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CTOP is a potent and highly selective μ-opioid receptor antagonist. CTOP antagonizes the acute morphine-induced analgesic effect and hypermotility. CTOP enhances extracellular dopamine levels in the nucleus accumbens. CTOP dose-dependently enhances locomotor activity[1][2].—Neuroscience-Neuromodulation–C50H67N11O11S2—-[1]Gulya K, et al. Central effects of the potent and highly selective μ opioid antagonist D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) in mice. Eur J Pharmacol. 1988 Jun 10;150(3):355-60.|[2]Badiani A, et al. Intra-VTA injections of the mu-opioid antagonist CTOP enhance locomotor activity. Brain Res. 1995 Aug 28;690(1):112-6. –103429-31-8–1062.26—-C(C=1C=2C(NC1)=CC=CC2)[C@H]3NC(=O)[C@H](CC4=CC=C(O)C=C4)NC(=O)[C@@H](NC([C@@H](CC5=CC=CC=C5)N)=O)CSSC(C)(C)[C@@H](C(N[C@@H]([C@@H](C)O)C(N)=O)=O)NC(=O)[C@]([C@@H](C)O)(NC(=O)[C@H](CCCN)NC3=O)[H]–Neurological Disease–10 mM in DMSO–Opioid Receptor–μ Opioid Receptor/MOR–GPCR/G Protein;Neuronal Signaling–Peptides