 Next, let's discuss the ADP receptor blockers. ADP receptor blockers irreversely block ADP from binding to the P2Y12 receptor, which will prevent subsequent platelet aggregation. The P2Y12 G-coupled receptor is activated when ADP binds to it, causing an inhibition of the adenomal cyclase, therefore decreasing intracellular levels of cyclic AMP. When we see that decrease of cyclic AMP, it's going to reduce the phosphorylation of a vasodilator stimulated phosphoprotein, which will cause an activation of glycoprotein 2B in 3A receptors. Therefore, no platelet aggregation occurs due to this expression of this G2B3A platelet on the surface of the platelets. We use this in acute coronary syndrome and coronary stinting. So if you have stints placed into your heart, we can use the ADP receptor blocker to keep anything from binding to that stint, causing a clot, and completely reversing the effects that we have been able to establish with the use of that stint. Side effects for ADP receptor blockers include neutropenia, and we can also see really TTP, which is thrombotic thrombocytopenic perpura. Examples of ADP receptor blockers include clopidogrel, which is also known as plavix, parasugral, ticagralor, and ticlotopine. Finally, let's discuss our glycoprotein 2B3A inhibitors. As with our previous ADP receptor blockers, glycoprotein 2B3A inhibitors are going to be inhibiting platelet aggregation. They do this, however, by binding to the actual receptor that's on activated platelets. Our ADP blockers that we previously discussed keeps this glycoprotein from even being expressed on platelets, so they're not even activated. This medication, however, will block the receptor on platelets that have already been activated. Therefore, that's going to prevent our platelet from aggregating. This is used in unstable angina and during percutaneous coronary intervention. Side effects include bleeding as well as thrombocytopenia. Examples of our glycoprotein 2B3A inhibitors include absyximab, epithepotide, and tyrophibin.