Date published: 2025-9-23

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EPCR Inhibitors

The class of EPCR inhibitors encompasses a diverse array of compounds targeting various cellular pathways to modulate the expression and function of Endothelial Protein C Receptor (EPCR). One notable group includes tyrosine kinase inhibitors such as R547 and Dasatinib, which act on focal adhesion kinase (FAK) and Src family kinases, respectively. Disruption of these kinases indirectly influences EPCR by interfering with integrin-mediated signaling and downstream processes associated with EPCR modulation. Additionally, small molecules like SB203580 and LY294002 play a crucial role as indirect EPCR inhibitors. SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor, disrupts the p38 MAPK pathway, impacting cellular events linked to EPCR modulation. LY294002, a selective phosphoinositide 3-kinase (PI3K) inhibitor, alters downstream processes related to EPCR, illustrating the intricate interplay between PI3K signaling and EPCR regulation.

Furthermore, compounds such as BAY 11-7082 and Wortmannin provide indirect modulation of EPCR by targeting the NF-κB and PI3K-related kinase pathways, respectively. These inhibitors disrupt the inflammatory signaling cascades and cellular processes associated with EPCR, emphasizing the complexity of regulatory networks involved in EPCR expression. The class also includes inhibitors like SP600125, U0126, and BMS-345541, targeting JNK, MEK1/2, and IκB kinase (IKK), respectively. Through their actions on these key signaling components, these inhibitors exert downstream effects on pathways connected to EPCR, showcasing the diverse strategies employed by this class to influence EPCR expression and function. In summary, the class of EPCR inhibitors encompasses a range of chemical compounds that intricately modulate cellular pathways associated with EPCR. These inhibitors act through well-defined mechanisms, providing a nuanced understanding of how specific biochemical and cellular pathways influence the expression and activity of EPCR.

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