Coagulation & thrombus formation

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Coagulation & thrombus formation

Tissue-factor-triggered coagulation, thrombin generation and fibrin polymerization forming the occlusive coronary thrombus; fibrinolytic turnover markers.

91 molecules · 38 druggable · 5 with clinical trials

Canonical markers: Fibrinogen, D-dimer, thrombin-antithrombin, F1+2, tissue factor, PAI-1

D-dimer indicates active coagulation and thrombus formation during acute coronary events.

60 refs1 trials

Fibrinogen is the substrate for thrombin-driven fibrin polymerization forming the occlusive coronary thrombus.

60 refsdruggable

Plasminogen activator inhibitor-1SERPINE1

PAI-1 inhibits fibrinolysis and promotes a prothrombotic state favoring coronary thrombus formation and persistence.

60 refsgeneticdruggable

Thrombin-antithrombin complex

Thrombin-antithrombin complex is a marker of tissue-factor-triggered coagulation activation and thrombin generation, indicating active thrombus formation in acu

Tissue FactorF3

Tissue Factor is exposed on thrombogenic lipid-core material after plaque rupture, triggering Factor VIIa and thrombin generation.

41 refs1 trialsdruggable

Tissue plasminogen activatorPLAT

Tissue plasminogen activator is released during coronary thrombosis and serves as a marker of fibrinolytic activity and thrombus burden in acute MI.

38 refsgeneticdruggable

Fibrinopeptide A

Fibrinopeptide A is released during thrombin-catalyzed fibrin polymerization, marking coagulation activation in coronary thrombosis.

Prothrombin fragment 1+2F2

F1+2 release quantifies activated prothrombin conversion, reflecting the rate of thrombin generation and coagulation activation.

29 refsgeneticdruggable

Thrombin is generated by tissue-factor-triggered coagulation and drives fibrin polymerization and platelet activation in coronary thrombosis.

25 refs1 trials

Fibrinogen Beta ChainFGB

Fibrinogen polymerizes into fibrin scaffolding the occlusive coronary thrombus and amplifies platelet aggregation.

25 refsdruggable

Prothrombin Fragment 1+2

Prothrombin fragment 1+2 is released during tissue-factor-triggered coagulation, indicating thrombin generation during coronary thrombosis.

Fibrin polymerization forms the structural matrix of the occlusive coronary thrombus, with impaired fibrinolysis predicting worse outcomes.

antithrombin IIISERPINC1

Antithrombin III is consumed during thrombin-driven thrombus formation, and its depletion indicates active coagulation in acute infarction.

17 refsgeneticdruggable

Plasminogen activation to plasmin drives fibrin degradation and thrombus resolution in coronary occlusion.

16 refs1 trialsgeneticdruggable

FVII activity initiates tissue-factor-mediated coagulation and fibrin-thrombus formation in MI.

14 refsdruggable

Factor XI activation by thrombin and contact factors amplifies intrinsic coagulation in post-rupture and post-erosion thrombosis, driving coronary occlusion.

12 refsdruggable

Coagulation factor VIIIF8

Factor VIII elevation reflects a pro-coagulative state and augments the intrinsic tenase complex, increasing thrombin generation risk.

11 refsdruggable

Factor V acts as a cofactor in the prothrombinase complex to amplify thrombin generation and drive fibrin polymerization during coronary thrombus formation.

11 refsdruggable

Tissue factor pathway inhibitorTFPI

Tissue factor pathway inhibitor antagonizes coagulation activation and thrombus formation, with inverse association to MI risk.

11 refsdruggable

Coagulation Factor XIIF12

Factor XII activation in the contact system amplifies coagulation and contributes to thrombus formation and fibrinolytic-induced reactivation in MI.

10 refsdruggable

Protein C deficiency or inactivation impairs anticoagulant regulation, promoting prothrombotic thrombus formation in acute MI.

10 refsgeneticdruggable

Fibrin degradation products

Products of plasmin-mediated fibrin degradation indicating active fibrinolysis in acute coronary thrombosis.

Alpha-2-antiplasminSERPINF2

Alpha-2-antiplasmin inhibits plasmin-mediated fibrin degradation; its depletion reflects active fibrinolytic turnover and indicates a hypofibrinolytic environme

7 refsdruggable

Kininogen-1KNG1

KNG1 drives contact-triggered coagulation cascade activation and is a marker of plaque rupture and thrombus formation in Type 1 MI.

7 refsdruggable

Prothrombin fragment F1+2

F1+2 is released during prothrombin activation, quantifying thrombin generation and thrombotic activity in acute MI.

Thrombin-Activatable Fibrinolysis InhibitorCPB2

TAFI cross-links fibrin and inhibits plasmin-mediated fibrinolysis, stabilizing the occluding thrombus in Type 1 MI.

7 refsdruggable

Coagulation Factor XIII A ChainF13A1

Transglutaminase-catalyzing coagulation factor that stabilizes fibrin thrombus and modulates hemostatic platelet aggregation.

6 refsdruggable

Protease-activated receptor 1F2R

G-protein-coupled receptor activated by thrombin; drives both platelet activation and endothelial pro-inflammatory signaling during thrombosis.

6 refsgeneticdruggable

sphingosine-1-phosphate

Sphingosine-1-phosphate is a thrombin-downstream lipid mediator that amplifies platelet activation and coagulation responses.

Coagulation Factor XF10

Activated Factor X catalyzes prothrombin conversion to thrombin, a central step in occlusive coronary thrombus formation.

5 refsgeneticdruggable

Fibrinogen Gamma ChainFGG

Fibrinogen gamma chain polymerizes into fibrin and modulates platelet aggregation; genetic variants alter MI risk.

5 refsdruggable

Plasmin-α2-antiplasmin complex

Plasmin-α2-antiplasmin complex indicates active fibrinolysis and proteolytic thrombus remodeling during acute coronary occlusion.

uPA degrades fibrin and facilitates fibrinolysis, with downregulation post-MI predicting adverse cardiac remodeling and heart failure risk.

Plasma kallikreinKLKB1

Kallikrein activation in the contact phase amplifies coagulation and contributes to MI risk, particularly during thrombolytic therapy-induced reactivation.

4 refsdruggable

Complement C3C3

Central complement component driving local inflammatory amplification and thrombus-associated innate immune activation.

3 refsdruggable

Complement component 1q

C1q initiates classical complement activation driving thrombus formation and myocardial injury in acute MI.

D-dimers reflect fibrin deposition and plasmin-mediated fibrinolysis, marking active thrombotic and fibrinolytic activity in acute coronary occlusion.

Endogenous thrombin potential

Elevated endogenous thrombin potential indicates heightened coagulation capacity promoting thrombus formation.

Inter-alpha-trypsin inhibitor heavy chain 4ITIH4

Serine-protease inhibitor produced in atherosclerotic plaques and released in exosomes, predicting coronary thrombosis and acute MI.

3 refsdruggable

Lymphatic vessel endothelial hyaluronan receptor-1LYVE1

LYVE1 marks lymphatic endothelial and macrophage infiltration in thrombus and plaque.

3 refsdruggable

Plasma protease C1 inhibitorSERPING1

C1-inhibitor suppresses both contact-phase coagulation and complement-driven inflammation during coronary thrombus formation.

3 refsdruggable

Plasmin-antiplasmin complexes

Plasmin-antiplasmin complexes quantify active fibrinolysis of the coronary thrombus, indicating both thrombus formation and the fibrinolytic response in acute M

Soluble fibrin monomer

Intermediate in fibrin polymerization indicating active coronary thrombus formation and fibrinogen consumption.

Thrombin-antithrombin complexes

TAT complexes quantify active thrombin generation at the site of coronary injury, marking the intensity of coagulation cascade activation in acute MI.

Kallikrein-generated vasodilatory mediator providing endothelial signaling and cardioprotection during acute thrombosis.

Anticardiolipin Antibody

Anticardiolipin antibodies promote arterial thrombosis by enhancing coagulation and platelet activation.

antiphospholipid antibodies

Antiphospholipid antibodies induce a hypercoagulable state and thrombosis, causing MI in young patients.

Antithrombin IIISERPENC1

Antithrombin III consumption during MI reflects thrombin and Factor Xa generation; low AT-III impairs anticoagulation and predicts thrombotic burden.

Coagulation Factor IXF9

Factor IX is a serine protease in the intrinsic coagulation cascade whose activity predicts venous-thromboembolism and thrombotic risk.

2 refsdruggable

D2-40 podoplaninPDPN

D2-40/podoplanin marks lymphatic endothelial involvement in coronary thrombus architecture.

2 refsdruggable

Heparin Cofactor IISERPIND1

SERPIND1 inhibits thrombin and intrinsic tenase, regulating coagulation amplification during acute MI.

2 refsdruggable

Histidine-Rich GlycoproteinHRG

Histidine-rich glycoprotein regulates coagulation and platelet adhesion, influencing thrombus formation in Type 1 MI.

2 refsdruggable

miR-197-5p dysregulation in unstable angina and STEMI associates with altered coagulation and platelet activation cascades.

miR-361-5p dysregulation in acute MI associates with altered coagulation cascade activation and adverse major events.

Plasmin-inhibitor complex

Plasmin-inhibitor complex marks active fibrinolysis and thrombus remodeling in myocardial infarction.

Vascular endothelial growth factor receptor 3FLT4

VEGFR3 expression marks lymphatic endothelial cells infiltrating coronary thrombus.

2 refsdruggable

Activated Protein CPC

Activated Protein C generation marks thrombin-driven anticoagulant feedback and reflects acute coagulation activation during MI.

1 refsdruggable

AGBL1 variants influence activated partial thromboplastin time, a coagulation trait linked to CAD thrombotic risk.

Alpha-2 macroglobulinA2M

Broad-spectrum protease inhibitor involved in thrombin inhibition and fibrinolytic regulation during acute thrombosis.

1 refsdruggable

Annexin V-binding small microparticles

Annexin V-binding microparticles provide a procoagulant surface promoting thrombus formation in acute coronary syndromes.

Anti-β2-glycoprotein I antibodies

Anti-β2-glycoprotein I antibodies promote a prothrombotic state through phospholipid-dependent coagulation activation.

APC-PCI (activated protein C-protein C inhibitor complex) reflects ongoing thrombin generation and coagulation amplification during coronary thrombosis.

C4b-binding protein alpha-chainC4BPA

C4b-binding protein modulates complement activation and anticoagulation during coronary thrombus formation.

1 refsdruggable

CD144+ tissue-factor+ microparticles

CD144+TF+ microparticles from activated endothelium carry tissue factor to trigger thrombin generation and fibrin deposition.

Cross-linked fibrin degradation products

Cross-linked fibrin degradation products reflect active thrombus formation and fibrinolytic activity, indicating thrombus burden and complexity in MI.

Crosslinked fibrin degradation products

Crosslinked fibrin degradation products reflect Factor XIII-stabilized thrombus formation and endogenous fibrinolytic activation.

Erythrocyte Membrane Particles

Erythrocyte-derived microparticles serve as markers of vascular injury and contribute to coagulation amplification in acute coronary syndrome.

Fibrin degradation product

Fibrin degradation products indicate active fibrinolytic remodeling and coagulation turnover during acute MI.

Fibrin fragment beta 15-42

Fibrin-derived peptide released during fibrin polymerization and plasmin-mediated degradation in acute thrombus.

Fibrin/fibrinogen degradation products

Fibrin/fibrinogen degradation products reflect active thrombus formation and plasmin-driven fibrinolysis within the occlusive thrombus.

Fibrinogen B-beta 15-42 peptide

Fibrinogen B-beta 15-42 peptide is a fibrin-specific breakdown product marking active fibrinolysis and thrombus remodeling.

Fibrinogen/fibrin fragment E

Fragment E released during fibrin degradation reflects active coagulation and fibrinolytic turnover in the coronary thrombus.

Fragment D neoantigen

Neoepitope released during fibrinolytic degradation of cross-linked fibrin in coronary thrombus.

Fibrin degradation product marking thrombin-driven coagulation and fibrinolytic turnover in acute coronary thrombosis.

Fragment E neoantigen

Neoepitope released during fibrinolytic degradation indicating active thrombus formation and fibrin turnover.

FX-06 is a fibrin-derived peptide that mitigates ischemia-reperfusion injury following coronary thrombus resolution.

Homocysteine thiolactone

Homocysteine thiolactone modulates fibrin structure and plasmin-mediated lysis, influencing thrombus stability and fibrinolytic resistance in acute MI.

Lupus Anticoagulant

Lupus anticoagulant promotes coronary thrombosis through tissue-factor and coagulation pathway activation.

Myosin-driven actin sliding powers platelet contraction and thrombus compaction, enabling the transition from loose plug to stable occlusive clot.

P-selectin+ tissue-factor+ microparticles

CD62P+TF+ microparticles simultaneously mark platelet activation and deliver tissue factor to amplify thrombus formation.

PAI-2 regulates fibrinolysis by inhibiting tissue plasminogen activator and urokinase, modulating thrombus stabilization and resolution.

1 refsdruggable

Plasmin-alpha2-plasmin inhibitor complex

Plasmin-alpha2-plasmin inhibitor complex quantifies fibrinolysis and thrombus burden in acute coronary thrombosis.

Protein C activation peptide

Peptide released during activated Protein C generation, marking endogenous anticoagulant pathway engagement.

Protein Z is a vitamin K-dependent anticoagulant that influences coagulation balance and thrombotic risk.

1 refsdruggable

Red blood cell-derived microparticles

RBC-derived microparticles marking thrombotic activation and hemolysis during acute coronary occlusion.

Thrombin peak (generation)

Thrombin peak represents the maximum rate of thrombin generation, reflecting coagulation cascade activation and fibrin formation intensity.

Tissue Plasminogen Activator / Plasminogen Activator Inhibitor-1 Ratio

The tPA/PAI-1 ratio quantifies net fibrinolytic activity; low ratio signals impaired thrombus lysis and predicts worse reperfusion in acute MI.

tPA/PAI-1 complex

tPA/PAI-1 complex imbalance (excess PAI-1) suppresses fibrinolysis and promotes thrombus persistence in coronary occlusion.

Tropomyosin stabilizes actin filaments in the platelet cytoskeleton, reinforcing thrombus structural organization and mechanical integrity.

ABO Histo-Blood GroupABO

Blood-group determinant modulating von Willebrand factor and clotting-factor levels.

gamma-glutamyl carboxylaseGGCX

Catalyzes vitamin K-dependent carboxylation of coagulation factors (II, VII, IX, X) and vascular Gla proteins (MGP, osteocalcin); deficiency impairs thrombus re

geneticdruggable