Bioactivity | 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]. | ||||||
In Vivo | 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]. Animal Model: | ||||||
Name | CTOP TFA | ||||||
Sequence | Phe-Cys-Tyr-Trp-{Orn}-Thr-{Pen}-Thr-NH2 (Disulfide bridge:Cys2-Pen7) | ||||||
Shortening | FCYW{Orn}T{Pen}T-NH2 (Disulfide bridge:Cys2-Pen7) | ||||||
Formula | C52H68F3N11O13S2 | ||||||
Molar Mass | 1176.28 | ||||||
Appearance | Solid | ||||||
Transport | Room temperature in continental US; may vary elsewhere. | ||||||
Storage | Sealed storage, away from moisture and light
*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light) |
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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. |