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.

 

Хайраа хуваалцаарай

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.

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 цаг.

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

Its core mechanism lies in multi-pathway modulation of төв мэдрэлийн систем функц.

First and foremost, NA Semax Amidate acts as a powerful upregulator of тархины гаралтай нейротрофийн хүчин зүйл (BDNF), which in turn enhances neuronal survival, axonal growth, синаптик уян хатан чанар болон long-term potentiation (LTP) — the molecular basis for learning and memory.

Moreover,NA Semax Amidate potentiates dopaminergic, serotonergic, and noradrenergic neurotransmission, thereby optimizing урд талын кортекс 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, гипокси, trauma, болон neurodegeneration.

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

Товчхондоо, NA Semax Amidate utilizes chemical modifications to overcome the limitations of the natural peptide, thereby surpassing conventional Semax in танин мэдэхүйн сайжруулалт, neuroprotection, mood regulation, and injury repair.

This holds significant clinical importance for the treatment of мэдрэлийн доройтлын өвчин and the promotion of central nervous system functional recovery.

Дараалал

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

CAS дугаар

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Молекулын томъёо

C39H54N10O10S

Молекулын жин

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 үүсэх, 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 синаптик уян хатан чанар thresholds through profound activation of the нейротроф хүчин зүйл network.

2.Neuroprotection and Repair

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

Concurrently, it upregulates супероксид дисмутаза expression and inhibits excessive inflammatory цитокин үйлдвэрлэл.

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 энкефалин болон β-endorphin while inhibiting G protein-coupled receptor kinase (GRK)-mediated receptor internalization and desensitization, thereby prolonging analgesic дохио өгөх.

It also reduces FTO-mediated inflammatory pain hypersensitivity.

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

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 руу 6 цаг.

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

MS

(1) Дмитриева, В. Г.; Поварова, О. В.; Скворцова, В. I.; Лимборска, С. А.; Мясоедов, Н. Ф.; Дергунова, Л. В. Semax ба Pro-Gly-Pro нь тархины ишемийн дараа нейротрофин ба тэдгээрийн рецепторын генийн транскрипцийг идэвхжүүлдэг.. Эсийн ба молекулын нейробиологи 2009, 30 (1), 71-79. DOI: 10.1007/s10571-009-9432-0.

(2) Эрэмин, К. О.; Кудрин, В. С.; Сарансари, П.; Бүтээгдэхүүн, С. С.; Гривенников, I. А.; Мясоедов, Н. Ф.; Раевский, К. С. Битгий сонс, ACTH(4-10) Ноотроп шинж чанартай аналог, Мэрэгчдийн допаминергик ба серотонинергик тархины системийг идэвхжүүлдэг. Нейрохимийн судалгаа 2005, 30 (12), 1493-1500. DOI: 10.1007/s11064-005-8826-8.

(3) Глазова, Н. Ю.; Манченко, Д. М.; Володина, М. А.; Мерчиева, С. А.; Андреева, Л. А.; Кудрин, В. С.; Мясоедов, Н. Ф.; Левицкая, Н. Г. Битгий сонс, синтетик ACTH(4-10) аналог, Цагаан харханд флувоксаминыг хэрэглэсний дараа зан үйлийн болон нейрохимийн өөрчлөлтийг сулруулдаг.. Нейропептидүүд 2021, 86. DOI: 10.1016/j.npep.2020.102114.

(4) Зардал, Н. В.; Соколов, О.; Габаева, М. В.; Гривенников, I. А.; Андреева, Л. А.; Миасоедов, Н. Ф.; Зозулиа, А. А. [Semax болон selank нь хүний ​​ийлдэс дэх энкефалиныг задалдаг ферментийг саатуулдаг]]. Биорг Хим 2001, 27 (3), 180-183. DOI: 10.1023/а:1011373002885 NLM Medline-аас.

(5) Медведева, Э. В.; Дмитриева, В. Г.; Лимборска, С. А.; Мясоедов, Н. Ф.; Дергунова, Л. В. Битгий сонс, ACTH-ийн аналог(4−7), харханд тархины ишемийн гэмтлийн үед дархлааны хариу урвалын генийн илэрхийлэлийг зохицуулдаг. Молекул генетик ба геномик 2017, 292 (3), 635-653. DOI: 10.1007/s00438-017-1297-1.

(6) Пае, C.-U. "Семакс" -ын сэтгэл гутралын эмчилгээний боломж. Төв мэдрэлийн системийн спектрүүд 2014, 13 (1), 20-21. DOI: 10.1017/s1092852900016102.

(7) Власова, I. М.; Буравцов, Д. Э.; Салецки, А. М. Тархины ишемийн үед "Семакс" эмийн мэдрэлийн хамгаалалтын шинж чанарыг судлахад цусны бүрэлдэхүүн хэсгүүдийн гэрлийн шинжилгээ.. Хэрэглээний спектроскопийн сэтгүүл 2009, 76 (1), 121-126. DOI: 10.1007/s10812-009-9141-y.

Дараалал:

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

CAS:

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М.В:

854.98 г/моль

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