N7161
Nogo-66(1-40) antagonist peptide
≥84% (HPLC)
Synonym(s):
NEP (1-40)
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About This Item
Empirical Formula (Hill Notation):
C204H322N56O64 · xC2HF3O2
Molecular Weight:
4583.08 (free base basis)
MDL number:
UNSPSC Code:
12352202
NACRES:
NA.32
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Assay
≥84% (HPLC)
form
lyophilized solid
color
white
solubility
H2O: 1 mg/mL
UniProt accession no.
storage temp.
−20°C
Gene Information
human ... RTN4(57142)
Amino Acid Sequence
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
Application
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.
Legal Information
Sold under a non-exclusive license. For research use only, and not for diagnostic or therapeutic use or for use in humans.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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Neutralization of Nogo-A enhances synaptic plasticity in the rodent motor cortex and improves motor learning in vivo.
Zemmar A, Weinmann O, Kellner Y, et al.
The Journal of Neuroscience, 34(26), 8685-8698 (2014)
Wei Xu et al.
Neuroscience, 431, 103-114 (2020-02-19)
Focal cerebral infarction leads to autophagic activation, which contributes to secondary neuronal damage in the ipsilateral thalamus. Although Nogo-A deactivation enhances neuronal plasticity, its role in autophagic activation in the thalamus after ischemic stroke remains unclear. This study aimed to
Xiaofei Sun et al.
Biochemical and biophysical research communications, 527(1), 131-137 (2020-05-25)
To investigate the expression of Nogo-A in dorsal root ganglion (DRG) in rats with cauda equina injury and the therapeutic effects of blocking Nogo-A and its receptor. Fifty-eight male Sprague-Dawley rats were divided randomly into either the sham operation group
Tadzia GrandPré et al.
Nature, 417(6888), 547-551 (2002-05-31)
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. A 66-residue domain of Nogo (Nogo-66) is expressed on the surface of oligodendrocytes and
Christoph Eckharter et al.
Frontiers in cellular neuroscience, 9, 454-454 (2015-12-05)
In contrast to the central nervous system (CNS) nerve fibers do regenerate in the peripheral nervous system (PNS) although in a clinically unsatisfying manner. A major problem is excessive sprouting of regenerating axons which results in aberrant reinnervation of target
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