaIs versus DTIs after adjustment (ROR = 0.687, 95% CI: 0.650-0.727, P < 0.001). Analysis of 32 detailed cases revealed distinct clinical patterns: DTI-associated injury featured higher proteinuria rates (P = 0.029), while FXaI-associated injury occurred more frequently in settings of polypharmacy (P = 0.006) and was associated with poorer renal recovery (P = 0.023). This study demonstrates distinct kidney injury risks among DOAC classes and individual agents, with DTIs and edoxaban showing particularly strong signals. These findings emphasize the need for individualized DOAC selection and enhanced renal monitoring in clinical practice.

PMID 42717832
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PubMedFrontiers in neurology2026-09-10

Stimuli-responsive nanozyme-hydrogel systems for ischemic stroke: toward spatiotemporal catalytic control of the neurovascular unit.

Yan Sen S, Wang Xiaohong X, Li Cai C, Wang Rong R

The development of ischemic stroke involves swiftly changing and spatially varied states, including oxidative burst, acidosis, hypoxia, endothelial dysfunction, blood-brain barrier disruption, neuroinflammation, and later tissue remodeling. This temporal structure is poorly matched by conventional single-dose neuroprotectants. Nanozyme-hydrogel systems that respond to stimuli provide a promising approach by integrating catalytic redox control with localized retention, lesion-adaptive mechanics, and release triggered by specific cues. This Mini Review critically examines the design logic of such systems for ischemic stroke. Initially, we categorize reactive oxygen and nitrogen species, low pH, hypoxia, thrombin, matrix metalloproteinases, and inflammatory signals as a pathological code for activating materials. Following this, we examine nanozyme catalytic modules, responsive hydrogel matrices, and integration approaches including encapsulation, anchoring, in situ assembly, and multi-input gating. Emphasis is on the phase-aligned management of the neurovascular unit, covering early reperfusion defense, endothelial stabilization, glial adjustment, angiogenesis, and neural reconfiguration. A key takeaway is that there is limited direct evidence of fully integrated nanozyme-hydrogel platforms specifically for stroke; the field largely relies on the intersection of advanced stroke nanozymes and responsive hydrogels. Consequently, we recommend translational benchmarks that emphasize phase-route alignment, exact catalytic activity, degradation tracking, production feasibility, and validation in various preclinical settings. Accordingly, this Mini Review is intended as a design framework for hypothesis generation and preclinical validation, rather than as evidence of clinical readiness.

PMID 42719665
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PubMedTH open : companion journal to thrombosis and haemostasis2026-09-09

Beyond Rebalanced Haemostasis: Haemostatic Phenotypes, Thrombin Generation, and Clinical Risk in Chronic Liver Disease.

Agouba Sohaib Mukhtar SM, Bradacova Pavla P, Mikler Jan J, Drotarova Miroslava M et al.

Advanced chronic liver disease (ACLD) profoundly remodels haemostasis through concurrent reductions in procoagulant factors and natural anticoagulants, qualitative platelet abnormalities, elevated von Willebrand factor and factor VIII, and dynamic alterations in fibrinolysis. Although rebalanced haemostasis has transformed understanding of coagulation in cirrhosis, accumulating evidence indicates that haemostatic balance varies according to disease aetiology, fibrosis severity, and clinical stage. This review advances a phenotypic framework for haemostasis in chronic liver disease and explores its implications for risk stratification and antithrombotic management. Three developments support this framework. First, thrombomodulin-modified thrombin generation assays identify distinct haemostatic phenotypes across the disease spectrum, distinguishing the hypercoagulable profile of compensated cirrhosis from hypocoagulable states observed in acute-on-chronic liver failure, whereas metabolic dysfunction-associated steatotic liver disease emerges as a particularly prothrombotic phenotype. Second, recent studies link liver stiffness measurement with thrombin-generation parameters, suggesting convergence between structural liver injury and functional haemostatic assessment. Third, complementary evaluation of fibrin structure, fibrinolysis, plasmin generation, and viscoelastic clot mechanics provides information beyond thrombin kinetics alone, despite important analytical limitations. The review applies this framework to clinically relevant complications, including bleeding, venous thromboembolism, atrial fibrillation, and portal vein thrombosis (PVT). Recent histopathological and clinical evidence challenges the traditional concept of cirrhotic PVT as a manifestation of systemic hypercoagulability and instead supports a predominantly vascular pathogenesis driven by portal-flow abnormalities, endothelial dysfunction, and intimal remodelling. Collectively, these findings support a transition from rebalanced haemostasis towards precision haemostatic phenotyping in ACLD.

PMID 42713243
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PubMedShock (Augusta, Ga.)2026-09-09

Early antithrombin depletion after trauma is associated with biomarkers of endotheliopathy and systemic protein loss: a retrospective observational study.

Matsumoto Hironori H, Kan Akihito A, Takezawa Mitsuaki M, Tanabe Tsunenori T et al.

Early antithrombin (AT) depletion after trauma may result from thrombin-related consumption, vascular leakage, and systemic protein loss. We examined the biomarker profile associated with early AT depletion and whether reduced AT activity identifies an adverse early injury phenotype. In this single-center retrospective observational study, 100 adult trauma patients were analyzed on admission. AT activity, albumin (Alb), syndecan-1 (SDC-1), and thrombin-antithrombin complex (TAT) were measured in residual blood samples obtained at hospital arrival. Associations among biomarkers were assessed using locally estimated scatterplot smoothing and generalized additive models. LASSO and elastic-net regression identified variables associated with AT activity, and exploratory Bayesian regression assessed directional associations. Clinical outcomes were compared between patients with reduced (<80%) and preserved (≥80%) AT activity. Reduced AT activity was present in 32% of patients and remained associated with shock (adjusted OR 9.42, 95% CI 1.32-109.00, p=0.037) and disseminated intravascular coagulation (DIC) (adjusted OR 12.20, 95% CI 2.17-113.00, p=0.010) after adjustment for age, sex, ISS, and lactate. AT activity was positively associated with Alb and negatively associated with SDC-1 and TAT. In regularized regression, Alb and SDC-1 were more consistently associated with AT activity, whereas TAT was not selected. Bayesian analyses showed stronger directional evidence for Alb and SDC-1 than for TAT. Early AT depletion after trauma was associated with adverse clinical features and biomarker patterns consistent with endothelial injury and circulating protein depletion, beyond thrombin-related consumption alone.

PMID 42713784
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PubMedHaemophilia : the official journal of the World Federation of Hemophilia2026-09-09

Plasma-Derived Factor VIIa/Factor X Improves Thrombin Generation Potential in a Plasma Model of Haemophilia A Supplemented With Direct Oral Anticoagulants.

Oh Shigeharu S, Nakajima Yuto Y, Onishi Tomoko T, Takami Eisuke E et al.

Patients with haemophilia (PwH) complicated with atrial fibrillation require direct oral anticoagulants (DOACs) to prevent thrombosis, but still require haemostatic management to control bleeding. However, specific recommendations for managing bleeding in PwH with inhibitors (PwH-inh) receiving DOACs remain lacking. In Japan, plasma-derived (pd-) factor (F)VIIa/FX products are available for clinical management of PwH-inh, and may also be beneficial for haemostatic treatment in PwH-inh receiving DOACs. To assess coagulation potential of pd-FVIIa/FX or other bypassing agents (BPAs) using an in vitro plasma model of PwHA-inh receiving DOACs. FVIII-deficient plasma was preincubated with anti-FVIII inhibitor (termed 'FVIII-depleted'). Pd-FVIIa/FX (1.5 µg/mL as FVIIa), recombinant (r)FVIIa (2.2 µg/mL), activated prothrombin complex concentrates (aPCC; 1.3 IU/mL), or FX preparation (520 nM) were added to FVIII-depleted plasmas supplemented with apixaban (100 ng/mL) or edoxaban (100 ng/mL). A similar model was prepared using plasma samples spiked with emicizumab (50 µg/mL). Coagulation potential was assessed utilizing thrombin generation assay (TGA). The addition of pd-FVIIa/FX to FVIII-depleted plasmas supplemented with DOACs increased TG potential to near-normal range, irrespective of the presence of emicizumab. However, the addition of rFVIIa or FX alone to the FVIII-depleted plasma with DOACs exhibited coagulation potential below the normal range. The addition of aPCC and emicizumab to FVIII-depleted plasmas with DOACs enhanced TG potential above the normal range. Pd-FVIIa/FX improved coagulation potential in the in vitro model plasma of PwHA-inh spiked with DOACs, irrespective of concomitant emicizumab. The clinical efficacy and safety of pd-FVIIa/FX require further evaluation.

PMID 42711667
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PubMedTH open : companion journal to thrombosis and haemostasis2026-09-09

A Novel Complete F8 Tandem Duplication Causing Elevated Factor VIII Activity and Associated with Venous Thromboembolism.

Mao Yinqi Y, Lu Yeling Y, Wu Wenman W, Ding Qiulan Q et al.

Background Coagulation factor VIII (FVIII) is a critical component of the intrinsic coagulation pathway. While elevated FVIII levels are an established risk factor for venous thromboembolism (VTE), genetic variants in the F8 gene directly causing such elevations remain scarce. Here, we report a novel complete F8 tandem duplication identified in a female patient with splanchnic venous thrombosis (SVT). Methods We performed genetic testing using a thrombophilia panel targeting 35 genes involved in thrombosis and haemostasis to detect both point variants and copy number variations (CNVs). Family co-segregation analysis and phenotypic assays for FVIII and von Willebrand factor (VWF) were conducted. The structural basis of the identified F8 copy number gain was elucidated using optical genome mapping (OGM). Full-length F8 mRNA amplification, quantitative PCR, plasma FVIII Western blotting, and X-chromosome inactivation analysis were performed to assess the functional consequences of the duplication. Thrombin generation test (TGT) was employed to assess the hypercoagulable state. Results Genetic testing identified three copies of all 26 exons of the F8 gene in the proband, which was also detected in her mother (CNVs = 3) and son (CNVs = 2). One-stage clotting and chromogenic assays confirmed persistently elevated FVIII activity in the proband and her mother, accompanied by increased FVIII antigen levels. The OGM analysis confirmed a 229 kb tandem duplication including the F8 gene on one of the proband's X chromosomes. The junction regions exhibited high sequence homology and were rich in repetitive sequences, which precluded precise breakpoint mapping. Full-length F8 mRNA amplification revealed no aberrant transcripts, whereas quantitative PCR showed increased F8 mRNA expression in all carriers. Plasma FVIII Western blotting indicated FVIII heavy and light chains of expected molecular weights with increased band intensity in carriers. X-chromosome inactivation analysis in female carriers showed no significant skewing. TGT in two available carriers showed increased thrombin generation compared with a normal control at both low (1 pM) and high (5 pM) tissue factor concentrations. Conclusion We identified a novel complete F8 tandem duplication associated with increased FVIII expression and a hypercoagulable phenotype in a female patient with SVT. These findings support F8 gene dosage gain as a rare gain-of-function mechanism contributing to elevated FVIII levels and thrombophilia, while variation in VWF levels and acquired risk factors may modify thrombotic penetrance.

PMID 42712804
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