Lung tissues produce a large amount of Thromboxane (Tx) A2. In addition to platelet aggregation and artery smooth muscle contraction, TxA2 strongly induces airway smooth muscle contraction and bronchial hyperresponsiveness. Not only TxA2, but many arachidonate cyclooxygenase metabolites such as PGD2, PGF2 alpha, PGH2, and others stimulate TP (PGH2/TxA2) receptor and can take a pathophysiological role for bronchial asthma. Several compounds competitively antagonizing TP receptor have been developed and being proved to have beneficial effects for treating of bronchial asthma in clinical. In this review the efficacy and usage of TP receptor antagonists for bronchial asthma was discussed.