475221-20-6

Basic information

• Product Name: AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2
• Synonyms: 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;AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2;NEP1-40;NOGO-66 (1-40);NOGO-66 (1-40) ANTAGONIST PEPTIDE;NOGO EXTRACELLULAR PEPTIDE, 1-40;M.W. 4625.11 C206H324N56O65
• CAS NO: 475221-20-6
• Molecular Formula: C206H324N56O65
• Molecular Weight: 4625.11
• Product Categories: Various Peptides
• Mol File: 475221-20-6.mol

Chemical Properties

• Appearance: white/solid
• Storage Temp.: −20°C
• Solubility: H2O: 1 mg/mL
• CAS DataBase Reference: AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2(CAS DataBase Reference)
• NIST Chemistry Reference: AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2(475221-20-6)
• EPA Substance Registry System: AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2(475221-20-6)

Safety Data

• Safety Statements: 22-24/25
• WGK Germany: 3
• Hazardous Substances Data: 475221-20-6(Hazardous Substances Data)

Usage

Uses

Used in Neuroscience Research:
AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 is used as a Nogo-66 receptor antagonist peptide for studying the preliminary therapeutic effect after inhibition of Nogo-A in the cauda equina compression (CEC) model. This helps researchers understand the potential of this peptide in treating conditions related to nerve compression and damage.
Used in Autophagy Studies:
AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 is used as a research tool to determine the effects of Nogo-A/NgR1 on autophagic activation. Autophagy is a cellular process that helps maintain cellular homeostasis and is involved in various diseases, including neurodegenerative disorders. Understanding the role of Nogo-A/NgR1 in autophagy can provide insights into the development of therapeutic strategies for these conditions.
Used in Axonal Growth and Regeneration Research:
AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 is used as a Nogo-66 receptor antagonist peptide to study its role in Nogo-B mediated axonal branching using Schwann cells and sensory neurons of mice. This research can help in understanding the molecular mechanisms underlying axonal growth and regeneration, which is essential for the development of treatments for nerve injury and neurodegenerative diseases.

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.