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thrombin (ThrombiRAAS)

✓ Approved

Shanghai RAAS Blood Products Co., Ltd. · F2 · Cell-based Therapies

What is thrombin?

thrombin is a cell-based therapies developed by Shanghai RAAS Blood Products Co., Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesThrombiRAAS
CompanyShanghai RAAS Blood Products Co., Ltd.
Drug ClassCell-based Therapies
Molecular TargetF2
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Shanghai RAAS Blood Products Co., Ltd.

Mechanism of Action

Molecular Targets

thrombin acts on 1 molecular target:

F2coagulation factor II, thrombin (THPH1, PT)
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Therapeutic Indications

thrombin is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersExtravasation blood✓ Approved
Vascular disordersHaemorrhage✓ Approved

Related Research Articles

PubMedSeminars in thrombosis and hemostasis2026-09-18

Age-related Global Coagulation Changes: From Neonate to Old Age.

Lu Vincent V, Attard Chantal C, Karlaftis Vasiliki V, Cai Tengyi T et al.

Global coagulation assays provide a comprehensive assessment of clotting and fibrinolytic dynamics and have shown potential in predicting bleeding and thrombotic risk. Successful clinical implementation, however, requires understanding of normal age-specific changes, which remains limited. This study aims to evaluate age- and sex-related differences in global coagulation assays from neonates to older adults. A total of 546 citrated plasma samples from 380 healthy pediatric participants (0 to < 18 years) and 166 adults (20-79 years, without known cardiovascular risk factors or medications affecting coagulation) were tested for thrombin generation (CAT-TG), modified overall hemostatic potential (mOHP), and plasmin generation (PG). This study demonstrated that hemostatic capacity was lowest at birth and increased rapidly throughout early childhood, with endogenous thrombin and plasmin potentials peaking in the fourth decade of life. Fibrin generation continued to rise, peaking in the sixth decade, accompanied by a decline in fibrinolytic capacity. Sex differences showed a hypercoagulable shift in females beginning at puberty, peaking during the reproductive years. These sex differences attenuated post-menopause, reflecting the convergence of cardiovascular risk in older age. These findings provide essential normative data to support age- and sex-adjusted interpretation of global coagulation assays. Overall, the most pronounced hemostatic changes occur in early life, consistent with developmental hemostasis. The midlife peak in procoagulant parameters and the decline in fibrinolytic capacity highlight progressive hemostatic changes associated with aging. While sex-related differences underscore the role of endogenous hormones in modulating coagulation, longitudinal studies in healthy and at-risk individuals are warranted to clarify trajectories and inform personalized interventions.

PMID 42759551
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PubMedBirth defects research2026-09-18

Compound Heterozygous Mutations in FGA Cause Congenital Afibrinogenemia: A Case Report and Literature Review.

Liu Liangliang L, Yuan Desheng D, Zhao Huaxing H, Yu Bacui B

Congenital afibrinogenemia is an extremely rare autosomal recessive bleeding disorder with an estimated incidence of one in one million, caused by mutations in the fibrinogen-encoding genes. We report a genetically confirmed case of FGA-related congenital afibrinogenemia in a 9-year-old female child. Comprehensive coagulation analysis revealed undetectable fibrinogen activity (FIB:C, < 0.2 g/L) as measured by the Clauss assay, along with significantly prolonged prothrombin time, activated partial thromboplastin time, and thrombin time. Next-generation sequencing targeting coagulation-related genes identified compound heterozygous mutations in FGA (NM_000508): a paternal nonsense mutation c.502C>T (p.Arg168Ter) in Exon 4 and a maternal frameshift mutation c.668delT (p.Leu223ArgfsX2) in Exon 5. These pathogenic variants were further confirmed by Sanger sequencing in the proband and her parents, which demonstrated that the proband carried the two FGA variants in a compound heterozygous state, with paternal inheritance of c.502C>T and maternal inheritance of c.668delT. This case expands the genotype-phenotype correlation database for fibrinogen disorders and underscores the necessity of molecular diagnosis for congenital coagulation defects.

PMID 42757861
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PubMedResearch and practice in thrombosis and haemostasis2026-09-18

Subcutaneous MG1113 in severe hemophilia A and B: phase 1b study for safety, pharmacokinetics, and pharmacodynamics.

You Chur-Woo CW, Baek Hee Jo HJ, Park Young-Shil YS, Kim Bo Ram BR et al.

MG1113 is an immunoglobulin G4 monoclonal antibody targeting the Kunitz-2 domain of tissue factor pathway inhibitor (TFPI), developed as a hemostatic rebalancing agent for patients with hemophilia A or B. We aimed to investigate the safety, pharmacokinetics (PK), pharmacodynamics, and preliminary hemostatic effects of MG1113. This phase 1b clinical trial was conducted in a multicenter, prospective, stepwise dose-escalating (2.0, 3.0, and 3.3 mg/kg) design. MG1113 was administered subcutaneously once weekly for 8 weeks. Fifteen male patients (n = 5/cohort) diagnosed with severe hemophilia A (n = 14) or B (n = 1) without inhibitors were enrolled. MG1113 was well tolerated, with an adverse event (AE) rate of 40.0% (6/15). No serious AEs, early withdrawals, or dose interruptions occurred. PK analysis demonstrated a nonlinear profile, with the peak plasma concentration at 33 to 48 hours post dose. Free TFPI and diluted prothrombin time (PT) decreased from baseline, while thrombin generation markers increased. Exploratory analysis showed a notable numerical reduction in annualized total bleeding rates at higher doses: 91.7% at 3.0 mg/kg and 76.2% at 3.3 mg/kg. The zero bleeding rate was 20.0%, 60.0%, and 40.0% at doses of 2.0, 3.0, and 3.3 mg/kg, respectively. MG1113, administered subcutaneously as a prophylaxis in patients with severe hemophilia A or B without inhibitors for 8 weeks, demonstrated an acceptable safety profile with a PK profile suitable for once-a-week dosing. The pharmacodynamics marker changes were consistent with TFPI inhibition, which was associated with reductions in bleeding events. This trial was prospectively registered at www.ClinicalTrials.gov (#NCT05493631).

PMID 42757060
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PubMedAnnali italiani di chirurgia2026-09-18

A Nomogram Model Based on Preoperative Coagulation-Fibrinolysis Biomarkers for Predicting Postoperative Hemorrhage After Pancreaticoduodenectomy: A Retrospective Study With Internal Validation.

Hu Yiling Y, Shen Weifeng W, Tang Dongmei D, Zhou Hui H

Post-pancreaticoduodenectomy hemorrhage (PPH) remains a life-threatening complication. However, conventional coagulation assays fail to capture the dynamic hemostatic disturbances preceding overt bleeding. This study aimed to evaluate whether preoperative coagulation-fibrinolysis biomarkers could improve PPH risk stratification and support the development of an interpretable predictive model. We retrospectively analyzed 315 adults who underwent elective pancreaticoduodenectomy, randomly allocated to a training cohort (n = 220) and an internal validation cohort (n = 95). Preoperative variables included routine coagulation indices and molecular markers, including thrombin-antithrombin complex (TAT), plasmin-α2-plasmin inhibitor complex (PIC), and D-dimer. Multivariable logistic regression was used to identify independent predictors and construct a predictive nomogram. Model performance was assessed in terms of discrimination (area under the curve [AUC]), calibration (Brier score and Hosmer-Lemeshow goodness-of-fit test), and decision curve analysis (DCA). In the training cohort, patients who developed PPH exhibited significantly higher levels of TAT, PIC, and D-dimer, and lower fibrinogen (FIB). Multivariable analysis identified four independent predictors: FIB (odds ratio (OR) = 0.46), PIC (OR = 1.79), D-dimer (OR = 1.59), and TAT (OR = 1.15). The nomogram demonstrated good discrimination, with an AUC of 0.81 in the training cohort and 0.75 in the validation cohort. Calibration performance was acceptable, with Brier scores of 0.11 (training) and 0.15 (validation). Although the Hosmer-Lemeshow test indicated no statistically significant lack of fit (p > 0.05 in both cohorts), visual inspection of the validation calibration curve suggested moderate deviations in the intermediate-risk range, likely reflecting the limited sample size. Shapley Additive exPlanations‌ (SHAP) analysis identified PIC as the most influential predictor in the model output. Preoperative coagulation-fibrinolysis "process markers" may provide additional information for assessing PPH risk. The four-marker nomogram (PIC, TAT, D-dimer, and FIB) offers an interpretable framework for perioperative risk stratification and demonstrates satisfactory overall performance. However, external validation in larger, independent cohorts is warranted to confirm model generalizability and calibration stability.

PMID 42755305
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PubMedFrontiers in cardiovascular medicine2026-09-18

A refined phenomenological model of viscoelastic clot formation and lysis in trauma-induced coagulopathy.

Liu Guanyun G, Shick Amanda E AE, Shamash Maya M, Cook Caroline M CM et al.

Hyperfibrinolysis is strongly associated with early post-injury mortality, but the condition is preventable with timely detection and targeted interventions. Unfortunately, current hyperfibrinolysis diagnostic assays such as thromboelastography (TEG) are time-consuming, making them infeasible for use in real-time treatment strategies to guide adjustable, precise, and personalized interventions. Computational models offer a fast alternative to current practice for ascertaining patient hemostatic state from quickly-measurable protein concentrations. However, few models exist to predict clot strength. Our prior biologically-interpretable, phenomenological, dynamical system TEG model does not often satisfactorily capture hyperfibrinolysis because this feature was missing from training data. Here, we present model improvements that are experimentally-driven and theoretically-grounded to better facilitate the replacement of slow patient viscoelastic clotting measurements, with and without hyperfibrinolysis, by rapid and accurate predictions of TEG parameters in silico. We created a tPATXA dataset to enable model refinements, and we validated TEG parameter predictions using the published Activation of Coagulation and Inflammation in Trauma (ACIT) dataset, which was excluded from model training. Our tPATXA dataset consists of 310 citrated native (CN) TEG assay profiles that were generated from healthy human donor whole blood samples spiked with tissue plasminogen activator (tPA) and tranexamic acid (TXA) at varying concentrations to provide added phenomenological information about fibrinolysis behavior. We then used ACIT clinical data from 93 trauma patients containing 254 citrated kaolin (CK) and 122 citrated kaolin with heparinase (CKH) TEG assays for model validation. We characterized model performance by: the coefficient of determination R 2 ; percent-error predictions of TEG parameters R-time, K-time, alpha angle, maximum amplitude, and time to maximum amplitude; and absolute errors of TEG parameters Ly30 and Ly60. Our key model update is to make a previously-constant parameter a time-varying function. Our updated model substantially outperforms the prior model in both datasets. On the tPATXA dataset that both models were trained on and then subsequently predicted to verify competency, the model updates improved R 2 from 0.9726 to 0.9983. On the ACIT validation dataset that was not used for training, the model updates improved R 2 from 0.9848 to 0.9993, and reduced TEG parameter prediction variance by over 99%. In addition, the updated model had low prediction errors of 1%-13% for R-time, K-time, alpha angle, maximum amplitude, and time to maximum amplitude, and 0.7%-2.2% for Ly30 and Ly60. A mechanistic interpretation of the new parameter is its capture of the formation and breakdown of a fibrin clot mesh over time. Our refined model offers higher accuracy, consistency, and biological interpretability than previously available. Our updated model's modular design supports future integration with literature phenomenological models that predict thrombin dynamics, as well as with externally-added controllers for automation. Thus, this work captures broad clinical coagulation insights and also lays the groundwork for real-time, personalized trauma care via control-theoretic tools.

PMID 42756045
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PubMedInternational journal for numerical methods in biomedical engineering2026-09-17

Mesoscale Simulations of Blood Coagulation in Flow and Quiescent Domains Using SDPD.

Ferrero Marina Echeverría ME, Moreno Nicolas N, Ellero Marco M

Blood coagulation is governed by tightly regulated reaction networks whose activation and early evolution are influenced by transport processes. While reduced kinetic models of the intrinsic and extrinsic pathways have been validated in well-mixed experimental settings, their behavior in spatially resolved domains remains insufficiently characterized. In this work, two established reduced coagulation networks are embedded within a thermodynamically consistent mesoscale particle-based framework that resolves fluid momentum transport together with multispecies advection-diffusion-reaction dynamics. Unlike conventional continuum coagulation solvers, the proposed formulation captures coupled transport and biochemical interactions through interacting particles within a unified hydrodynamic description. The framework is used to investigate the initiation phase of coagulation under controlled microvascular-like flow conditions in simplified channel geometries. The simulations reproduce characteristic thrombin generation curves (TGCs) across physiologically relevant parameter ranges while additionally revealing spatial transport effects that are not captured by outlet-averaged measures alone. In particular, the results show that transport-reaction coupling induces pronounced spatial heterogeneities in thrombin concentration, with transitions between localized activation, wall-aligned accumulation, and advective washout depending on Reynolds and Péclet regimes. Injury geometry is further shown to modulate coagulation amplification, with capped configurations producing enhanced thrombin accumulation due to localized surface-mediated activation. Complementary quiescent-domain simulations additionally reproduce qualitative trends observed in thrombodynamics assays, including fibrinogen-dependent variations in fibrin formation. Overall, the study introduces a unified mesoscale computational framework for analyzing how flow, transport, and biochemical kinetics jointly regulate early coagulation dynamics in spatially resolved domains.

PMID 42750253
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