Mast cells, basophils and eosinophils are the effector cells in Type I (imm
ediate hypersensitivity or immunoglobulin E (IgE)-associated) allergic diso
rders. The release of granule-associated/lipid mediators as well as the pro
duction of various cytokines/chemokines is intimately linked to the acute a
nd late phase symptoms observed in atopic patients. Perhaps standing at the
beginning of many if not all chronic allergic inflammatory conditions with
high specific IgE levels. Binding of IgE to the high affinity Fc epsilon R
I receptor, which is constitutively expressed on mast cells, basophils, and
some eosinophils, and its crosslinking via allergen initiates the resultin
g pathology. The relative specificity of the ligand (IgE)/receptor (Fc epsi
lon RI) interaction and the discovery of specific intracellular signalling
cascades in other cell types has prompted efforts to interfere at these lev
els with the activation of those effector cells. Here we report on the phar
maceutical endeavours over the last 5 years - reflected in the patent liter
ature in the area of mast cell signalling inhibitors. Those 'potential drug
s' are under development for several allergic manifestations such as allerg
ic rhinitis, allergic conjunctivitis, allergic asthma as well as acute and
chronic urticaria.