Table 4.

Selected situations in where rebinding is likely to prolong drug/ligand-target binding

Ligand	Target	System
(1)Thyrotropin	Thyrotropin receptors	Human thyroid membranes
(2)Naloxone	µ opioid receptor	Recombinant CHO cells
(3)Sartans	AT1 angiotensin II receptors	Recombinant CHO cells
(4)Spipeone	D2 dopamine receptors	Recombinant CHO cells
(5)Rimonabant, taranabant	CB1 cannabinoid receptors	Recombinant CHO cells
(6)Epidermal growth factor	EGF receptors	A431 cells
(7)Dinitrophenyl ligands	Cell-surface IgE	Rat basophilic leukemia cells
(8)Fibroblast growth factor-2	Heparan sulphate proteoglycans	Vascular smooth muscle cells
(9)Diprenorphine, naloxone	Opioid receptors	Rat brain, in vivo
(10)CH 23390	D1 dopamine receptors	Rat brain, in vivo
(11)Fasciculin 2	Acetylcholinesterase	Neuromuscular junction
(12)Lectins	Selectin	Cell-cell interactions
(13)Peptide-MHC class II ligands	T cell receptors	Cell-cell interactions
(14)Antibodies (also monomeric)	Immobilized ampicillin	BIAcore biosensor

Many other experimental observations in where target binding is shortened by the presence of an excess of other drugs/ligands have been published but they were, rightfully or not, merely commented in view of non-competitive interactions. References: (1) Powell-Jones et al., 1979; (2) Spivak et al., 2006; (3) Fierens et al., 1999; Le et al., 2007; (4) Packeu et al., 2008 (5) Szczuka et al., 2009; Wennerberg et al., 2010; (6) Wiley (1988); (7) Goldstein et al., 1989; Posner et al., 1992; (8) Chu et al., 2004; (9) Perry et al., 1980; (10) Gifford et al., 1998; (11) Krejci et al., 2006; (12) Lou et al., 2006; Thomas, 2006; (13) Germain, 1997; (14) Nieba et al., 1996.