Heparin is a glycosaminoglican used in prophylactic and treatment of thrombosis. Heparin possesses also non-anticoagulant properties, including modulation of various proteases, anticomplement activity, and anti-inflammatory actions. Inhaled heparin has been shown to reduce early phase of asthmatic reaction and suppress allergen induced rise in bronchial hyperreactivity. Heparin inhibits the acute cutaneous reaction due to allergens. Moreover, inhaled heparin prevents exercise-induced asthma. The exact mechanism of heparin action in bronchial asthma remains obscure. It has been observed that heparin acts as a specific blocker of IP3 receptors and inhibits IP3-mediated calcium release in various cell types, including vascular smooth muscle and airway smooth muscle. In this mechanism heparin inhibits allergen induced mast cell degranulation and prevents subsequent development of reaction cascade leading to inflammation, bronchial hyperreactivity and asthma. It also modulates migration of proinflammatory cells, eosinophils and neutrophils, into the site of allergic reaction. Furthermore, heparin inhibits the increased vascular permeability induced by a wide range of agonists acting via specific receptors located on the vascular endothelial cells. The cationic peroxidases, such as major basic protein and eosinophil peroxidase, are neutralized by the highly anionic heparin; thus heparin inhibits the epithelial damage induced by some of these cationic proteins. The mechanism involved in the control of bronchial hyperreactivity by heparin has been studied little and is yet poorly understood. Heparin deserves further investigations in large number of subjects to provide further insight into the pathophysiology of asthma. Heparin may also be of clinical importance and may form the basis of novel therapeutic approaches.