| Identification | Back Directory | [Name]
CTAP | [CAS]
103429-32-9 | [Synonyms]
CTAP
CTAP-NH2
CTAP,CTA
CTAP, ≥95%
7)-disulfide
CYS2, TYR3, ARG5, PEN7-AMIDE
M.W. 1104.30 C51H69N13O11S2
D-PHE-CYS-TYR-D-TRP-ARG-THR-PEN-THR-NH2
H-D-PHE-CYS-TYR-D-TRP-ARG-THR-PEN-THR-NH2
D-Phe-L-Cys-L-Tyr-D-Trp-L-Arg-L-Thr-L-Pen-L-Thr-NH2
H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2(Cys2-Pen7)
D-PHE-CYS-TYR-D-TRP-ARG-THR-PEN-THR-NH2(DISULFIDE BRIDGE:CYS2-PEN7)
H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (Disulfide bond between Cys2 and Pen7)
L-Threoninamide,D-phenylalanyl-L-cysteinyl-L-tyrosyl-D-tryptophyl-L-arginyl-L-threonyl-3-mercapto-L-valyl-,cyclic (2®
D-Phenylalanyl-L-cysteinyl-L-tyrosyl-D-tryptophyl-L-arginyl-L-threonyl-3-mercapto-L-valyl-L-threoninamide cyclic (2→
D-Phenylalanyl-L-cysteinyl-L-tyrosyl-D-tryptophyl-L-arginyl-L-threonyl-3-mercapto-L-valyl-L-threoninamide cyclic (2-7)-disulfide
L-Threoninamide, D-phenylalanyl-L-cysteinyl-L-tyrosyl-D-tryptophyl-L-arginyl-L-threonyl-3-mercapto-L-valyl-, cyclic (2→7)-disulfide | [Molecular Formula]
C51H69N13O11S2 | [MDL Number]
MFCD00671434 | [MOL File]
103429-32-9.mol | [Molecular Weight]
1104.3 |
| Chemical Properties | Back Directory | [storage temp. ]
-20°C | [form ]
Solid | [color ]
off-white | [Water Solubility ]
Soluble to 1 mg/ml in water | [Sequence]
{d-Phe}-Cys-Tyr-{d-Trp}-Arg-Thr-{Pen}-Thr-NH2 (Disulfide bridge:Cys2-Pen7) |
| Hazard Information | Back Directory | [Uses]
CTAP acts as a selective μ-opioid receptor antagonist with a multitude of applications including the regulation of aggressive behavior in mammals. Activation of μ-opioid receptors in the central nucleus of the amygdala, is responsible for mechanisms related to the control of sodium appetite and regulation of sodium intake. | [Uses]
CTAP has been used as a μ-opioid receptor (MOR) antagonist:
- to study the anti-hyperalgesic effect of dipeptidyl peptidase 4 (DPP4) inhibitor isoleucine-proline-isoleucine (IPI) and vildagliptin in carrageenan-induced inflammation
- to study the role of MOR in glutamate and gamma-aminobutyric acid (GABA) efflux during predator stress in rats
- to determine the endogenous opioid peptide involved in blocking pain induced by activated gastrin-releasing peptide (Grp+) neurons
| [Biochem/physiol Actions]
CTAP is a peptide antagonist produced from somatostatin analogs. | [in vivo]
CTAP (0-1 mg/kg, IP, single) blocks morphine’s antinociceptive effect[1].
CTAP (10 mg/kg; IP, single) has no effect on L-DOPA-induced limb, axial, orolingual, or locomotor abnormal involuntary movements[1].
CTAP is stable in the blood and serum of rats (T1/2 > 500 min), showing that the structure of this peptide offers enzymatic resistance[2].
CTAP is extensively protein-bound to albumin in the perfusion medium (68.2%) and to proteins in rat serum (84.2%)[2]. | Animal Model: | Male Sprague-Dawley rats[1] | | Dosage: | 0, 0.1, 0.5, 1 mg/kg | | Administration: | IP, single | | Result: | Completely blocked morphine’s antinociceptive effect at 0.5 or 1 mg/kg. |
| [IC 50]
μ Opioid Receptor/MOR: 3.5 nM (IC50); δ Opioid Receptor/DOR: 4500 nM (IC50) | [storage]
Desiccate at -20°C |
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Sigma-Aldrich
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