TFPI Specific Neutra™ Antibody Products
Product listTissue Factor Pathway Inhibitor (TFPI) is a crucial regulator of blood coagulation, exerting its effects by inhibiting the tissue factor (TF)-initiated coagulation pathway. It exists in two primary isoforms: TFPIα and TFPIβ, each with distinct structural and functional characteristics. TFPI is primarily produced by endothelial cells and megakaryocytes, and it is distributed in the vasculature and platelet surfaces. TFPI acts as a key anticoagulant, thereby impeding the activation of factor X and inhibiting thrombin generation. Additionally, TFPI modulates angiogenesis and inflammation, underscoring its multifaceted role beyond coagulation regulation.
Its Gene ID: 7035, UniProtKB ID: P10646, and OMIM ID: 152310.
TFPI in Coagulation Regulation
TFPI plays a critical role in regulating coagulation by inhibiting the activity of the TF-initiated coagulation pathway. TFPI primarily functions by binding to factor Xa. The Xa-TFPI complexes can also subsequently inhibit the TF-factor VIIa complexes, thereby blocking the activation of factor X and inhibiting thrombin generation. Additionally, TFPIα, the primary isoform of TFPI, can directly inhibit the formation of early prothrombinase complexes by interfering with the interaction between activated factor V and factor X. In cellular coagulation models, TFPI can impede thrombin generation by inhibiting the formation of coagulation complexes on the surface of activated platelets.
Fig.1 Signaling and interactions of TF and TFPI.1
TFPI in Disease
TFPI is implicated in several diseases related to coagulation dysregulation. Abnormalities in TFPI levels or function can contribute to both thrombotic and bleeding disorders. In thrombotic conditions, deficiencies or mutations in TFPI can cause an imbalance in the coagulation system, favoring excessive blood clot formation. This can lead to deep vein thrombosis (DVT), pulmonary embolism, and arterial thrombosis. Conversely, elevated levels of TFPI have been linked to a reduced risk of thrombotic events. In bleeding disorders, reduced TFPI levels or impaired TFPI function can exacerbate bleeding tendencies. For instance, in hemophilia, where there is a deficiency of clotting factors, decreased TFPI levels can further disrupt the coagulation cascade, leading to prolonged and spontaneous bleeding episodes. Understanding the role of TFPI in disease pathogenesis allows for the creation of targeted therapies. Strategies aimed at restoring TFPI levels and function could potentially help rebalance the coagulation system in both thrombotic and bleeding disorders, offering new treatment options for these conditions.
Antibodies Targeting TFPI
Research on therapeutic antibodies targeting TFPI has shown promise in modulating coagulation pathways for various clinical conditions. These antibodies play a crucial role in regulating TFPI activity, which is essential for maintaining hemostasis. Therapeutic antibodies targeting TFPI can function through multiple mechanisms. They may inhibit TFPI's anticoagulant function by blocking its interaction with coagulation factors, thereby promoting clot formation in bleeding disorders like hemophilia. Alternatively, antibodies can enhance TFPI activity by increasing its inhibitory effects on coagulation factors, potentially benefiting patients with thrombotic disorders. Studies have demonstrated the impact of TFPI-targeting antibodies in preclinical models and cell-based assays. These investigations have explored how antibody-mediated modulation of TFPI influences clot formation, bleeding tendencies, and overall coagulation balance. Continued research into the development and optimization of TFPI-targeting antibodies holds significant potential for advancing therapeutic strategies in coagulation-related disorders.
Fig.2 The mechanism of action of novel anti-TFPI antibodies treatments.2
Creative Biolabs offers up to one hundred and thirty highly specific and affinity anti-TFPI antibody products. These antibodies are recombinantly expressed and have nearly ten kinds of applications to meet your diverse research needs.
REFERENCES
- Okaygoun, Dide, et al. "Advances in the management of haemophilia: emerging treatments and their mechanisms." Journal of biomedical science 28 (2021): 1-13. Distributed under Open Access license CC BY 4.0. The image was modified by extracting and using only part of the original image.
- Gualtierotti, Roberta, et al. "Updates on novel non-replacement drugs for hemophilia." Pharmaceuticals 15.10 (2022): 1183. Distributed under Open Access license CC BY 4.0. The image was modified by extracting and using only part of the original image.
