FIGURES AND TABLES
FROM:
Pharmacological Onomastics: What's in a name?
T P Kenakin
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Figure 1.
A sample of interactions of seven transmembrane receptors with cellular components to generate phenotypes of efficacy. Specific assays are available to isolate these processes and define molecular activity associated with them. It should be noted that cellular response does not automatically indicate interactions of the ligand-bound receptor with some of these processes (that is, is not a universal indicator of molecular efficacy).
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Figure 2.
Schematic diagram of parathyroid hormone (PTH) and analogues as activators of two separate pathways for extracellular signal kinase activation, namely G-protein-dependent (blue) and 
-arrestin G-protein-independent (red). PTH-1A=[D-Trp12,Tyr34]PTH-(7–34). Data from Gesty-Palmer et al. (2006).
Figure 3.
The classification of
2-adrenoceptor ligands. Eight
2-adrenoceptor ligands can be distinguished as positive and inverse agonists and neutral antagonists for adenylate cyclase (Gs-protein-mediated response) and agonists or inverse agonists for ERK1/2 signalling. Data from Galandrin and Bouvier (2006), Azzi et al. (2003) and Baker et al. (2003).
Figure 4.
Hypothetical dose–response curves for four molecules with different patterns of efficacy. The system is constitutively active (fractional effect=0.4) and then placed under an additional endogenous agonist tone to a level of 0.6 fractional effect. A partial agonist decreases the endogenous tone but imposes its own intrinsic activity on the system, a neutral competitive antagonist abolishes the endogenous tone but does not eliminate constitutive activity, a protean agonist reduces the constitutive activity somewhat but imposes its own intrinsic effect and an inverse agonist abolishes both the endogenous tone and the constitutive activity.
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