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Stimulation of Cholecystokinin‐A Receptors With Gl181771X: A Failed Clinical Trial That Did Not Test the Pharmacogenetic Hypothesis for Reduction of Food Intake
Author(s) -
Roses AD
Publication year - 2009
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.2008.192
Subject(s) - context (archaeology) , cholecystokinin , clinical pharmacology , blame , pharmacology , pharmacogenetics , clinical trial , drug , medicine , psychology , receptor , psychiatry , biology , gene , paleontology , biochemistry , genotype
There are two interacting components in a clinical trial: the drug and the study design. When a trial does not work, we blame the drug—and the study is usually not published. This Commentary provides a context for the use of efficacy pipeline pharmacogenetics (PGx) in therapeutic programs. Jordan et al . published the results of an obesity trial with a cholecystokinin‐A (CCK‐A) receptor agonist and concluded that CCK‐A by itself does not have a central role in long‐term energy balance. The conclusions were sound, the report accurate, and the journal commendable for publishing a negative study, but the trial design was misdirected—it did not build on phase IIA information and did not test the proposed mechanism of action. The hypotheses should have been based on the original putative role of a central mechanism affecting appetite, which had been validated using efficacy PGx in phase IIA. Clinical Pharmacology & Therapeutics (2009); 85 , 4, 362–365 doi: 10.1038/clpt.2008.192