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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

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

PubMedOrganic letters2026-07-27

Site-Specific Tyrosine Sulfation of Triabin via Semi-Synthesis Enhances Thrombin Inhibition through Synergistic Multiple-Mode Interactions.

Xiao Zhenbang Z, Mo Zeyuan Z, Lin Litong L, He Chunmao C

Herein, we report the semisynthesis of site-specifically sulfated triabin─a 142-amino-acid lipocalin protein─at Tyr124. Functional assays reveal that sulfation enhances anticoagulant activity by ∼5-fold, demonstrating that even rigid scaffolds can benefit from this modification. Modeling studies uncover a synergistic mechanism wherein the sulfate group engages in a hydrogen-bond network, electrostatic bridging, and charge-complementary interactions with thrombin exosite I, while the hydrophobic core (notably Phe106 and Val126) remains the primary driving force.

PMID 42503796
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PubMedMedical engineering & physics2026-07-27

Spatiotemporal dynamics of blood coagulation in medium-sized vessels: numerical insights into the effects of vessel walls and blood flow.

Tsubota Ken-Ichi KI, Tajikawa Tsutomu T

The spatiotemporal distribution of coagulation factors fundamentally governs blood coagulation dynamics. Although these dynamics have been examined at the submillimeter scale (hundred micrometers), how this distribution influences thrombus formation at dimensions comparable to or larger than those of medium-sized vessels (on the order of 1 mm in diameter) remains insufficiently clarified. In this study, we performed numerical simulations using a well-established reaction-diffusion model of the intrinsic coagulation pathway to investigate coagulation kinetics over millimeter-scale domains, while explicitly incorporating the effects of walls and convection on coagulation. The simulation settings were validated against experimentally observed coagulation behaviors. Our results indicated that in blood domains adjacent to an active wall surface, the propagation velocities of the thrombin wave and the advancing clot front decreased with increasing distance from the wall and approached a constant value at approximately 200µm. This spatial variation in velocity led to domain-size-dependent behavior in the temporal evolution of the volume-averaged thrombin concentration in millimeter-scale domains analyzed in thrombin generation assays because the domain size determined the ratio of the active surface area to blood volume. In addition, simulations of coagulation along a 5 cm-long thin filament within a rat arteriovenous shunt showed a progressive increase in the coagulation rate along the flow direction, indicating that the longitudinal distribution of coagulation activity governs the total clot volume. Together, these findings underscore the need to resolve multiscale spatial distributions of coagulation, from the micrometer to centimeter scales, to improve understanding of thrombus formation under physiological conditions where the effects of walls and convection interact.

PMID 42504136
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PubMedJournal of the Society for Cardiovascular Angiography & Interventions2026-07-26

Radial Artery Pseudoaneurysm Following Transradial Catheterization: Recognition, Management, and Prevention.

Carvajal Michelle C MC, Shirodkar Shivani S, Briscoe Jessica B JB, Suga Hilkiah H et al.

Transradial cardiac catheterization is recommended over femoral artery catheterization for patients with acute coronary syndrome due to lower rates of bleeding and vascular complications. Despite its favorable safety profile, radial artery-specific complications occur, including spasm, occlusion, arteriovenous fistula, perforation, and pseudoaneurysm. Radial artery pseudoaneurysm (RAP) is an uncommon but potentially morbid access-site complication that remains incompletely characterized, with limited practical guidance on diagnosis and management. This review synthesizes published clinical experience on RAP following transradial catheterization, with key considerations for diagnosis, risk stratification, and management. Across published experience, patients with RAP most commonly present with localized pain, swelling, or a pulsatile mass at the access site, with symptom onset ranging from hours to weeks after catheterization. Duplex ultrasonography is the primary diagnostic modality, allowing assessment of pseudoaneurysm size, neck morphology, and flow characteristics. Management strategies range from observation and mechanical compression to ultrasound-guided thrombin injection and surgical repair, with treatment selection guided by lesion size, symptoms, stability, anticoagulation status, and the need to preserve the radial artery. Early recognition with ultrasound and individualized treatment can prevent progression and associated morbidity as transradial access continues to expand.

PMID 42502332
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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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