Rupture of atherosclerotic plaque and thrombosis are the main pathological mechanisms of ACS. Rupture of unstable atherosclerotic plaques in the coronary artery and destruction of coronary endothelium during and after PCI expose the lower vascular intima, platelet adhesion, activation and degranulation release various vasoactive substances such as ADP and 5-hydroxytryptamine, induce further aggregation and activation of platelets, and change the conformation of platelet GPⅡb/Ⅲa receptors. When the fibrinogen binding site is exposed, activated platelets cross-link with fibrinogen through conformational change of GPⅡb/Ⅲa receptors, and eventually a large number of platelets aggregate to form thrombosis, leading to the occurrence of ischemic complications of ACS. It can be seen from the above processes that platelet aggregation plays an important role in the pathogenesis of ACS. GPⅡb/Ⅲa receptor is the final common pathway for platelet thrombosis, and GPⅡb/Ⅲa receptor antagonists can effectively block this process. A number of large-scale clinical trials have found that the application of GPⅡb/Ⅲa receptor antagonists in ACS patients can improve myocardial ischemia, reduce mortality and the incidence of myocardial infarction. Etiba Chemicalbook peptide has a modified lysine-glycine-aspartate amino acid chain, which can bind to the GPⅡb/Ⅲa receptor, and block the GPⅡb/Ⅲa receptor, so that coagulation factor I can not bind to the platelet GPⅡb/Ⅲa receptor, and play an anti-platelet aggregation effect. The inhibition of etifibatide on GDPⅱb /Ⅲa receptor was competitive and concentration-dependent. Compared with the monoclonal antibody abximab, etifibatide binds to GPⅡb/Ⅲa more strongly, specifically and specifically due to the presence of a single conserved amino acid substitution - lysine substitution for arginine, and Abximab binds to the glass adhesion protein receptor αvβ3 in addition to GPⅡb/Ⅲa. In addition, the binding of etifibatide to the GPⅡb/Ⅲa receptor is reversible, the effect is reduced by half at 4h after withdrawal, and the drug effect can be rapidly reversed with the termination of administration without increasing the risk of bleeding. And some studies have shown that the administration of etifibatide did not detect serum antibodies, no immune response was found. Therefore, the application of etifibatide for a longer period of time or repeated treatment is feasible.

integrilin is a novel polypeptide platelet glycoprotein Ⅱb/Ⅲa receptor antagonist, which inhibits platelet aggregation and thrombosis through the last common pathway of inhibiting platelet aggregation. Compared with the monoclonal antibody abximab, etifibatide has stronger, more Chemicalbook directed and specific binding to GDPⅱB /Ⅲa due to the presence of a single conserved amino acid substitution, lysine substitution for arginine. Therefore, it should have a good therapeutic effect in the interventional therapy of acute coronary syndrome. Many platelet glycoprotein Ⅱb / Ⅲa receptor antagonists have been developed. At present, there are three preparations that can be used in clinical practice internationally, abciximab, eptifibatide and tirofiban.