CTOP acetate is a somatostatin analogue and a μ-opioid receptor antagonist.

CTOP acetate increased a K+ conductance with an EC50 of 560 nM. The K+ currents induced by high concentrations of CTOP acetate desensitized to 42% of the initial maximum after prolonged superfusion (t1/2 = 247 sec). In the presence of fully desensitized CTOP acetate responses, somatostatin (1 microM) still produced near-maximal K+ currents; i.e., there was no cross-desensitization, which suggests that CTOP acetate might act on a receptor distinct from somatostatin receptors. However, the converse did not apply; high concentrations of CTOP acetate (30 microM) did not produce any additional current in the presence of desensitized somatostatin responses[2].

Intracerebroventricular (i.c.v.) administration of CTOP acetate antagonized the analgesic effect of morphine in a dose-dependent manner, as measured by the heat-irradiant (tail-flick) method. CTOP acetate was more effective than naloxone in inhibiting analgesia on a molar basis. CTOP acetate also antagonized the acute morphine-induced hypermotility. CTOP acetate caused withdrawal hypothermia and a loss of body weight in morphine-dependent animals. After the development of morphine-induced chronic dependence, CTOP acetate administered i.c.v. caused a dose-dependent loss of body weight and hypothermia, and was about 10-400 times more potent than naloxone. CTOP acetate administered alone to drugnaive mice did not cause antinociception, changes in body weight or body temperature[1].