2. GPCR/G Protein Neuronal Signaling
  3. Opioid Receptor
  4. CTOP

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.

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CTOP Chemical Structure

CTOP Chemical Structure

CAS No. : 103429-31-8

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CTOP Related Antibodies

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Description

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].

IC50 & Target

μ Opioid Receptor/MOR

 

In Vivo

CTOP (0-0.5 nmol, ICV, once) antagonizes the analgesic effect of morphine in a dose-dependent manner[1].
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.

Animal Model: Male CFLP mice (25-30 g)[1]
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)
Administration: Intracerebroventricular (i.c.v.) administration, once
Result: Antagonized the analgesic effect of morphine in a dose-dependent manner, antagonized the morphine-induced hypermotility in a dose-dependent manner.
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]
Dosage: 0, 0.001, 0.05, 0.2, and 2 nmol
Administration: Intracerebroventricular (i.c.v.) administration, once
Result: Decreased the body temperature in a dose-dependent manner, and caused withdrawal hypothermia and a loss of body weight in morphine-dependent animals.
Animal Model: Long-Evans hooded rats (12, male, 350-450 g)[2]
Dosage: 0, 0.015, 0.15, and 1.5 nmol per side
Administration: Intra-VTA (ventral tegmental area) injection
Result: Enhanced extracellular dopamine levels in the nucleus accumbens, dose-dependently increased activity, whereas had no effect on feeding and drinking behavior.
Molecular Weight

1062.26

Formula

C50H67N11O11S2
CAS No.
Sequence

{D-Phe}-Cys-Tyr-{D-Trp}-{Orn}-Thr-{Pen}-Thr-NH2 (Disulfide bridge:Cys2-Pen7)
Sequence Shortening

{D-Phe}-CY-{D-Trp}-{Orn}T{Pen}T-NH2 (Disulfide bridge:Cys2-Pen7)
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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CTOP Related Classifications

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The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

CTOP103429-31-8Opioid Receptorμ-opioid receptorKORpepideMorphine-induced analgesiaHypermotilityventral tegmental areaNucleus accumbensLocomotor activityInhibitorinhibitorinhibit

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