For research use only. Not for therapeutic Use.
CTOP TFA is a potent and highly selective μ-opioid receptor antagonist. CTOP TFA antagonizes the acute analgesic effect and hypermotility. CTOP TFA enhances extracellular dopamine levels in the nucleus accumbens. CTOP TFA dose-dependently enhances locomotor activity[1][2].
CTOP TFA (0-0.5 nmol, ICV, once) antagonizes the analgesic effect in a dose-dependent manner[1].
CTOP TFA (0-2 nmol, ICV, once) causes withdrawal hypothermia and a loss of body weight in animals[1].
CTOP TFA (0-1.5 nmol per side, Intra-VTA injection) enhances extracellular dopamine levels in the nucleus accumbens and dose-dependently enhances locomotor activity[2].
Catalog Number | I045801 |
Molecular Formula | OC(C(F)(F)F)=O.O=C(N[C@@H]1CC2=CNC3=CC=CC=C23)[C@H](CC4=CC=C(O)C=C4)NC([C@@H](NC([C@@H](CC5=CC=CC=C5)N)=O)CSSC([C@@H](C(N[C@@H]([C@@H](C)O)C(N)=O)=O)NC([C@]([H])([C@@H](C)O)NC([C@H](CCCN)NC1=O)=O)=O)(C)C)=O.[x] |
Purity | ≥95% |
Reference | [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. |