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Factor X + Factor IX (Factor X P Behring)

✓ Approved

CSL Behring · F9 · Cell-based Therapies

What is Factor X + Factor IX?

Factor X + Factor IX is a cell-based therapies developed by CSL Behring. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesFactor X P Behring
CompanyCSL Behring
Drug ClassCell-based Therapies
Molecular TargetF9, F10
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

Factor X + Factor IX acts on 2 molecular targets:

F9coagulation factor IX (P19, F9 p22)
F10coagulation factor X (FXA, FX)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

Factor X + Factor IX is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersFactor IX deficiency✓ Approved
Congenital, familial and genetic disordersFactor X deficiency✓ Approved

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Reactive oxygen species-dependent regulation of hypoxia-inducible factor 1α/C-X-C motif chemokine receptor 4 signaling promotes ozone-induced cancer metastasis.

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Air pollutants, including vehicle emissions and photochemical smog such as ozone, have become a significant health concern in most industrialized nations. Inhaling ozone has repeatedly been linked to increased lung inflammation, immune responses, and cancer development, ultimately speeding up lung cancer metastasis and leading to higher death rates. However, the direct connection between ozone exposure and tumor cell migration has not yet been definitively established. This study aims to investigate the effects of ozone exposure on cancer spread and its underlying mechanisms, focusing on the hypoxia-inducible factor 1α (HIF-1α)/C-X-C motif chemokine receptor 4 (CXCR4) pathway, which influences cancer cell migration and epithelial-mesenchymal transition (EMT). Using B16F10 melanoma and LL2 Lewis lung carcinoma cells, we examined how 1 ppm ozone exposure affects reactive oxygen species (ROS) production and its subsequent impact on the HIF-1α/CXCR4 pathway. Our results show a significant increase in HIF-1α/CXCR4 expression and EMT-related proteins after ozone exposure. Additionally, the use of arbutin, a known ROS scavenger, significantly reduced HIF-1α/CXCR4 levels and cell migration, confirming the role of ROS in ozone-induced metastasis. In summary, our research suggests that ozone promotes cancer spread by activating the HIF-1α/CXCR4 signaling pathway, highlighting an environmental factor that could facilitate cancer progression.

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[This corrects the article DOI: 10.3389/fbinf.2025.1674791.].

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(A) Formation of the platelet-fibrin haemostatic plug. Vascular injury exposes von Willebrand factor (VWF) and tissue factor (TF) to flowing blood. VWF mediates platelet adhesion, leading to platelet activation and aggregation, while TF triggers the coagulation cascade, generating thrombin that converts fibrinogen to fibrin. Thrombin also amplifies platelet activation, integrating the two arms so that platelet aggregates and a fibrin mesh combine to form a stable platelet-fibrin haemostatic plug. (B) Anatomical correlation between bleeding phenotype and tissue factor expression. Typical bleeding sites in haemophilia A and B (intra-articular and intramuscular) are shown relative to the tissue-specific pattern of high tissue factor (TF) expression. Vital organs such as the brain, heart and lungs exhibit high TF expression, proposed to provide additional haemostatic protection, whereas the low TF expression in joints and skeletal muscle leaves these sites more reliant on FVIII- and FIX-dependent amplification and therefore vulnerable to bleeding when these factors are deficient. Figure created with BioRender.com.

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