Target intelligence / Profile preview

Coagulation factor II, Coagulation factor VII, Coagulation factor IX, Coagulation factor X (FII (or II), FVII (or VII), FIX (or IX), FX (or X))

Target
FII (or II), FVII (or VII), FIX (or IX), FX (or X)
Molecular classification
Enzyme, Serine protease, Vitamin K-dependent coagulation factor
01

Overview

The four factors—Coagulation factor II (Prothrombin), Coagulation factor VII, Coagulation factor IX, and Coagulation factor X—are serine protease enzymes that are essential for the normal process of blood coagulation[3][5]. They are synthesized in the liver as vitamin K–dependent zymogens, each with a characteristic domain structure (Gla domain, EGF-like domains, serine protease domain)[3][6]. Upon activation, they function sequentially in the coagulation cascade to generate thrombin and fibrin, which are necessary for the formation of a stable blood clot. Deficiency or dysfunction of any leads to bleeding disorders, while their over-activation is a key contributor to pathologic thrombosis[3][5][6]. Each factor is a validated drug target for anticoagulant therapy and for replacement in congenital or acquired bleeding disorders.

Other names
FIIProthrombinFVIIFIXChristmas factorFXStuart–Prower factor
02

Mechanism of action

Inhibition: small molecule or biologic drugs inhibit enzymatic activity to prevent thrombin generation and fibrin clot formation (e.g., FXa inhibitors) Replacement: recombinant or plasma-derived factor replacement for treating deficiencies (e.g., FIX concentrates for hemophilia B)

03

Biological functions

Blood coagulation (hemostasis)Thrombin generationActivation of downstream coagulation factors
04

Disease associations

Cardiovascular disease (thrombosis, stroke, myocardial infarction)Bleeding disorders (e.g., hemophilia B for FIX deficiency)Liver disease (factors synthesized in liver)Rare coagulation factor deficiencies
05

Safety considerations

Bleeding (major risk with inhibition of these targets)Thrombosis (with excess therapeutic factor replacement)Hypersensitivity/adverse reactions with biologicsVitamin K antagonists: narrow therapeutic window, many drug and dietary interactions
06

Interacting drugs

Vitamin K antagonists (e.g., warfarin)

3 more in the full profile.

07

Biomarkers

Plasma levels and activity assays for each factor (PT for FII, FVII, FX; aPTT for FIX)Thrombin generation assaysD-dimer (as an indirect marker of increased thrombin and fibrin formation/degradation)

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