Background
CTOP is a peptide antagonist of the μ-opioid receptor (IC50 = 2.8 nM).1 It is selective for μ-opioid receptors over δ-opioid receptors (IC50 = 13,500 nM) and somatostatin receptors (IC50 = 24,000 nM). CTOP inhibits the antinociceptive effect of morphine in the tail flick test in mice (ED50 = 0.018 nmol) and reverses morphine-induced increases in locomotor activity (ED50 = 0.02 nmol).2 It also induces withdrawal symptoms in a mouse model of chronic, but not acute, morphine dependence.
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