Nogo-66(1-40) antagonist peptide

C₂₀₄H₃₂₂N₅₆O₆₄ · xC₂HF₃O₂

4583.08 (free base basis)

MFCD06411437

NA.32

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

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

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.

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

100

≥84% (HPLC)

lyophilized solid

white

H₂O: 1 mg/mL

Q9NQC3

−20℃

human ... RTN4(57142)

1 mg in glass bottle

13 - Non Combustible Solids

WGK 3

Eyeshields, Gloves, type N95 (US)