Abstract
When we became interested in the antiallergic field in 1971 at May & Baker, we knew from the studies of Austen et.al. (1) that the inhibition of the anaphylactic release of histamine from human lung could be related to raised tissue levels of cyclic AMP. Furthermore, Lichtenstein and Margolis (2) observed that methylxanthines such as caffeine or theophylline (I) inhibit the antigen-induced release of histamine from human basophilic leukocytes probably by their well-known ability to inhibit phosphodiesterases. We therefore examined the methylxanthines in the passive cutaneous anaphylactic (PCA) reaction mediated by reaginic antibodies in the rat, and found them to be weak inhibitors. They did not inhibit the PCA reaction reactions mediated by non-reaginic antibodies and therefore in this respect the methylxanthines resembled disodium cromoglycate (DSG). Accordingly the xanthines were regarded as a lead to compounds of potential interest for antiallergic therapy, and totally unrelated chemically to DSG. In addition
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