Leukotrienes B4, C4, D4 and E4 are highly effective mediators of asthmatic airway inflammation. These phospholipid mediators are newly synthezised and released during inflammatory reactions by a number of cells, e.g. mast cells, basophils, neutrophils, eosinophils, alveolar macrophages, and also epithelial cells, in different quantities. Leukotrienes may cause a number of proasthmatic reactions such as bronchoconstriction, chemotaxis, increase in permeability of airway vessels, mucosal hypersecretion, and they may contribute to the development of airway hyperresponsiveness. Therefore leukotriene antagonists with different pharmacological actions have been developed. They are either leukotriene synthesis inhibitors, such as BAY X1005, or zileuton, which reduce leukotriene (B4, D4) synthesis by different mechanisms, or they are leukotriene receptor antagonists, available for leukotriene C4, D4, E4, but not for LTBA, such as ICI 204,219 [Accolate], MK-571, ONO-1078 (Pranlukast), RG-12525, and SKandF 104,353. Moderate bronchodilatation, together with a reduction in asthmatic symptoms and concomitant medication, has been demonstrated with a number of substances. It has, however, not been established if leukotriene antagonists act as true antiinflammatory agents, or if they reduce airway hyperresponsiveness. In addition, it is not yet clear which of the different pharmacological classes will be the most effective one. Some antagonists are orally effective, others by inhalation only. Oral drugs were preferentially investigated because an orally effective antiasthmatic drug would clearly improve patients' compliance. From the available data it can be suggested that leukotriene antagonists may be effective in mild to moderate asthma. The potential efficacy in severe asthma remains to be determined. Leukotriene antagonists appear to be a promising class of new antiasthmatic drugs. However, their definite place in asthma therapy needs to be clarified in further clinical studies.