NA Selank Amidate

NA Selank Amidate exhibits improved molecular stability and in vivo pharmacokinetic profile through a double-modification strategy of N-terminal acetylation and C-terminal amidation based on the original structure of Selank.

This results in an increased half-life, enhanced blood-brain barrier penetration efficiency, and prolonged bioactivity in both molecular and animal models.

Moreover, NA Selank Amidate exhibits potent immunomodulation and anti-stress activity.

Sequence

ac-thr-lys-pro-arg-pro-gly-pro-nh2

CAS Number

Molecular Formula

C35H60N12O9

Molecular Weight

792.94

Research Of NA Selank Amidate

1.Retained and Enhanced Efficacy

Efficacy-wise,NA Selank Amidate retains all of the characteristics of Selank, regulating gamma-aminobutyric acid (GABA) neurotransmission in the brain while also modulating the dopaminergic and serotonergic systems to deliver outstanding anxiolytic and antidepressant effects.

It also shows better efficacy than Selank in enhancing cognitive and neuroprotective functions, producing pronounced positive effects on learning, memory, and attention.

2.Anxiolytic and Mood-Stabilizing Effects

In a concentration-dependent and subtype-selective manner, NA Selank Amidate allosterically modulates the GABA-A receptor by potentiating the binding efficacy of GABA to its receptor or enhancing chloride ion channel opening efficiency.

This significantly increases the inhibitory tone in key brain circuits, producing marked anxiolytic effects.

Furthermore, the side effects of this anxiolytic action are significantly milder than those of conventional anxiolytic drugs, making NA Selank Amidate a more attractive mood-stabilizing compound.

3.Cognitive Enhancement and Neuroprotection

NA Selank Amidate directly activates BDNF gene transcription by inducing phosphorylation of the promoter-located CREB transcription factor and acetylation of histone H3, increasing BDNF mRNA levels 3.2-fold in hippocampal dentate gyrus granule cells and prefrontal cortical pyramidal neurons and protein secretion 2.8-fold within 24 hours.

This activates the TrkB receptor signaling pathway downstream, inducing the Ras-MAPK and PI3K-Akt cascade to increase dendritic spine density by 39%, upregulate synaptophysin expression by 45%, and restore LTP amplitude to baseline.

This successfully prevents stress-induced hippocampal neuronal injury and cognitive decline, demonstrating distinct neuroprotective properties.

4.Immunomodulatory and Anti-Stress Effects

NA Selank Amidate is a competitive inhibitor of enkephalin-degrading enzyme, protecting endogenous opioid peptides from hydrolysis and thereby elevating their levels, while it inhibits LPS (lipopolysaccharide)-induced expression of pro-inflammatory cytokines including IL-6 and TNF-α by 40–60% in astrocytes.

NA Selank Amidate also represses NF-κB nuclear translocation by interfering with the recruitment of MyD88 adaptor protein, providing protective regulation in the neuroinflammatory microenvironment.