ArticleScientific reports2025
NADPH oxidase 2 inhibitor GSK2795039 exerts antiplatelet and antithrombotic activity.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Nicotinamide adenine dinucleotide phosphate hydrogen oxidase 2 exacerbates abdominal aortic aneurysm formation by inducing oxidative stress through autophagy inhibition.Histology and histopathology · 2026Article
- Review
- Hemostasis-Sparing Antiplatelet Therapy: Current Concepts and Emerging Targets in Arterial Thrombosis.Biomolecules & therapeutics · 2026Review
- Aβ₁₋₄₀ Enhances Platelet Sensitivity to Thrombin via NADPH Oxidase-ROS Signaling and Integrin αBiomolecules & therapeutics · 2026Article
- Integrated transcriptomic and functional analyses reveal that NOX2 inhibition rewires the inflammatory landscape of macrophages.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Reactive oxygen species (ROS) production by NADPH oxidase (NOX) is a key promoter of platelet activation, making NOX inhibition an attractive antiplatelet strategy. This study evaluated the effects of the novel NOX2 inhibitor, GSK2795039, on human platelet functional responses and ROS-mediated signaling pathways. GSK2795039 effectively suppressed both extracellular and intracellular ROS production in collagen-stimulated platelets. Consequently, GSK2795039 treatment significantly inhibited collagen-induced platelet aggregation, dense-granule ATP release, and α-granule P-selectin exposure. Furthermore, GSK2795039 attenuated tyrosine phosphorylation-mediated activation of spleen tyrosine kinase (Syk), linker for the activation of T cells (LAT), vav guanine nucleotide exchange factor 1 (Vav1), and Bruton tyrosine kinase (Btk) within the collagen receptor signaling pathway, leading to decreased phospholipase Cγ2 (PLCγ2) activation and calcium mobilization. GSK2795039 also inhibited collagen-induced integrin αIIbβ3 activation, associated with increased cyclic guanosine monophosphate (cGMP) levels and vasodilator-stimulated phosphoprotein (VASP) phosphorylation. Additionally, the inhibitor reduced collagen-induced p38 mitogen-activated protein kinase (MAPK) activation, which led to lower cytosolic phospholipase A
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Registered trials
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