NA Semax Amidate is a structure-optimized analog of 没听到. 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 小时.
It also enhances room temperature storage stability and nasal mucosal absorption efficiency, thereby ensuring more reliable penetration of the blood-brain barrier (血脑屏障) and the sustained maintenance of an effective concentration gradient in brain tissue.
Its core mechanism lies in multi-pathway modulation of 中枢神经系统 功能.
First and foremost, NA Semax Amidate acts as a powerful upregulator of brain-derived neurotrophic factor (脑源性神经营养因子), which in turn enhances neuronal survival, axonal growth, 突触可塑性 和 long-term potentiation (LTP) — the molecular basis for learning and memory.
而且,NA Semax Amidate potentiates dopaminergic, 血清素能, and noradrenergic neurotransmission, thereby optimizing prefrontal cortex executive functions, including attention selectivity and working memory 容量.
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, 缺氧, 创伤, 和 neurodegeneration.
It is approved in Russia as adjunctive therapy for acute stroke, traumatic brain injury, and early-stage Parkinson’s disease.
总之, NA Semax Amidate utilizes chemical modifications to overcome the limitations of the natural peptide, thereby surpassing conventional Semax in cognitive enhancement, 神经保护, mood regulation, and injury repair.
This holds significant clinical importance for the treatment of 神经退行性疾病 and the promotion of central nervous system functional recovery.
顺序
AC-met-glu-his-phe-pro-gly-pro-nh2
CAS 号
/
分子式
C39H54N10O10S
分子量
854.98
Research Of NA Semax Amidate
NA Semax Amidate demonstrates efficacy comparable to classical 抗焦虑药 drugs in several preclinical models.
1.Cognitive Enhancement and Neural Plasticity
NA Semax Amidate activates the transcription factor CREB, upregulating 脑源性神经营养因子 gene expression and increasing neuronal BDNF levels by over 40%.
This in turn promotes 树突棘 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 测试.
Brain slice electrophysiological recordings confirm increased LTP amplitude and duration, indicating that NA Semax Amidate reshapes 突触可塑性 thresholds through profound activation of the 神经营养因子 network.
2.Neuroprotection and Repair
NA Semax Amidate activates the adenylate cyclase (AC)-cAMP-PKA pathway to stabilize mitochondrial membrane potential, inhibits 细胞色素C 发布, and suppresses caspase-3 cascade activation, thereby blocking the execution phase of 细胞凋亡.
同时, it upregulates 超氧化物歧化酶 expression and inhibits excessive inflammatory 细胞因子 生产.
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 多巴胺能 neuron survival by 35%, demonstrating potent neuroprotection.
3.Anxiolytic and Analgesic Effects
NA Semax Amidate increases affinity for endogenous 脑啡肽 和 β-内啡肽 while inhibiting G protein-coupled receptor kinase (GRK)-mediated receptor internalization and desensitization, thereby prolonging analgesic 信令.
It also reduces FTO-mediated inflammatory pain hypersensitivity.
In mouse models, pain thresholds were elevated by 30-40% and remained elevated for 4 到 6 小时.
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.
同时, 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 到 6 小时.
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
高效液相色谱法
多发性硬化症
