| Identification | Back Directory | [Name]
AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 | [CAS]
475221-20-6 | [Synonyms]
NEP1-40
NOGO-66 (1-40)
PubChem ID: 90488731
Nogo Extracellular Peptide
M.W. 4625.11 C206H324N56O65
NOGO EXTRACELLULAR PEPTIDE, 1-40
NOGO-66 (1-40) ANTAGONIST PEPTIDE
NEP1-40; NOGO EXTRACELLULAR PEPTIDE; 1-40
AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2
ARG-ILE-TYR-LYS-GLY-VAL-ILE-GLN-ALA-ILE-GLN-LYS-SER-ASP-GLU-GLY-HIS-PRO-PHE-ARG-ALA-TYR-LEU-GLU-SER-GLU-VAL-ALA-ILE-SER-GLU-GLU-LEU-VAL-GLN-LYS-TYR-SER-ASN-SER-NH2 | [Molecular Formula]
C206H324N56O65 | [MDL Number]
MFCD06411437 | [MOL File]
475221-20-6.mol | [Molecular Weight]
4625.11 |
| Chemical Properties | Back Directory | [storage temp. ]
-20°C | [solubility ]
H2O: 1 mg/mL
| [form ]
solid
| [color ]
white
| [Water Solubility ]
Soluble to 1 mg/ml in water | [Sequence]
Ac-Arg-Ile-Tyr-Lys-Gly-Val-Ile-Gln-Ala-Ile-Gln-Lys-Ser-Asp-Glu-Gly-His-Pro-Phe-Arg-Ala-Tyr-Leu-Glu-Ser-Glu-Val-Ala-Ile-Ser-Glu-Glu-Leu-Val-Gln-Lys-Tyr-Ser-Asn-Ser-NH2 |
| Hazard Information | Back Directory | [Uses]
Nogo-66(1-40) antagonist peptide has been used as a Nogo-66 receptor antagonist peptide:
- to study the preliminary therapeutic effect after inhibition of Nogo-A in the cauda equina compression (CEC) model
- to determine the effects of Nogo-A/NgR1 on autophagic activation
- to study its role in Nogo-B mediated axonal branching using Schwann cells and sensory neurons of mice
| [Biochem/physiol Actions]
Myelin-derived axon outgrowth inhibitors, such as Nogo, may account for the lack of axonal regeneration in the central nervous system (CNS) after trauma in adult mammals. Nogo-66 can inhibit axonal outgrowth through an axonal Nogo-66 receptor (NgR). Competitive antagonists of NgR derived from amino-terminal peptide fragments of Nogo-66. The Nogo-66(1 40) antagonist peptide (NEP1 40) blocks Nogo-66 or CNS myelin inhibition of axonal outgrowth in vitro, demonstrating that NgR mediates a significant portion of axonal outgrowth inhibition by myelin. Intrathecal administration of NEP1 40 to rats with mid-thoracic spinal cord hemisection results in significant axon growth of the corticospinal tract, and improves functional recovery. Thus, Nogo-66 and NgR have central roles in limiting axonal regeneration after CNS injury, and NEP1-40 provides a potential therapeutic agent. | [in vivo]
NEP(1-40) (89 μg/kg, ip, 15 min and 19 h post-injury) administration further shifts distributions of microglia away from an injury-induced activated morphology towards greater proportions of rod and macrophage-like morphologies[1]. | Animal Model: | 74 male Sprague-Dawley rats (328-377 g)[1]. | | Dosage: | 89 μg/kg (97.5% PBS and 2.5% DMSO). | | Administration: | IP, 15 min and 19 h post-injury. | | Result: | Reduced NgR function immediately post-injury.
Increased number of amoeboid microglia/macrophages at 2 days post-injury
|
| [storage]
Store at -20°C |
|
| Company Name: |
Sigma-Aldrich
|
| Telephone: |
021-61415566 800-8193336 |
| Website: |
https://www.sigmaaldrich.cn |
|