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Fluticasone propionate Anti-inflammatory Lymphocyte Adhesion molecules Eosinophil CD4+ cells Interleukin-5 Antigen challenge Protease inhibitor Correspondence to: Dr. M. Johnson, Respiratory Commercial Strategy, Glaxo plc, Stockley Park West, Uxbridge, Middlesex UB11 1BU (UK) Fluticasone propionäte (FP) is a new corticosteroid based on the androstane nucleus [1]. It is more lipophilic than beclomethasone dipropionate (BDP) and budesonide, and both binding and retention in human lung tissue in vitro is in the rank order: FP > BDP > beclomethasone 17mono-propionate (17-BMP) > budesonide > flunisolide > hydro-cortisone [2]. FP has an absolute affinity (Kd) for the gluco-corticoid receptor of 0.5 nM, and a relative receptor affinity 1.5and 3-fold higher than 17-BMP and budesonide, respectively. The rate of association with the receptor is 4-fold faster, and the rate of dissociation 10-fold slower than with standard steroids. The resulting half-life of the active steroid-receptor complex is > 10 h, compared with 1, 5, 7.5 and 4h for dexamethasone, budesonide, 17-BMP and triamci-nolone, respectively [2]. FP is also highly selective for the glucocorticoid receptor, with little or no activity at proges-tagen, androgen, oestrogen or mineralocorticoid receptors [1]· The properties of FP have been investigated in a number of systems relevant to the pathophysiology of allergic inflammation. FP is more potent in vitro than dexamethasone, BDP and budesonide in inhibiting anti-CD3-induced human T lymphocyte proliferation, with IC50 values of 0.3, 5.9, 2.0 and 0.8 nM, respectively. Similarly, FP attenuates the expression of adhesion molecules (Eselectin, VCAM) on human endothelial cells in culture stimulated with the cyto-kine, tumour necrosis factor (TNF)-α. The IC5() against E-selectin was 1 nM, compared with 23 nM for dexamethasone and 9.5 nM for budesonide. Higher concentrations of FP (100 nM) were required to inhibit TNF-α-induced VCAM and there was little effect on ICAM expression. In human airway epithelial cells, FP (10 nM) increased mRNA levels for secretory leukocyte protease inhibitor within 24 h and maximal transcript accumulation occurred at 48 h [3]. The rank order of potency of corticosteroids was: FP (EC50: 0.1 ∏M) > triamcinolone (1 nM) > dexamethasone (2nM) > methylprednisolone (5 nM) > hydrocortisone (25 nM). In vivo, by the inhaled route in the guinea pig, FP had an approximately 100-fold higher potency than dexamethasone, BDP and budesonide in inhibiting eosinophil accumulation in the airway