Table 1.

Typical drugs and biomolecules for anti-thrombosis and anti-restenosis treatment.

Type	Therapeutic substance	Mechanism of action	Therapeutic ability	Drawbacks	References
Drugs	Paclitaxel	Inhibit cell proliferation, adhesion, and migration	Reduce intimal hyperplasia	Indiscriminate cell suppression, delayed re-endothelialization and impaired endothelial functions	(Lundberg et al., 2015; Palmerini et al., 2015)
	Sirolimus/zotarolimus	Interfere cell cycle by inhibiting the mammalian target of rapamycin	Promote re-endothelialization	Long-term safety concerns, late stent thrombosis	(Joner et al., 2006; Park et al., 2010)
Biomolecules	NO and NO-producing materials	Activate soluble guanylate cyclase related signal pathway	Vasodilatation, stimulate EC growth, inhibit SMC proliferation and platelet activation/aggregation	Short-lived, limited diffusion distance, by-products during NO-producing process	De (Mel et al., 2011; Carpenter and Schoenfisch, 2012)
	Antibodies (e.g., CD34 antibody)	Selectively recruit endothelial progenitor cells	Enhance growth of neointimal layer and prevent adhesion of thrombotic tissues	Complex preparation process, high cost, immune response	(Hristov et al., 2003; De Visscher et al., 2012)
	Cell-adhesive peptides (e.g., Arg-Glu-Asp-Val)	Mediate the adsorption and migration of targeted cells	Enhance re-endothelialization and anti-restenosis	Immune response, concerns on complications or undesired tissue growth	(Wei et al., 2013; Mahara et al., 2015)
	Growth factors (e.g., endothelial growth factor)	Promotes EC recruitment, adhesion, migration, and proliferation	Facilitate re-endothelialization	Short half-life, high dose with high cost	(Poh et al., 2010; Shin et al., 2012)
	Heparin	Inhibit the activation of thrombin	Possess anti-coagulant effect and reduce platelet aggregation	Hemorrhage and thrombocytopenia	(Gurbel and Bliden, 2003; Chuang and Masters, 2009)