Since its introduction more than 10 years ago, coronary angioplasty has been limited by a 30-40% incidence of restenosis, typically de-veloping within 3-6 months of the procedure. 12 The interactive biological processes responsible for re-stenosis have generally been attributed to varying degrees of three pathological mechanisms. First, depending on the relative fibrocellular, sclerotic, and calcium contents of the atherosclerotic lesion, passive vascular recoil may result in progressive diminution of the maximal coronary dimensional improvement imparted by balloon dilatation. 3 Second, ballooninduced vascular barotrauma, resulting in severe intimal and medial disruption, platelet deposition, and thrombus formation, may provide a potent nidus on which mural thrombus organization, 4 collagen matrix formation, and myointimal proliferation can occur. 5, 6 Last, mitogenic factors released as a result of vascular injury at the time of coronary angioplasty may induce smooth muscle cell hyperplasia, 5 culminating in excessive myointimal proliferation and luminal compromise in some patients. 6 Unfortunately, multiple pharmacological strategies aimed at prevention of restenosis have thus far failed to demonstrate a convincing reduction in its incidence. 7-17 The profound economic importance of the identification of an agent or combination of agents that will reduce restenosis after coronary angioplasty has led to an impressive investment of resources into clinical restenosis trials. Because the number of agents that can be tested in this setting is exceptionally large, for descriptive purposes, these agents can be divided into those that primarily inhibit platelet-specific receptors, platelet mediators, and thrombus formation at the site of coronary angioplasty; smooth muscle cell proliferation; and growth factors (Figure 1). Currently, at least 11 placebo-controlled clinical restenosis trials are ongoing, each varying in preclinical investigation, timingand duration of dosing, and