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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

PubMedBlood2026-07-25

Factor V is an anticoagulant of the extrinsic pathway of coagulation and modifier of thrombin generation in hemophilia A.

Jewell Megan M, Baird Christine H CH, Thornhill Dianne D, Ashour Zaina Z et al.

Factor V (FV) links procoagulant amplification to anticoagulant feedback, but how FV limits tissue factor-initiated coagulation are not fully defined. We hypothesized that procofactor FV downregulates factor X (FX) activation by tissue factor:factor VIIa (TF:FVIIa), independently of tissue factor pathway inhibitor α (TFPIα), and that this mechanism is especially important in hemophilia. Thrombin generation was measured in FV/FVIII‑immunodepleted plasma and synthetic plasma while titrating FV, with TFPIα removed, blocked, or re-added. TF:FVIIa activation of FX was measured on phosphatidylserine‑containing or phosphatidylserine‑free liposomes with antibodies against the FV light chain and C2 domain. FV and TFPIα levels modulated thrombin generation in plasma from people with hemophilia A. In TF‑initiated coagulation lacking TFPIα, thrombin generation peaked at 2 nM FV and decreased as FV increased; at 20 nM FV (normal concentration), peak thrombin and thrombin generation rate were reduced by up to 50-80%, with larger effects at low FVIII. In purified TF:FVIIa assays, FV reduced FX activation by ~80% at physiologic concentration and inhibited FX activation on TF-expressing fibroblasts. Increasing PS content enhanced FX activation and increased the FV-sensitive component, while blocking the FV light chain or C2 domain partially relieved inhibition. In hemophilia A plasma, higher FV was associated with longer lag time and time-to-peak, and lower peak thrombin independent of TFPIα. Thus, FV is an endogenous anticoagulant that inhibits TF-initiated coagulation by limiting FX activation by TF:FVIIa through a membrane-dependent mechanism. This mechanism refines models of coagulation initiation and may help explain how FV variation contributes to bleeding and thrombosis.

PMID 42498286
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PubMedArthroscopy techniques2026-07-25

The Biologically Enhanced Anterior Cruciate Ligament Reconstruction With Combined Injection of Harvested Platelet-Rich Plasma, Thrombin, and Bone Marrow Aspirate Concentrate.

Aldawoudy Akram A, Hirschmann Micheal T MT, Abdelgawad Ahmed Abdalla Ahmed AAA, Gawish Hesham Mohamed HM

Despite continuous advances, anterior cruciate ligament reconstruction still struggles to restore full native knee function, as most techniques improve mechanical stability but overlook biological healing. The described superenhanced anterior cruciate ligament reconstruction technique aims to address this biological problem through a quadruple approach. The native anterior cruciate ligament stump is preserved, autologous bone "biosticks" are used to enhance tunnel osteointegration, and incorporates platelet-rich plasma, and the bone marrow aspirate concentrate in a gel-like structure to boost graft revascularization.

PMID 42499953
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PubMedThe American journal of pathology2026-07-25

Synergistic cytokine signaling drives angiofibrotic gene pathways in primary human retinal endothelial cells.

McLellan Fergus C FC, Liang George G, Jin Yuting Y, Madigan Michele C MC et al.

Neovascularization of the posterior eye is a progressive disease state, marked by an inflammatory initiation, angiogenic growth, and subsequent fibrotic degeneration of ECs (ECs). Although implicated in age-related macular degeneration (AMD) and proliferative diabetic retinopathy (PDR) as a leading cause of irreversible vision loss worldwide, the mechanisms underpinning retinal EC dysregulation in neovascularization and fibrosis are not well understood. This study presents a transcriptomic investigation of cultured primary human microvascular retinal EC dysregulation following exposure to 10 ng/mL of six retinal neovascularization-associated signaling molecules (IL-6, TNF-α, TGF-β1, TGF-β2, thrombin, and VEGF-A) both individually and as a combined treatment for 24 hours. TNF-α, thrombin and TGF-β2 alone induced significant enhancement of inflammatory and angiofibrotic pathways, including PI3K/Akt, NF-κB and SMAD. BGN, CD34, COL1A2, CXCL8, IGFBP5, INHBA, SERPINE1, SNAI1, TGFB2 and TNFSF11 were identified as having overlapping, nodal roles in the pathological dysfunction of retinal ECs. Co-treatment with all six ligands significantly enhanced differential gene expression, revealing 889 unique differentially expressed genes. Using a novel network-based gene correlation engine, GeneBunny, the cocktail group was found to mimic published retinal and choroidal EC transcriptomes from AMD patient tissue more accurately than individual treatment groups. These findings provide a biologically relevant characterization of the pathological mechanisms driven by key retinal neovascularization-associated signaling molecules in retinal, enabling the identification of novel anti-fibrotic therapeutic targets.

PMID 42498181
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PubMedWorld journal of otorhinolaryngology - head and neck surgery2026-07-25

The Relationship Between Blood Lipids, Coagulation Indexes, Blood Homocysteine and Sudden Deafness: A Retrospective Study and Mendelian Randomization Analysis.

Yang Feng-Xin FX, Song Yu-Wan YW, Wang Yan Y, Zhao Kun K et al.

Certain blood components, including blood lipids, coagulation parameters, and homocysteine, have been suggested to correlate with the incidence and prognosis of sudden sensorineural hearing loss (SSNHL). However, the nature of these associations remains controversial. A retrospective study was conducted between January 2020 and December 2024. A total of 308 patients with SSNHL who received short-term combined therapy and 169 healthy controls were included from our hospital. Initially, baseline clinical indicators were compared between the patient group and the control group. Subsequently, patients were further stratified into four subgroups according to their hearing recovery outcomes for more detailed inter-group comparisons, and the impact of these indicators on SSNHL incidence and prognosis was assessed. To further investigate potential causality, Mendelian randomization (MR) analysis was performed to examine the relationship between genetically predicted blood components and SSNHL. Our retrospective analysis revealed significant differences between the patient and control groups in the following parameters at admission: plasma fibrinogen at admission (PRE-FIB), activated partial thromboplastin time (APTT), thrombin time (TT), prothrombin time (PT), total cholesterol (CHOL), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG). Among the four groups stratified by hearing recovery, differences were observed in admission hearing level (dB), the change in plasma fibrinogen after the first batroxobin injection relative to baseline (DIFF-FIB), and CHOL. MR analysis using the random-effects inverse-variance weighted (IVW) method indicated a significant causal relationship between genetically predicted lipid levels and SSNHL. Additionally, genetically predicted S-adenosylhomocysteine and fibrinogen were identified as potential risk factors for SSNHL. PRE-FIB, APTT, TT, PT, CHOL, HDL-C, LDL-C, and TG may be associated with the onset of SSNHL. Admission hearing level (dB), DIFF-FIB, and CHOL could play a role in predicting hearing recovery after SSNHL. MR analysis provides causal evidence supporting lipids, fibrinogen, and S-adenosylhomocysteine as potential risk factors for SSNHL.

PMID 42500069
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PubMedMolecular therapy : the journal of the American Society of Gene Therapy2026-07-24

Prothrombin recognition and conformational modulation by anti-thrombin anticoagulant aptamers.

Troisi Romualdo R, Cangiano Alessandro A, Cowieson Nathan N, Spiridonova Vera V et al.

Disorders of the blood coagulation cascade continue to pose a major clinical challenge, necessitating the development of new therapeutic agents capable of modulating this process. Several oligonucleotide aptamers targeting coagulation factors have been developed, and some are undergoing preclinical or clinical evaluation. Among them, anti-thrombin anticoagulant aptamers are promising dual-targeting agents in that, in addition to inhibiting enzyme activity, they may limit thrombin generation by binding to its precursor, prothrombin. In the present study, combined calorimetric and spectroscopic analyses reveal that these aptamers recognize proexosite I of prothrombin and exosite I of thrombin through broadly similar thermodynamic binding mechanisms. Integration of structural SAXS studies and limited proteolysis shows that aptamer binding to proexosite I alters prothrombin structure, shifting the equilibrium from its more abundant closed form to the open conformation. Taken together, these results support the classification of these aptamers as dual-targeting agents capable of recognizing both thrombin and prothrombin and provide guidance for their continued development as anticoagulant therapeutics.

PMID 42494063
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PubMedACS omega2026-07-24

High-Performance Thrombin Aptamers with a Peptide-Extended Recognition Interface.

Varizhuk Irina V IV, Kolganova Natalia A NA, Gordeeva Olga B OB, Stomakhin Andrey A AA et al.

Improving the affinity and inhibitory characteristics of aptamers is important in the context of their applications in therapy and diagnostics. The use of peptide-aptamer conjugates with an extended aptamer-protein interface is an efficient strategy toward this goal. Here, we report GLE peptide conjugates of the bimodular duplex-quadruplex thrombin aptamers Re31 and NU172. Biophysical studies of the aptamer conjugates revealed that the presence of the tripeptide subunit does not have a significant effect on the thermodynamic stability or structure of the aptamers. In contrast, the affinity and anticoagulant activity of the conjugates were significantly improved. The NU172-GLE conjugate appeared to be the most effective inhibitor of thrombin-induced fibrinogen polymerization. Further clotting studies in human plasma showed that due to the presence of prothrombin, an alternative target for aptamers, the antithrombin activity of aptamers in plasma samples may be significantly underestimated.

PMID 42495377
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