Abstract:
Introduction. Antiplatelet medication plays an essential role in prevention and healing of thrombotic
affections such as myocardial infarction or cerebrovascular accident. Despite the shown efficiency in the
prevention of ischemic events, bleeding issues, thrombocytopenia, and recurrent thrombotic events serve
as an impulse for the elaboration of new medicine that will remove thrombotic risks without effects on
hemostasis. Platelet adhesive receptors, coagulation process phases and thrombin receptors represent the
main targets in the elaboration of new antiplatelet medicine.
Aim of study. The goal is to identify the progress of new antiplatelet medicine development in scientific
literature.
Methods and materials. This workpaper is realized on the analytical basis of the articles published
between 2018-2022 on PubMed and Google Scholar. The most relevant articles were selected with the help
of key word antiplatelet and the generic name of medicines.
Results. In current therapy are more commonly used cyclooxygenase inhibitors (acetylsalicylic acid,
triflusal), P2Y12 purinergic receptors antagonists (clopidogrel, prasugrel, ticagrelor, cangrelor, regrelor,
elinogrel), GPIIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban, xemilofiban, orbofiban,
sibrafiban, etc.) and PAR-1 antagonists (voraxapar, atopaxar). The new antiplatelet drugs are in preclinical
and clinical trials, targeting the following platelet receptors and pathways: receptors P2Y12 (selatogrel,
AZD1283, SAR21647) and P2Y1 (BMS-884775), phosphoinositide 3-kinase (AZD6482, TGX-221,
idelalisib), protein disulfide-isomerase (isoquercetin, ML359), GPIIb/IIIa receptor (elarofiban, RUC-1,
RUC-4), protease-activated receptor 4 (BMS-986120), GPVI (revacept, losartan, scFv9012, Troa6 și
Troa10), GPIb-IX-V (caplacizumab, antifibatide), 12-lipoxygenase (ML355), P-selectin (rPSGL-Ig, PSI697, PSI-421), CD40 (anti-CD40, Ab), prostacyclin analogs (iloprost, treprostinil, beraprost),
phosphodiesterase 3 (dipiridamol, cilostazol, anagrelide, milrinone), glucagon like peptide 1 receptor
(exenatide), thromboxane–prostaglandin receptor (ramatroban, ridogrel, seratrodast, terutroban), serotonin
5-HT2A receptor (APD791), prostanoid EP3 receptor, nitric oxide donors.
Conclusion. The studies on mechanism of platelet blood clots formation have developed new antiplatelet
therapies that would reduce side effects and would offer new perspectives on adapting the antiplatelet
therapy on patient´s pathophysiology. For the realization of this goal, new studies are needed that should
evaluate the therapeutic efficiency and the ability of new medications to prevent recurrent thrombotic
events.
