It has been established that platelet aggregation plays an important role in the physiopathology of unstable angina. Despite conventional therapy associating aspirin and heparin, the morbidity and mortality of unstable angina remain high with 8 to 10% of fatalities or infarcts in the weeks following the acute episode. Research for new antiplatelet agents has been concentrated on developing molecules which block the GPIIb/IIIa receptors which are the final step of platelet aggregation. Two main families of the GPIIb/IIIa receptor inhibitors may be distinguished: 1) non-specific inhibitors which are the best known and most widely studied, amongst which the c7E3, 2) specific antagonists such as cyclic peptides or "peptido-mimetic" agents. Most clinical experience has been obtained with c7E3 (ReoPro) which has been shown to be very effective in reducing the complications of coronary angioplasty in patients with unstable angina in the CAPTURE and EPIC trials. However, this agent increases the risk of bleeding, especially in cases of overdosage of heparin. The efficacy of specific inhibitors (integrelin, lamifiban, tirofiban) has been suggested in clinical trials but on limited numbers of patients. In conclusion, blockers of the GPIIb/IIIa receptors are an interesting therapeutic innovation in patients with unstable angina. The optimal mode of usage and precise indications of this new therapeutic class should become clear after several phase III trials under way at present.