NA Semax Amidate

NA セマックスアミデート

NA セマックスアミデート

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.

 

商品コード: 198886 カテゴリー:
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NA Semax Amidate is a structure-optimized analog of 聞こえませんでした. 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 時間.

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 central nervous system 関数.

First and foremost, NA Semax Amidate acts as a powerful upregulator of 脳由来神経栄養因子 (BDNF), which in turn enhances neuronal survival, axonal growth, シナプス可塑性 そして long-term potentiation (LTP) — the molecular basis for learning and memory.

さらに,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, 低酸素症, trauma, そして neurodegeneration.

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

要約すれば, 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 neurodegenerative diseases and the promotion of central nervous system functional recovery.

順序

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

CAS番号

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分子式

C39H54N10O10S

分子量

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 形成, 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 シナプス可塑性 thresholds through profound activation of the 神経栄養因子 network.

2.Neuroprotection and Repair

NA Semax Amidate activates the adenylate cyclase (AC)-cAMP-PKA pathway to stabilize ミトコンドリア membrane potential, inhibits cytochrome C release, and suppresses caspase-3 cascade activation, thereby blocking the execution phase of アポトーシス.

Concurrently, it upregulates スーパーオキシドジスムターゼ expression and inhibits excessive inflammatory サイトカイン 生産.

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 そして 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 に 6 時間.

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 に 6 時間.

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) ドミトリエワ, V. G.; ポヴァロワ, ○. V.; スクヴォルツォワ, V. 私。; リンボルスカ, S. A.; ミャソエドフ, N. F.; デルグノバ, L. V. Semax と Pro-Gly-Pro は脳虚血後のニューロトロフィンとその受容体遺伝子の転写を活性化します. 細胞分子神経生物学 2009, 30 (1), 71-79. 土肥: 10.1007/s10571-009-9432-0.

(2) エレミン, K. O.; クドリン, V. S.; サランサリ, P.; 製品, S. S.; グリヴェニコフ, 私. A.; ミャソエドフ, N. F.; ラエフスキー, K. S. 聞かないでください, ACTH(4-10) 向知性特性を持つ類似体, げっ歯類のドーパミン作動性およびセロトニン作動性の脳システムを活性化します. 神経化学研究 2005, 30 (12), 1493-1500. 土肥: 10.1007/s11064-005-8826-8.

(3) グラゾヴァ, N. Y.; マンチェンコ, D. M.; ヴォロディナ, M. A.; メルキエワ, S. A.; アンドレーバ, L. A.; クドリン, V. S.; ミャソエドフ, N. F.; レヴィツカヤ, N. G. 聞かないでください, 合成ACTH(4–10) アナログ, 白色ラットにおける幼少期のフルボキサミン曝露後の行動および神経化学的変化を軽減する. 神経ペプチド 2021, 86. 土肥: 10.1016/j.npep.2020.102114.

(4) 料金, N. V.; ソコロフ, O.; ガバエバ, M. V.; グリヴェニコフ, 私. A.; アンドレーバ, L. A.; ミャソエドフ, N. F.; ゾズリア, あ. あ. [Semax と selank はヒト血清のエンケファリン分解酵素を阻害します]]. バイオオルグ・キム 2001, 27 (3), 180-183. 土肥: 10.1023/ある:1011373002885 NLM メドラインより.

(5) メドベージェワ, E. V.; ドミトリエワ, V. G.; リンボルスカ, S. A.; ミャソエドフ, N. F.; デルグノバ, L. V. 聞かないでください, ACTHの類似体(4−7), ラットの虚血性脳損傷時の免疫応答遺伝子の発現を調節する. 分子遺伝学とゲノミクス 2017, 292 (3), 635-653. 土肥: 10.1007/s00438-017-1297-1.

(6) ペー, C.-U. うつ病に対する「Semax」の治療可能性. 中枢神経系スペクトル 2014, 13 (1), 20-21. 土肥: 10.1017/s1092852900016102.

(7) ヴラソワ, 私. M.; ブラフツコフ, D. E.; サレツキー, あ. M. 脳虚血における薬物「Semax」の神経保護特性の研究における血液成分の発光分析. 応用分光学ジャーナル 2009, 76 (1), 121-126. 土肥: 10.1007/s10812-009-9141-y.

順序:

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

CAS:

/

M.W:

854.98 グラム/モル

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