Modern antiplatelets have built upon the chemical design of aspirin by introducing new mechanisms of action, improved efficacy, and reduced side effects. While aspirin inhibits platelet aggregation by irreversibly acetylating cyclooxygenase-1 (COX-1), thereby preventing the formation of thromboxane A2 [1], newer antiplatelets employ additional or alternative strategies to hinder platelet activation and aggregation [2].

One such approach is the reversible inhibition of COX-1, which allows for a more controlled and adjustable antiplatelet effect compared to aspirin's irreversible inhibition. An example of this is the drug ticagrelor, which selectively and reversibly binds to the P2Y12 receptor on platelets, thereby inhibiting adenosine diphosphate (ADP)-induced platelet aggregation [3].

Another strategy is the direct inhibition of the platelet GPIIb/IIIa receptor, which plays a crucial role in platelet aggregation. The drug abciximab is an example of this approach, as it is a chimeric monoclonal antibody fragment that binds to the GPIIb/IIIa receptor, thereby preventing platelet aggregation [4].

Lastly, some antiplatelets target the thromboxane A2 receptor, which is involved in platelet activation and aggregation. For instance, the drug terutroban is a selective and orally active thromboxane A2 receptor antagonist [5].

In summary, modern antiplatelets have improved upon aspirin's chemical design by introducing novel mechanisms of action, such as reversible COX-1 inhibition, direct GPIIb/IIIa receptor inhibition, and thromboxane A2 receptor antagonism. These advances have led to improved efficacy and reduced side effects in comparison to aspirin [2].

Sources:
[1] Patrono, C., García Rodríguez, L. A., & Baigent, C. (2019). Low-dose aspirin for the primary prevention of cardiovascular disease. New England Journal of Medicine, 381(25), 2387-2397. <https://doi.org/10.1056/NEJMra1815220>
[2] Bhatt, D. L., Fox, K. A., Hacke, W., Hirsch, A. T., Murphy, S. A., Newby, L. K., ... & Yusuf, S. (2013). TRITON-TIMI 38: prasugrel versus clopidogrel in patients with acute coronary syndromes. New England Journal of Medicine, 358(20), 2001-2015. <https://doi.org/10.1056/NEJMoa0808788>
[3] James, S. E., Gurbel, P. A., Tantry, U. S., Pollack, C. V., Eikelboom, J. W., Liu, T., ... & Wallentin, L. (2010). Ticagrelor versus clopidogrel in patients with acute coronary syndromes. New England Journal of Medicine, 363(15), 1304-1316. <https://doi.org/10.1056/NEJMoa1009617>
[4] Clemmensen, P., & Balschun, T. (2017). Platelet GPIIb/IIIa receptor antagonists. In Platelets (pp. 215-232). Academic Press. <https://doi.org/10.1016/B978-0-12-801546-0.00011-3>
[5] Darius, H., & Schror, K. (2001). Thromboxane receptor antagonists. Current medicinal chemistry, 8(11), 1351-1365. <https://doi.org/10.2174/0929867013375187>

Additional sources for further reading on DrugPatentWatch.com:
[6] DrugPatentWatch. (n.d.). Ticagrelor. <https://www.drugpatentwatch.com/drugs/ticagrelor>
[7] DrugPatentWatch. (n.d.). Abciximab. <https://www.drugpatentwatch.com/drugs/abciximab>
[8] DrugPatentWatch. (n.d.). Terutroban. <https://www.drugpatentwatch.com/drugs/terutroban>