Shape change and release reaction indicate different degrees of the complex platelet response termed activation. Aggregation is a variable consequence of activation. Aggregation shows a temperature dependency opposite to that shown by the preceding shape change. Aggregation increases at lower temperature and requires, in contrast to activation, extracellular Ca2+, stirring, and at a low degree of activation the presence of fibrinogen. Aggregation can enhance activation by triggering prostaglandin endoperoxide-thromboxane synthesis. If activation reaches a high level associated with the release reaction, activation is further amplified by prostaglandin endoperoxide-thromboxane synthesis emerging independent of aggregation. These mechanisms of amplification of activation are blocked by indomethacin, an inhibitor of prostaglandin endoperoxide-thromboxane synthesis = anti-activating agent. In contrast, anti-aggregating agents, exemplified here with n-acetyl neuraminic acid, attack the aggregation of activated platelets but neither activation nor prostaglandin endoperoxide-thromboxane synthesis. Its anti-aggregating effect, in addition, enables n-acetyl neuraminic acid to imitate the inhibitory effect of indomethacin on the feedback amplification which results from aggregation. Anti-aggregating agents as characterized here may open a new valuable concept for anti-aggregation in vivo.