The thromboxanes were isolated from blood platelets, and whilst TXA2 showed high biological activity TXB2 was only weakly active. TXA2 causes blood platelets to aggregate to form a clot or thrombus, by increasing cytoplasmic calcium concentrations and thus deforming the platelets which then fuse together. It has the opposite effect to PGI2, and presumably the development of thrombosis reflects an imbalance in the two activities. Both compounds are produced from the same precursor, PGH2, which is converted in the blood platelets to TXA2, and in the blood vessel wall to PGI2. Thromboxanes A3 and B3 have also been isolated from blood platelets, are structurally analogous to prostaglandins in the 3-series, and are derived from A5'8'11'14'17-eicosapentaenoic acid. TXA3 is not strongly aggregatory towards blood platelets. The highly unstable nature of the biologically active thromboxanes has made their synthesis difficult, and drug use of natural structures will probably be impracticable. It is likely that most efforts will be directed towards thromboxane antagonists to help reduce blood platelet aggregation in thrombosis patients. The value of aspirin in preventing cardiovascular disease is now known to be related to inhibition of thromboxane A2 biosynthesis in platelets.

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