Substance P (SP) is a peptide comprising eleven amino acids. In 1931 von Euler and Gaddum1 suggested its ex-istence in the extract of mammalian and avian guts. The confirmed structure of SP was finally sequenced by Chang et al. 2 in 1971 as Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2. SP is a member of the tachykinin family of peptides which have similar amino acidsequences at the car boxy terminal. Three particular peptides within the family, namely SP, neurokinin A (NKA), 3 and neuro-kinin B (NKB), 4 are termed neurokinins. The receptors of the neurokinins are now classified into the following three subtypes, NK1 (NK2, and NK3, which have high affinity to SP, NKA, and NKB, respectively. 5 Numerous physiological activities of SP such as vasodilation, saliva-tion, contraction of smooth muscle, and so forth have been reported as reviewed. 6 Conventional research on the etiology of asthma has focused on the allergic reaction as mediated by histamine, leukotrienes, prostaglandins, PAF, and so on. Recently, however, Barnes and Lundberg have proposed another mechanism in which SP participates. 7 SP is distributed in sensory nerves C-fibers in the human airway. Thestimuli to the epithelium of the airway results in the release of SP from its nerve endings by the so called axon reflex mechanism. The physiological actions of re-leased SP lead to the pathological features of asthma, eg bronchoconstriction, mucus hypersecretion, and microvascular leakage. This mechanism is referred as “neurogenic inflammation” by Barnes et al. Standing on the foundation of these roles of SP in asthma, we assumed that an antagonist of SP would be able to modulate the SP-induced functions in the airway and consequently could be developed as a new type of antiasthmatic drug totally different fromthe currently available antihistamines, mediator release inhibitors, and bronchodilators.