TXA Synthase Activators represent a class of chemicals that can exert influence on the TXA Synthase (TBXAS1) pathway, a crucial component in the synthesis of thromboxane A2. Arachidonic Acid is one of the primary agents associated with this pathway, serving as the precursor for thromboxane A2 synthesis. An increase in its levels can amplify TXA production. The Calcium ionophore A23187 has been shown to induce the release of arachidonic acid, thus acting as an indirect activator by supplying more of the TXA precursor. Phorbol 12-myristate 13-acetate (PMA) is another chemical that exerts its influence on the TXA Synthase pathway by activating PKC, which in turn induces arachidonic acid release, a significant factor in enhancing TXA production. Furthermore, Forskolin can modulate TXA Synthase activity by raising cAMP levels. On the other hand, Eicosapentaenoic acid (EPA) has a dual role. While it competes with arachidonic acid, high doses of EPA can increase TXA production.
Additionally, a series of COX inhibitors can indirectly influence TXA Synthase activity by altering the synthesis of prostaglandins, which play a role in the TXA pathway. Rofecoxib and Celecoxib are selective COX-2 inhibitors that can bring about this alteration. Non-selective COX inhibitors, such as Indomethacin, Aspirin (acetylsalicylic acid), Naproxen, and Ibuprofen, can also impact the prostaglandins and thereby the thromboxane synthesis pathway. Meloxicam, as a preferential COX-2 inhibitor, can modify the prostaglandin levels, which in turn affect TXA Synthase activity.
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