ABSTRACT
The identification of platelet activating factor (PAF) as glycero-3-phosphocholine,1-3 a number of constitutional analogs of PAF have been reported. CV-3988 inhibits PAF-induced platelet aggregation, but has no effect on the aggregation induced by arachidonic acid, ADP, collagen, or calcium ionophore. In experimental animal models, CV-3988 has been utilized to demonstrate important evidence for the involvement of PAF in several diseases. Biological evaluation of CV-3988, CV-6209, and the other PAF antagonists gave interesting results. These results can be explained by the differences in the affinity of PAF antagonists for the PAF receptors of platelets and nonplatelets; the former mediates platelet aggregation and the latter mediates PAF-induced hypotension. PAF-related analogs might have similar affinity for the receptor of both platelets and nonplatelets. The chapter suggests that CV-3988 and CV-6209 may be useful drugs for investigating the pathophysiological role of PAF in diseases and beneficial drugs for treating diseases such as anaphylaxis, disseminated intravascular coagulation and endotoxin shock.
