Potential non-glycoprotein IIb IIIa effects of abciximab

The antithrombotic effect of abciximab is believed to be primarily due to i ts blockade of platelet glycoprotein IIb/IIIa receptors, leading to the inh ibition of platelet aggregation. Studies have, however, identified that ant ibody 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, intim al hyperplasia offer vascular injury, reperfusion injury, and thrombin gene ration, it is possible that some of abciximab's effects relate to this reac tivity. Similarly, because alpha V beta 3 has been implicated in platelet a dhesion to osteopontin, intimal hyperplasia after vascular injury, and plat elet-mediated thrombin generation, ii is possible that some of abciximab's beneficial effects relate to this reactivity. Blockade of alpha V beta 3 re ceptors may also be beneficial in other disease states because, in animal m odels, such blockade inhibits tumor angiogenesis and sickle cell adhesion t o blood vessel endothelium. Despite these intriguing observations, there ar e no direct data to support any beneficial roles or any unwanted side effec ts related to the reactivities of abciximab with "activated" alpha M beta 2 or alpha V beta 3 receptors.