Abciximab, a chimeric (murine/human) monoclonal antibody fragment (c7E3 Fab), is a glycoprotein IIb/IIIa antagonist [1]. Abciximab inhibits platelet aggregation and leucocyte adhesion by binding to the glycoprotein IIb/IIIa, vitronectin and Mac-1 receptors [2]. Abciximab has been used to destabilize coronary thrombi and disperse mural thrombi [3].
In vitro, Abciximab treatment for 24 hours significantly inhibited the chemotaxis and invasion of human coronary smooth muscle cells (hcSMCs), with IC50 value of 33.0μg/ml and 0.5μg/ml, respectively [4]. Treatment with 10μg/ml Abciximab for 30 minutes decreased generation of new thrombin on both collagen-coated platelets and clot-adherent platelet [5].
References:
[1] Tcheng J E, Kereiakes D J, Lincoff A M, et al. Abciximab readministration: results of the ReoPro Readministration Registry[J]. Circulation, 2001, 104(8): 870-875.
[2] Ibbotson T, McGavin J K, Goa K L. Abciximab: an updated review of its therapeutic use in patients with ischaemic heart disease undergoing percutaneous coronary revascularisation[J]. Drugs, 2003, 63(11): 1121-1163.
[3] Marciniak Jr S J, Mascelli M A, Furman M I, et al. An additional mechanism of action of abciximab: dispersal of newly formed platelet aggregates[J]. Thrombosis and haemostasis, 2002, 87(06): 1020-1025.
[4] Blindt R, Bosserhoff A K, Zeiffer U, et al. Abciximab inhibits the migration and invasion potential of human coronary artery smooth muscle cells[J]. Journal of Molecular and Cellular Cardiology, 2000, 32(12): 2195-2206.
[5] Ilveskero S, Lassila R. Abciximab inhibits procoagulant activity but not the release reaction upon collagen-or clot-adherent platelets[J]. Journal of Thrombosis and Haemostasis, 2003, 1(4): 805-813.