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N7161

Nogo-66(1-40) antagonist peptide

≥84% (HPLC), Nogo-66 blocker, lyophilized solid

Sinónimos:

NEP (1-40)

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Tamaño de envaseSKUDisponibilidadPrecio
1 mg
Comprobar disponibilidad del carrito
$637.00

Acerca de este artículo

Fórmula empírica (notación de Hill):
C204H322N56O64 · xC2HF3O2
Peso molecular:
4583.08 (free base basis)
UNSPSC Code:
12352202
NACRES:
NA.32
MDL number:

$637.00


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Nombre del producto

Nogo-66(1-40) antagonist peptide, ≥84% (HPLC)

Quality Level

assay

≥84% (HPLC)

form

lyophilized solid

color

white

solubility

H2O: 1 mg/mL

UniProt accession no.

storage temp.

−20°C

SMILES string

[nH]1cnc(c1)C[C@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)CNC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)[C@@H](NC(=O)C)CCCNC(=N)N)[C@H](CC)C)Cc6ccc(cc6

InChI

1S/C206H324N56O65/c1-23-104(15)163(258-169(292)109(20)226-174(297)126(59-67-148(210)272)240-201(324)166(107(18)26-4)261-199(322)160(101(9)10)255-153(277)92-223-171(294)120(41-30-33-75-207)230-186(309)138(86-115-51-57-119(271)58-52-115)249-202(325)165(106(

InChI key

OLEKMOOQFWTQGD-SJQNMCRDSA-N

Gene Information

human ... RTN4(57142)

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[1]
  • to determine the effects of Nogo-A/NgR1 on autophagic activation[2]
  • to study its role in Nogo-B mediated axonal branching using Schwann cells and sensory neurons of mice[3]

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.
Nogo-66(1-40) promotes axonal regeneration; it blocks effects of axon outgrowth inhibitors such as Nogo66.

Legal Information

Sold under a non-exclusive license. For research use only, and not for diagnostic or therapeutic use or for use in humans.

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Este artículo
AB5664PAB5666PPRS4087
assay

≥84% (HPLC)

assay

-

assay

-

assay

-

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

form

lyophilized solid

form

-

form

-

form

buffered aqueous solution

Gene Information

human ... RTN4(57142)

Gene Information

human ... RTN4(57142)

Gene Information

human ... RTN4(57142)

Gene Information

human ... RTN4(57142)

storage temp.

−20°C

storage temp.

-

storage temp.

-

storage temp.

−20°C

UniProt accession no.

Q9NQC3

UniProt accession no.

Q9NQC3

UniProt accession no.

Q9NQC3

UniProt accession no.

Q9NQC3


Clase de almacenamiento

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)



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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



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SKUGTIN
N7161-1MG04061826739600

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