CTOP
Based on 1 publication(s) in Google Scholar
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.
For research use only. We do not sell to patients.
- CAS No.: 103429-31-8
- Formula: C50H67N11O11S2
- Molecular Weight:1062.26
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) CTOP
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Biological Activity
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μ Opioid Receptor/MOR |
CTOP (0-2 nmol, ICV, once) causes withdrawal hypothermia and a loss of body weight in morphine-dependent animals[1].
CTOP (0-1.5 nmol per side, Intra-VTA injection) enhances extracellular dopamine levels in the nucleus accumbens and dose-dependently enhances locomotor activity[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male CFLP mice (25-30 g)[1]
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Dosage: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)
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Administration:Intracerebroventricular (i.c.v.) administration, once
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Result:Antagonized the analgesic effect of morphine in a dose-dependent manner, antagonized the morphine-induced hypermotility in a dose-dependent manner.
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Animal Model: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]
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Dosage:0, 0.001, 0.05, 0.2, and 2 nmol
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Administration:Intracerebroventricular (i.c.v.) administration, once
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Result:Decreased the body temperature in a dose-dependent manner, and caused withdrawal hypothermia and a loss of body weight in morphine-dependent animals.
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Animal Model:Long-Evans hooded rats (12, male, 350-450 g)[2]
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Dosage:0, 0.015, 0.15, and 1.5 nmol per side
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Administration:Intra-VTA (ventral tegmental area) injection
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Result:Enhanced extracellular dopamine levels in the nucleus accumbens, dose-dependently increased activity, whereas had no effect on feeding and drinking behavior.
Chemical Information
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CAS No. 103429-31-8
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Molecular Weight 1062.26
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Formula C50H67N11O11S2
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Sequence
{D-Phe}-Cys-Tyr-{D-Trp}-{Orn}-Thr-{Pen}-Thr-NH2 (Disulfide bridge:Cys2-Pen7)
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Sequence Shortening
{D-Phe}-CY-{D-Trp}-{Orn}T{Pen}T-NH2 (Disulfide bridge:Cys2-Pen7)
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
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J Neurosci
HDAC6 inhibition reverses cisplatin-induced mechanical hypersensitivity via tonic delta opioid receptor signaling. [Abstract]2022 Oct 19;42(42):7862-7874. PMID: 36096670
Purity & Documentation
References
[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. [Content Brief]
[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. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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