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Thromboxane A2 inhibitors

Monge, A., Aldana, L, Erro, A., Parrado, P., Font, M., Rocha, E., Prieto, L, Fremont-Smith, M. and Fernandez-Alvarez, E. 1984. New synthetic thromboxane A2 inhibitors with the pyridazine[4,5-b]indole and pyridazine[4,5-a]indole structures as platelet antiaggre-gants. Anal. R. Acad. Farm. 50(3) 365-377. [Pg.64]

The advent of COX-2-selective inhibitors has led to unexpected results. By selectively inhibiting the COX-2 isoform, COX-2-selective NSAIDs increase the risk of cardiovascular events in certain patientsP COX-2 is responsible for the production of prostacyclin, a vasodilatory and antiplatelet substance. On the other hand, COX-1 controls the production of thromboxane A2, a vasoconstrictor and platelet aggregator. Selective inhibition of COX-2 results in decreased prostacyclin levels in the face of stable thromboxane A2 levels. An imbalance in the thromboxane A2 prostacyclin ratio ensues, which creates an environment that favors thrombosis. [Pg.886]

The widely used platelet inhibitor aspirin or acetylsalicylic acid, by acetylating the enzyme cyclooxygenase, inhibits platelet function by preventing the formation of thromboxane A2 and the synthesis of prostaglandin I2 (PGI2) (68). Aspirin has been used in combination with other antiplatelet agents such as ticlopidine, which inhibits ADP-induced platelet aggregation (69). [Pg.151]

Drugs that target other sites of platelet action include thromboxane synthetase inhibitors, serotonin or 5-hydroxytryptamine (5-HT2) receptor blockers, and thromboxane A2 receptor blockers, in addition to cyclooxygenase inhibitors and prostaglandin analogues. [Pg.151]

Dipyridamole is a platelet adhesion inhibitor, although the mechanism of action has not been fully elucidated. The mechanism may relate to 1) Inhibition of red blood cell uptake of adenosine, itself an inhibitor of platelet reactivity, 2) phosphodiesterase inhibition leading to increased cyclic-3 , 5 -adenosine monophosphate within platelets and, 3) inhibition of thromboxane A2 formation,... [Pg.95]

Certain structural indications of thromboxane A2 biosynthesis inhibition and hence potential therapeutic utility in arterial thrombosis prompted the synthesis of the pyridine prostanoid 544 (Scheme 165) (83TL3291). Brief metalation of 42 followed by DMF quench afforded aldehyde 541, which upon Homer-Emmons chain extension, reduction, and protection gave 542. Having served as a DMG, the bromo function was subjected to metal-halogen exchange, transmetalation (CuCN), and condensation with an iodo allene to furnish the 3,4-disubstituted pyridine 543. The latter was transformed into two derivatives 544 (with and without double bond), which were shown to be effective inhibitors of thromboxane A2. [Pg.281]

Synthesis of quinone derivatives containing saturated O-heterocyclic substituents as 5-lipoxygenase inhibitors and antagonists of thromboxane A2 receptors 92YGK786. [Pg.307]


See other pages where Thromboxane A2 inhibitors is mentioned: [Pg.1984]    [Pg.170]    [Pg.1984]    [Pg.185]    [Pg.192]    [Pg.132]    [Pg.1984]    [Pg.170]    [Pg.1984]    [Pg.185]    [Pg.192]    [Pg.132]    [Pg.169]    [Pg.866]    [Pg.874]    [Pg.137]    [Pg.84]    [Pg.160]    [Pg.17]    [Pg.520]    [Pg.98]    [Pg.95]    [Pg.1]    [Pg.61]    [Pg.328]    [Pg.328]    [Pg.542]    [Pg.316]    [Pg.9]    [Pg.19]    [Pg.70]    [Pg.263]    [Pg.593]    [Pg.4]    [Pg.10]    [Pg.39]    [Pg.59]    [Pg.95]    [Pg.129]    [Pg.15]    [Pg.457]    [Pg.126]    [Pg.131]   
See also in sourсe #XX -- [ Pg.177 ]




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