NA Semax Amidate

NA Semax Amidate

NA Semax Amidate

NA Semax Amidate is a structure-optimized analog of semax. It is an N-terminally acetylated and C-terminally amidated derivative of the Semax peptide, which preserves the core sequence.

 

SKU: 198886 ምድብ:
ፍቅራችሁን አካፍሉን

NA Semax Amidate is a structure-optimized analog of አልሰማም።. It is an N-terminally acetylated and C-terminally amidated derivative of the Semax peptide, which preserves the core sequence.

This artificial modification markedly improves the resistance of the peptide chain against exo- and endopeptidases (for example leucine aminopeptidase), extending its half-life by about 30 minutes compared with the original Semax, with an overall duration of action of 6-12 ሰዓታት.

It also enhances room temperature storage stability and nasal mucosal absorption efficiency, thereby ensuring more reliable penetration of the blood-brain barrier (ቢቢቢ) and the sustained maintenance of an effective concentration gradient in brain tissue.

Its core mechanism lies in multi-pathway modulation of central nervous system ተግባር.

First and foremost, NA Semax Amidate acts as a powerful upregulator of ከአእምሮ የተገኘ ኒውሮትሮፊክ ሁኔታ (BDNF), which in turn enhances neuronal survival, axonal growth, የሲናፕቲክ ፕላስቲክነት እና long-term potentiation (LTP) — the molecular basis for learning and memory.

ከዚህም በላይ,NA Semax Amidate potentiates dopaminergic, serotonergic, and noradrenergic neurotransmission, thereby optimizing prefrontal cortex executive functions, including attention selectivity and working memory capacity.

NA Semax Amidate also exhibits significant neuroprotective effects by suppressing inflammatory cytokine release, reducing oxidative stress damage, and stabilizing mitochondrial membrane potential.

It is effective against various pathological insults such as cerebral ischemia, ሃይፖክሲያ, trauma, እና neurodegeneration.

It is approved in Russia as adjunctive therapy for acute stroke, traumatic brain injury, and early-stage Parkinson’s disease.

በማጠቃለል, NA Semax Amidate utilizes chemical modifications to overcome the limitations of the natural peptide, thereby surpassing conventional Semax in cognitive enhancement, neuroprotection, mood regulation, and injury repair.

This holds significant clinical importance for the treatment of የነርቭ በሽታ አምጪ በሽታዎች and the promotion of central nervous system functional recovery.

ቅደም ተከተል

AC-met-glu-his-phe-pro-gly-pro-nh2

የ CAS ቁጥር

/

ሞለኪውላር ፎርሙላ

C39H54N10O10S

ሞለኪውላዊ ክብደት

854.98

Research Of NA Semax Amidate

NA Semax Amidate demonstrates efficacy comparable to classical anxiolytic drugs in several preclinical models.

1.Cognitive Enhancement and Neural Plasticity

NA Semax Amidate activates the transcription factor CREB, upregulating BDNF gene expression and increasing neuronal BDNF levels by over 40%.

This in turn promotes dendritic spine ምስረታ, axonal guidance, and aggregation of postsynaptic density protein 95 (PSD-95), thereby enhancing learning capacity.

Biological simulation experiments demonstrate a 35-50% improvement in memory retention rates in contextual fear conditioning ፈተናዎች.

Brain slice electrophysiological recordings confirm increased LTP amplitude and duration, indicating that NA Semax Amidate reshapes የሲናፕቲክ ፕላስቲክነት thresholds through profound activation of the ኒውሮሮፊክ ፋክተር network.

2.Neuroprotection and Repair

NA Semax Amidate activates the adenylate cyclase (AC)-cAMP-PKA pathway to stabilize ሚቶኮንድሪያል membrane potential, inhibits ሳይቶክሮም ሲ መልቀቅ, and suppresses caspase-3 cascade activation, thereby blocking the execution phase of አፖፕቶሲስ.

Concurrently, it upregulates ሱፐርኦክሳይድ መበታተን expression and inhibits excessive inflammatory ሳይቶኪን ማምረት.

In a rat middle cerebral artery occlusion model, it reduced cerebral infarction volume by over 50%.

In an MPTP model of Parkinson’s disease, it increased dopaminergic neuron survival by 35%, demonstrating potent neuroprotection.

3.Anxiolytic and Analgesic Effects

NA Semax Amidate increases affinity for endogenous enkephalins እና β-ኢንዶርፊን while inhibiting G protein-coupled receptor kinase (GRK)-mediated receptor internalization and desensitization, thereby prolonging analgesic ምልክት መስጠት.

It also reduces FTO-mediated inflammatory pain hypersensitivity.

In mouse models, pain thresholds were elevated by 30-40% and remained elevated for 4 ወደ 6 ሰዓታት.

In chronic constriction injury (CCI) models, mechanical allodynia was alleviated by 50%, further confirming NA Semax Amidate’s clear anti-stress and mood-stabilizing properties.

NA Semax Amidate demonstrates efficacy comparable to classical anxiolytic drugs in several preclinical models.

4.Cognitive Enhancement and Neural Plasticity

NA Semax Amidate activates the transcription factor CREB, upregulating BDNF gene expression and increasing neuronal BDNF levels by over 40%.

This in turn promotes dendritic spine formation, axonal guidance, and aggregation of postsynaptic density protein 95 (PSD-95), thereby enhancing learning capacity.

Biological simulation experiments demonstrate a 35-50% improvement in memory retention rates in contextual fear conditioning tests.

Brain slice electrophysiological recordings confirm increased LTP amplitude and duration, indicating that NA Semax Amidate reshapes synaptic plasticity thresholds through profound activation of the neurotrophic factor network.

5.Neuroprotection and Repair

NA Semax Amidate activates the adenylate cyclase (AC)-cAMP-PKA pathway to stabilize mitochondrial membrane potential, inhibits cytochrome C release, and suppresses caspase-3 cascade activation, thereby blocking the execution phase of apoptosis.

Concurrently, it upregulates superoxide dismutase expression and inhibits excessive inflammatory cytokine production.

In a rat middle cerebral artery occlusion model, it reduced cerebral infarction volume by over 50%.

In an MPTP model of Parkinson’s disease, it increased dopaminergic neuron survival by 35%, demonstrating potent neuroprotection.

6.Anxiolytic and Analgesic Effects

NA Semax Amidate increases affinity for endogenous enkephalins and β-endorphin while inhibiting G protein-coupled receptor kinase (GRK)-mediated receptor internalization and desensitization, thereby prolonging analgesic signaling.

It also reduces FTO-mediated inflammatory pain hypersensitivity.

In mouse models, pain thresholds were elevated by 30-40% and remained elevated for 4 ወደ 6 ሰዓታት.

In chronic constriction injury (CCI) models, mechanical allodynia was alleviated by 50%, further confirming NA Semax Amidate’s clear anti-stress and mood-stabilizing properties.

COA

HPLC

ኤም.ኤስ

(1) ዲሚትሪቫ, ቪ. ጂ.; ፖቫሮቫ, ኦ. ቪ.; Skvortsova, ቪ. አይ.; ሊምቦርስካ, ኤስ. ሀ.; ማይሶዶቭ, ኤን. ኤፍ.; Dergunova, ኤል. ቪ. ሴሜክስ እና ፕሮ-ግሊ-ፕሮ ከሴሬብራል ኢሽሚያ በኋላ የኒውሮትሮፊኖች እና ተቀባይ ጂኖች ቅጂን ያግብሩ. ሴሉላር እና ሞለኪውላር ኒውሮባዮሎጂ 2009, 30 (1), 71-79. DOI: 10.1007/s10571-009-9432-0.

(2) ኤሬሚን, ኬ. ኦ.; ኩድሪን, ቪ. ኤስ.; ሳራንሳሪ, ፒ.; ምርት, ኤስ. ኤስ.; ግሪቨኒኮቭ, አይ. ሀ.; ማይሶዶቭ, ኤን. ኤፍ.; ሬይቭስኪ, ኬ. ኤስ. አትስማ, አንድ ACTH(4-10) አናሎግ ከኖትሮፒክ ንብረቶች ጋር, Dopaminergic እና Serotoninergic Brain Systems በሮደንትስ ውስጥ ያነቃል።. ኒውሮኬሚካል ምርምር 2005, 30 (12), 1493-1500. DOI: 10.1007/s11064-005-8826-8.

(3) ግላዞቫ, ኤን. ዋይ; ማንቼንኮ, ዲ. ኤም.; ቮሎዲና, ኤም. ሀ.; Merchieva, ኤስ. ሀ.; አንድሬቫ, ኤል. ሀ.; ኩድሪን, ቪ. ኤስ.; ማይሶዶቭ, ኤን. ኤፍ.; ሌቪትስካያ, ኤን. ጂ. አትስማ, ሠራሽ ACTH(4-10) አናሎግ, በነጭ አይጦች ውስጥ ቀደምት ህይወት የፍሎቮክሳሚን መጋለጥን ተከትሎ የባህሪ እና የነርቭ ኬሚካላዊ ለውጦችን ያዳክማል. ኒውሮፔፕቲዶች 2021, 86. DOI: 10.1016/j.npep.2020.102114.

(4) ወጪ, ኤን. ቪ.; ሶኮሎቭ, ኦ.; ጋቤቫ, ኤም. ቪ.; ግሪቨኒኮቭ, አይ. ሀ.; አንድሬቫ, ኤል. ሀ.; Miasoedov, ኤን. ኤፍ.; ዞዙሊያ, ሀ. ሀ. [ሴማክስ እና ሴላንክ ኢንኬፋሊንን የሚያበላሹ ኢንዛይሞችን ከሰው ሴረም ይከለክላሉ]]. Bioorg Khim 2001, 27 (3), 180-183. DOI: 10.1023/ሀ:1011373002885 ከ NLM Medline.

(5) ሜድቬዴቫ, ኢ. ቪ.; ዲሚትሪቫ, ቪ. ጂ.; ሊምቦርስካ, ኤስ. ሀ.; ማይሶዶቭ, ኤን. ኤፍ.; Dergunova, ኤል. ቪ. አትስማ, የ ACTH አናሎግ(4-7), በአይጦች ላይ ischemic የአንጎል ጉዳት በሚደርስበት ጊዜ የበሽታ መቋቋም ምላሽ ጂኖችን መግለፅን ይቆጣጠራል. ሞለኪውላር ጄኔቲክስ እና ጂኖሚክስ 2017, 292 (3), 635-653. DOI: 10.1007/s00438-017-1297-1.

(6) ፔ, ሲ.ዩ. ለድብርት "ሴማክስ" የሕክምና ዕድል. የ CNS Spectrums 2014, 13 (1), 20-21. DOI: 10.1017/s1092852900016102.

(7) ቭላሶቫ, አይ. ኤም.; ቡራቭትኮቭ, ዲ. ኢ.; ሳሌትስኪ, ሀ. ኤም. በሴሬብራል ኢስኬሚያ ውስጥ "ሴሜክስ" የተባለው መድሃኒት የነርቭ መከላከያ ባህሪያትን በሚመለከት ጥናት ውስጥ የደም ክፍሎችን የብርሃን ትንተና.. የተተገበረ ስፔክትሮስኮፒ ጆርናል 2009, 76 (1), 121-126. DOI: 10.1007/s10812-009-9141-ይ.

ቅደም ተከተል:

AC-met-glu-his-phe-pro-gly-pro-nh2

CAS:

/

ኤም.ደብሊው:

854.98 ግ/ሞል

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