NA Semax Amidate

एनए सेमैक्स एमिडेट

एनए सेमैक्स एमिडेट

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.

 

अपना प्यार बांटें

NA Semax Amidate is a structure-optimized analog of नहीं सुना. 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 घंटे.

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 केंद्रीय तंत्रिका तंत्र समारोह.

First and foremost, NA Semax Amidate acts as a powerful upregulator of मस्तिष्क-व्युत्पन्न न्यूरोट्रॉफिक कारक (बीडीएनएफ), which in turn enhances neuronal survival, axonal growth, सूत्रयुग्मक सुनम्यता और long-term potentiation (एलटीपी) — the molecular basis for learning and memory.

इसके अतिरिक्त,NA Semax Amidate potentiates dopaminergic, serotonergic, and noradrenergic neurotransmission, thereby optimizing prefrontal cortex executive functions, including attention selectivity and working memory क्षमता.

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, हाइपोक्सिया, सदमा, और neurodegeneration.

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

सारांश, 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.

अनुक्रम

एसी-मेट-ग्लू-हिज़-फे-प्रो-ग्लाइ-प्रो-एनएच2

सीएएस संख्या

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आण्विक सूत्र

C39H54N10O10S

आणविक वजन

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 बीडीएनएफ gene expression and increasing neuronal BDNF levels by over 40%.

This in turn promotes dendritic spine गठन, 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 परीक्षण.

Brain slice electrophysiological recordings confirm increased एलटीपी amplitude and duration, indicating that NA Semax Amidate reshapes सूत्रयुग्मक सुनम्यता thresholds through profound activation of the न्यूरोट्रॉफिक कारक नेटवर्क.

2.Neuroprotection and Repair

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

Concurrently, it upregulates सुपरऑक्साइड डिसम्यूटेज़ expression and inhibits excessive inflammatory साइटोकाइन उत्पादन.

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 और β-endorphin while inhibiting G protein-coupled receptor kinase (GRK)-mediated receptor internalization and desensitization, thereby prolonging analgesic संकेतन.

It also reduces FTO-mediated inflammatory pain hypersensitivity.

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

In chronic constriction injury (CCI) मॉडल, 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 को 6 घंटे.

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

सीओए

एचपीएलसी

एमएस

(1) दमित्रिएवा, वी. जी।; पोवारोवा, हे. वी; स्कोवर्त्सोवा, वी. मैं।; लिम्बोर्स्का, एस. एक।; Myasoedov, एन. एफ।; डर्गुनोवा, एल. वी. सेमैक्स और प्रो-ग्लाइ-प्रो सेरेब्रल इस्केमिया के बाद न्यूरोट्रॉफिन और उनके रिसेप्टर जीन के प्रतिलेखन को सक्रिय करते हैं. सेलुलर और आणविक तंत्रिका जीव विज्ञान 2009, 30 (1), 71-79. डीओआई: 10.1007/s10571-009-9432-0.

(2) एरेमिन, के. ओ; कुद्रिन, वी. एस।; सारणसारी, पी।; उत्पाद, एस. एस।; Grivennikov, मैं. एक।; Myasoedov, एन. एफ।; रेयेव्स्की, के. एस. मत सुनो, एक ACTH(4-10) नूट्रोपिक गुणों के साथ एनालॉग, कृंतकों में डोपामिनर्जिक और सेरोटोनर्जिक मस्तिष्क प्रणालियों को सक्रिय करता है. न्यूरोकेमिकल अनुसंधान 2005, 30 (12), 1493-1500. डीओआई: 10.1007/s11064-005-8826-8.

(3) ग्लेज़ोवा, एन. वाई; मैनचेंको, डी. एम।; वोलोडिना, एम. एक।; मर्चिएवा, एस. एक।; एंड्रिवा, एल. एक।; कुद्रिन, वी. एस।; Myasoedov, एन. एफ।; लेवित्स्काया, एन. जी. मत सुनो, सिंथेटिक ACTH(4-10) अनुरूप, सफेद चूहों में प्रारंभिक जीवन फ़्लूवोक्सामाइन के संपर्क के बाद व्यवहार और न्यूरोकेमिकल परिवर्तनों को कम करता है. न्यूरोपेप्टाइड्स 2021, 86. डीओआई: 10.1016/जे.एन.पी.ई.पी.2020.102114.

(4) लागत, एन. वी; सोकोलोव, ओ; गबाएवा, एम. वी; Grivennikov, मैं. एक।; एंड्रिवा, एल. एक।; मियासोएडोव, एन. एफ।; ज़ोज़ुलिया, ए. ए. [सेमैक्स और सेलांक मानव सीरम से एन्केफेलिन-डिग्रेडिंग एंजाइम को रोकते हैं]]. बायोऑर्ग खिम 2001, 27 (3), 180-183. डीओआई: 10.1023/ए:1011373002885 एनएलएम मेडलाइन से.

(5) मेदवेदेवा, ई. वी; दमित्रिएवा, वी. जी।; लिम्बोर्स्का, एस. एक।; Myasoedov, एन. एफ।; डर्गुनोवा, एल. वी. मत सुनो, ACTH का एक एनालॉग(4-7), चूहों में इस्केमिक मस्तिष्क की चोट के दौरान प्रतिरक्षा प्रतिक्रिया जीन की अभिव्यक्ति को नियंत्रित करता है. आणविक आनुवंशिकी और जीनोमिक्स 2017, 292 (3), 635-653. डीओआई: 10.1007/s00438-017-1297-1.

(6) पीएई, सी.-यू. अवसाद के लिए "सेमैक्स" की चिकित्सीय संभावना. सीएनएस स्पेक्ट्रम 2014, 13 (1), 20-21. डीओआई: 10.1017/s1092852900016102.

(7) व्लासोवा, मैं. एम।; बुरावतकोव, डी. ई.; सालेत्स्की, ए. एम. सेरेब्रल इस्किमिया में दवा "सेमैक्स" के न्यूरोप्रोटेक्टिव गुणों के अध्ययन में रक्त घटकों का ल्यूमिनसेंस विश्लेषण. एप्लाइड स्पेक्ट्रोस्कोपी जर्नल 2009, 76 (1), 121-126. डीओआई: 10.1007/s10812-009-9141-y.

अनुक्रम:

एसी-मेट-ग्लू-हिज़-फे-प्रो-ग्लाइ-प्रो-एनएच2

कैस:

/

एम.डब्लू:

854.98 जी/मोल

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