Other notable TP receptor antagonists are Seratrodast (AA-2414), Terutroban (S18886), PTA2, 13-APA, GR-32191, Sulotroban (BM-13177), SQ-29,548, SQ-28,668, ONO-3708, Bay U3405, EP-045, BMS-180,291, and S-145. Many of these TP receptor antagonists have been evaluated as potential therapeutic agents for asthma, thrombosis and hypertension. These evaluations indicate that TP receptor antagonists can be more effective than drugs which selectively block the production of TXA2 thromboxane synthase inhibitors. This seemingly paradoxical result may reflect the ability of PGH2, whose production is not blocked by the inhibitors, to substitute for TXA2 in activating TP. Novel TP receptor antagonists that also have activity in reducing TXA2 production by inhibiting cyclooxygenases have been discovered and are in development for testing in animal models. TP is classified as a contractile type of prostenoid receptor based on its ability to contract diverse types of smooth muscle-containing tissues such as those of the lung, intestines, and uterus. TP contracts smooth muscle and stimulates various response in a wide range of other cell tytes by coupling with and mobilizing one or more families of the G protein class of receptor-regulated cell signaling molecules. When bound to TXA2, PGH2, or other of its agonists, TP mobilizes members of the:  Following its activation of these pathways, the TP receptors's cell-stimulating ability rapidly reverses by a process termed homologous desensitization, i.e. TP is no longer able to mobilize its G protein targets or further stimulate cell function. Subsequently, the β but not α isoform of TP undergoes receptor internalization. These receptor down regulating events are triggered by the G protein-coupled receptor kinases mobilized during TP receptor activation. TP receptor-independent agents that stimulate cells to activate protein kinases C or protein kinases A can also down-regulate TP in a process termed heterologous desensitization. For example, prostacyclin I2 (PGI2)-induced activation of its prostacyclin receptor (IP) and prostaglandin D2-induced activation of its prostaglandin DP1 receptor cause TP receptor desensitization by activating protein kinases A while prostaglandin F2alpha-induced activation of its prostaglandin F receptor and prostaglandin E2-induced activation of its prostaglandin EP1 receptor receptor desensitizes TP by activating protein kinases C.