Abstract
The introduction of SCG for the treatment of bronchial asthma was viewed by many as the advent of a new era, the era of the antiallergic drug which acted by suppressing the release of inflammatory mediators from mast cells. However, some 17 years on, SCG is the only drug of its type on the market. Efforts to improve its efficacy by chemical modification have not succeeded. As it is now clear that all of the beneficial effects of SCG in asthma cannot be attributed to its effects on mast cell mediator secretion, it is not surprising that mast cell models are not predictive of clinical activity. Perhaps a clearer understanding of the basic bio-chemical mechanisms of SCG and its actions in animals and man may lead to development of more relevant models and to a more potent drug.
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