Potential non-glycoprotein IIb IIIa effects of abciximab

The antithrombotic effect of abciximab is believed to be primarily due to its blockade of platelet glycoprotein IIb/IIIa receptors, leading to the inhibition of platelet aggregation. Studies have, however, identified that antibody 7E3, the parent molecule of abciximab, and/or abciximab itself, binds to both "activated" alpha M beta 2 receptors and alpha V beta 3 receptors. Because alpha M beta 2 receptors are present on granulocytes and monocytes, cells that have been implicated in contributing to atherosclerosis, intimal hyperplasia offer vascular injury, reperfusion injury, and thrombin generation, it is possible that some of abciximab's effects relate to this reactivity. Similarly, because alpha V beta 3 has been implicated in platelet adhesion to osteopontin, intimal hyperplasia after vascular injury, and platelet-mediated thrombin generation, ii is possible that some of abciximab's beneficial effects relate to this reactivity. Blockade of alpha V beta 3 receptors may also be beneficial in other disease states because, in animal models, such blockade inhibits tumor angiogenesis and sickle cell adhesion to blood vessel endothelium. Despite these intriguing observations, there are no direct data to support any beneficial roles or any unwanted side effects related to the reactivities of abciximab with "activated" alpha M beta 2 or alpha V beta 3 receptors.