CTOP TFA is a specific μ-opioid receptor antagonist. CTOP TFA antagonizes morphine-induced acute analgesia and hyperkinesia. CTOP TFA increases extracellular dopamine levels in the nucleus accumbens. CTOP TFA dose-dependently enhances exercise capacity.

Physicochemical Properties

Molecular Formula	C52H68F3N11O13S2
Molecular Weight	1176.28
Related CAS #	CTOP;103429-31-8
Appearance	White to off-white solid powder
HS Tariff Code	2934.99.9001
Storage	Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.
Shipping Condition	Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Biological Activity

Targets	μ Opioid Receptor/MOR
ln Vivo	In a dose-dependent manner, CTOP TFA (0-0.5 nmol, ICV, once) counteracts the analgesic effect[1]. Animals exposed to CTOP TFA (0–2 nmol, ICV, once) experience withdrawal hypothermia and body weight loss[ 1]. In the nucleus accumbens, CTOP TFA (0–1.5 nmol per side, Intra-VTA injection) raises extracellular dopamine levels and dose-dependently increases locomotor activity[2].
Animal Protocol	Animal/Disease Models: Male CFLP mice (25-30 g)[ 1] Doses: 0, 0.001, 0.05, 0.075, 0.1, and 0.5 nmol (made up in artificial cerebrospinal fluid (CSF) and kept in plastic tubes at -25℃ until use) Route of Administration: Intracerebroventricular (icv) administration, once Experimental Results: Antagonized the analgesic effect in a dose-dependent manner, antagonized the induced hypermotility in a dose-dependent manner. Animal/Disease Models: Male CFLP mice (25-30 g, Acute dependence to morphine was induced by a single dependence-inducing (100 mg/ kg) dose of morphine-HC1)[1] Doses: 0, 0.001, 0.05, 0.2, and 2 nmol Route of Administration: Intracerebroventricular (icv) administration, once Experimental Results: diminished the body temperature in a dose-dependent manner, and caused withdrawal hypothermia and a loss of body weight in animals. Animal/Disease Models: Long-Evans hooded rats (12, male, 350-450 g)[2] Doses: 0, 0.015, 0.15, and 1.5 nmol per side Route of Administration: Intra-VTA (ventral tegmental area) injection Experimental Results: Enhanced extracellular dopamine levels in the nucleus accumbens, dose-dependently increased activity, whereas had no effect on feeding and drinking behavior.
References	[1]. 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]. Intra-VTA injections of the mu-opioid antagonist CTOP enhance locomotor activity. Brain Res. 1995 Aug 28;690(1):112-6.

Solubility Data

Solubility (In Vitro)	H2O :~50 mg/mL (~42.51 mM)
Solubility (In Vivo)	Solubility in Formulation 1: 100 mg/mL (85.01 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.  (Please use freshly prepared in vivo formulations for optimal results.)

Preparing Stock Solutions		1 mg	5 mg	10 mg
	1 mM	0.8501 mL	4.2507 mL	8.5014 mL
	5 mM	0.1700 mL	0.8501 mL	1.7003 mL
	10 mM	0.0850 mL	0.4251 mL	0.8501 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.