NA Selank Amidate nthuav tawm kev txhim kho molecular stability thiab hauv vivo pharmacokinetic profile los ntawm kev hloov kho ob lub tswv yim ntawm N-terminal acetylation thiab C-terminal amidation raws li tus qauv qub ntawm Selank.
Qhov no ua rau muaj kev nce ib nrab-lub neej, txhim kho ntshav-hlwb barrier nkag mus efficiency, thiab ntev bioactivity nyob rau hauv ob qho tib si molecular thiab tsiaj qauv.
Ntxiv mus, NA Selank Amidate nthuav tawm muaj zog immunomodulation thiab tiv thaiv kev ntxhov siab.
Ib ntus
ac-thr-lys-pro-arg-pro-gly-pro-nh2
CAS Nr
/
Molecular Formula
C35H60N12O9
Molecular Luj
792.94
Kev tshawb fawb ntawm NA Selank Amidate
1.Khaws cia thiab ua kom muaj txiaj ntsig zoo
Efficiency-wise,NA Selank Amidate khaws tag nrho cov yam ntxwv ntawm Selank, tswj hwm gamma-aminobutyric acid (GABA) neurotransmission in the brain while also modulating the dopaminergic thiab serotonergic systems to deliver outstanding anxiolytic thiab 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 tus 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.
Tsis tas li ntawd xwb, 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.Kev paub txog kev txawj ntse thiab Neuroprotection
NA Selank Amidate ncaj qha qhib BDNF gene transcription los ntawm inducing phosphorylation ntawm tus txhawb nqa-nyob CREB transcription factor thiab acetylation ntawm histone H3, nce BDNF mRNA qib 3.2-fold hauv hippocampal dentate gyrus granule cells thiab prefrontal cortical pyramidal neurons thiab protein secretion 2.8-fold hauv 24 teev.
Qhov no activates lub TrkB receptor signaling pathway downstream, inducing Ras-MAPK thiab PI3K-Akt cascade nce dendritic qaum ceev los ntawm 39%, upregulate synaptophysin qhia los ntawm 45%, thiab rov qab LTP amplitude rau hauv paus.
Qhov no ua tiav tiv thaiv kev ntxhov siab vim hippocampal neuronal raug mob thiab kev paub tsis meej, ua kom pom qhov txawv neuroprotective zog.
4.Immunomodulatory thiab Anti-Stress Effects
NA Selank Amidate yog ib qho kev sib tw inhibitor ntawm enkephalin-degrading enzyme, tiv thaiv endogenous tshuaj opioid peptides los ntawm hydrolysis thiab yog li no nce lawv qib, thaum nws inhibits LPS (lipopolysaccharide)-induced qhia ntawm pro-inflammatory cytokines suav nrog IL-6 thiab TNF-α los ntawm 40-60% nyob rau hauv astrocytes.
NA Selank Amidate tseem txwv tsis pub NF-κB nuclear kev hloov pauv los ntawm kev cuam tshuam nrog kev nrhiav neeg ua haujlwm ntawm MyD88 adapter protein, muab kev tiv thaiv kev cai nyob rau hauv lub neuroinflammatory microenvironment.
COA
HPLC
MS
