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 hours.
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 function.
First and foremost, NA Semax Amidate acts as a powerful upregulator of factor neurotròfic derivat del cervell (BDNF), which in turn enhances neuronal survival, axonal growth, synaptic plasticity and long-term potentiation (LTP) — the molecular basis for learning and memory.
Moreover,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, hipòxia, trauma, and neurodegeneration.
It is approved in Russia as adjunctive therapy for acute stroke, traumatic brain injury, and early-stage Parkinson’s disease.
In summary, 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.
Seqüència
AC-met-glu-his-phe-pro-gly-pro-nh2
Número CAS
/
Fórmula molecular
C39H54N10O10S
Pes molecular
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 formació, 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.
2.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.
3.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 to 6 hours.
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 to 6 hours.
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
