tcv-309 and lexipafant

Acute pancreatitis (AP) causes release of platelet-activating factor (PAF), which induces systemic effects that contribute to circulatory disturbances and multiple organ failure. PAF is a cell surface secretion of bioactive lipid, which could produce physiological and pathological effects by binding to its cell surface receptor called platelet-activating factor receptor (PAF-R). Studies showed that PAF participate in the occurrence and development of AP and administration of platelet-activating factor receptor antagonists (PAF-RAs) could significantly reduce local and systemic events after AP. PAF has also been implicated as a key mediator in the progression of severe AP, which can lead to complications and unacceptably high mortality rates. Several classes of compounds show significant PAF-RAs, and significant local and systemic effects on reducing inflammatory changes. As a preventive treatment, PAF-RA could block a series of PAF-mediated inflammatory injury and thus improve the prognosis of AP. This review introduces the important role of PAF-RA in the treatment of AP.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents; Azepines; Ginkgolides; Humans; Imidazoles; Lactones; Leucine; Pancreatitis; Platelet Aggregation Inhibitors; Platelet Membrane Glycoproteins; Pyridinium Compounds; Receptors, G-Protein-Coupled; Tetrahydroisoquinolines; Treatment Outcome; Triazoles