{"product_id":"semax-ac-semax-nh2-5-10mg-pen-test","title":"Semax (AC-Semax-NH2) | 15 Mg Pen","description":"\u003cp\u003eSemax is a synthetic regulatory peptide derived from the ACTH (4–10) fragment and widely studied in neurotrophic and cognitive-signaling research. Across preclinical and selected human research contexts, it has been explored for its relationship to neurotrophin expression (including BDNF-related pathways), neurotransmission markers, and stress-response signaling under controlled experimental conditions. Information on this page is provided for scientific and educational context only and does not represent medical guidance or therapeutic claims.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eSupports\u003c\/strong\u003e\u003c\/p\u003e\n\u003col\u003e\n\u003cli\u003eNeurotrophic signaling context (BDNF\/TrkB-related) tracked in neuronal and glial model systems.\u003c\/li\u003e\n\u003cli\u003eNeuroplasticity and synaptic adaptation endpoints monitored in learning and stress paradigms.\u003c\/li\u003e\n\u003cli\u003eMonoaminergic signaling context associated with dopamine\/serotonin pathway markers in models.\u003c\/li\u003e\n\u003cli\u003eNeuroinflammation and immune-response gene-expression readouts in neurobiology research settings.\u003c\/li\u003e\n\u003cli\u003eCellular resilience markers assessed in ischemia\/oxidative-stress model frameworks.\u003c\/li\u003e\n\u003c\/ol\u003e\n\u003ch2\u003eDescription\u003c\/h2\u003e\n\u003cp\u003e\u003cstrong\u003eSemax\u003c\/strong\u003e is an ACTH-fragment–based synthetic peptide (commonly referenced as MEHFPGP) developed within the class of neuroactive regulatory peptides. It is frequently used in experimental neurobiology to map how neurotrophin signaling, neurotransmission balance, and inflammatory-marker patterns shift under stress, cognitive load, or injury-like conditions in controlled models.\u003c\/p\u003e\n\u003cp\u003eIn mechanistic literature, Semax is often discussed in connection with \u003cstrong\u003eBDNF-related signaling\u003c\/strong\u003e and downstream pathways involved in synaptic function and adaptation. In parallel, multiple studies examine transcriptomic and immune-response readouts, positioning Semax as a probe compound in designs that evaluate neuroimmune crosstalk alongside behavioral or electrophysiologic endpoints.\u003c\/p\u003e\n\u003cp\u003eSemax is presented here for controlled research and educational context only. It is not marketed as an approved therapeutic product, and reported observations can vary substantially by model, endpoints, timing, and study design.\u003c\/p\u003e\n\u003ch2\u003eClinical Status\u003c\/h2\u003e\n\u003cp\u003eSemax has extensive preclinical and in vitro investigation and is also referenced in regional human research contexts, including studies that evaluate neurological recovery-associated endpoints. It is not presented here as an approved therapeutic product, and interpretation should remain study-specific and endpoint-driven.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eEvidence type:\u003c\/strong\u003e\u003cbr\u003eHuman RCT \u003cspan\u003e▣\u003c\/span\u003e | Observational ✔ | Animal ✔ | In vitro ✔ | Regulatory approval ☐\u003c\/p\u003e\n\u003ch2\u003eMechanism of Action\u003c\/h2\u003e\n\u003cp\u003eMechanistic discussions around Semax commonly emphasize changes in \u003cstrong\u003eneurotrophin signaling\u003c\/strong\u003e and gene-expression programs linked to neuronal survival and synaptic plasticity. Several experimental studies report BDNF-related expression changes in brain regions following Semax exposure, supporting its use in neuroplasticity-focused research frameworks.\u003c\/p\u003e\n\u003cp\u003eBeyond neurotrophins, Semax has been evaluated in models of ischemic injury and stress exposure where transcriptomic signatures include immune-response and inflammation-related gene clusters. These molecular readouts are often paired with functional measures (behavioral, electrophysiologic, or recovery-associated endpoints) depending on the study design.\u003c\/p\u003e\n\u003ch2\u003eBenefits\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cb\u003eUpregulation Of Neurotrophic Factors:\u003c\/b\u003e\u003cbr\u003eSemax has been studied for its ability to increase expression of brain-derived neurotrophic factor (BDNF) in both animal and human neurological research. BDNF plays a central role in synaptic plasticity, dendritic spine formation, and neuronal survival. Research demonstrates ↑ BDNF mRNA and protein levels in hippocampal regions following administration. This effect supports enhanced neuronal connectivity in experimental learning models. Neurotrophic activation is considered one of the core mechanisms underlying its cognitive research profile. Evidence type: Human clinical studies ✔ | Animal ▣.\u003c\/li\u003e\n\u003cli\u003e\n\u003cb\u003eEnhanced Synaptic Plasticity And Memory Signaling:\u003c\/b\u003e\u003cbr\u003eClinical studies have evaluated Semax in cognitive impairment and attentional performance models. Improvements in memory recall and executive function scores have been documented in controlled settings. Mechanistically, ↑ CREB activation contributes to long-term potentiation processes within hippocampal circuits. Preclinical data show improved synaptic density under stress conditions. These findings support its role in experimental neuroplasticity enhancement.\u003c\/li\u003e\n\u003cli\u003e\n\u003cb\u003eModulation Of Dopamine And Serotonin Systems:\u003c\/b\u003e\u003cbr\u003eSemax has been observed to influence monoaminergic neurotransmission, particularly dopamine and serotonin turnover. Laboratory studies indicate regulation of transporter activity and receptor sensitivity in cortical regions. This modulation contributes to balanced neurotransmitter signaling in stress-related research models. Improved attentional performance metrics have been associated with this pathway in human studies. Evidence type: Human ✔ | Animal ▣.\u003c\/li\u003e\n\u003cli\u003e\n\u003cb\u003eNeuroprotection Under Ischemic And Oxidative Stress Conditions:\u003c\/b\u003e\u003cbr\u003eIn ischemic animal models, Semax administration has been associated with ↓ infarct volume and improved behavioral recovery scores. Research demonstrates ↓ glutamate excitotoxicity and ↓ oxidative stress biomarkers in neuronal tissue. Enhanced neuronal survival pathways have been documented through BDNF-mediated signaling. These effects position Semax within experimental stroke and neuroprotection research domains.\u003c\/li\u003e\n\u003cli\u003e\n\u003cb\u003eGene Expression Regulation And Anti-Inflammatory Modulation:\u003c\/b\u003e\u003cbr\u003eGene expression profiling studies show modulation of inflammatory cytokines and stress-response proteins following Semax exposure. Research indicates ↓ expression of certain pro-inflammatory mediators in brain tissue models. This regulatory influence contributes to a stabilized neuronal microenvironment. Evidence remains primarily preclinical with supporting clinical observations.\u003c\/li\u003e\n\u003cli\u003e\n\u003cb\u003eCognitive Resilience In Stress Models:\u003c\/b\u003e\u003cbr\u003eSemax has been studied in models of acute and chronic stress exposure. Behavioral testing demonstrates improved performance compared to control groups under stress conditions. Mechanistic hypotheses suggest stabilization of monoamine signaling and neurotrophic pathways. These findings support inclusion in cognitive resilience research.\u003c\/li\u003e\n\u003cli\u003e\n\u003cb\u003eSelective ACTH Fragment Without Cortisol Stimulation:\u003c\/b\u003e\u003cbr\u003eUnlike full ACTH peptides, Semax does not significantly stimulate adrenal corticosteroid production. This selective activity allows neurological pathway modulation without systemic endocrine activation. Clinical endocrine markers confirm absence of significant cortisol elevation in controlled studies.\u003c\/li\u003e\n\u003cli\u003e\n\u003cb\u003eHigh Bioavailability Through Subcutaneous Administration:\u003c\/b\u003e\u003cbr\u003eProvided in a stabilized pre-mixed injection pen for SubQ administration, ensuring consistent systemic exposure in research protocols. Subcutaneous delivery supports reliable peptide absorption and simplifies laboratory handling. Each unit is freshly prepared and intended strictly for research use only.\u003cbr\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003ch2\u003eResearch Data\u003c\/h2\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"10\" style=\"width: 100%;\"\u003e\n\u003ctbody\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003eStudy\/model\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported effect\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003eAstrocyte cultures \/ basal forebrain models (in vitro \/ preclinical context)\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported stimulation of BDNF-related synthesis\/expression readouts in controlled experimental systems.\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003eRat brain region studies (in vivo; neurotrophin expression)\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported increases in BDNF expression in multiple brain areas following Semax exposure (endpoint- and timing-dependent).\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003eHippocampal BDNF\/TrkB signaling studies (preclinical)\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported modulation of hippocampal BDNF\/TrkB system markers linked to cognitive-function research hypotheses.\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003eFocal cerebral ischemia models (rat; transcriptomics)\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported changes in gene-expression clusters related to immune response and vascular-function pathways under ischemia conditions.\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003ePermanent\/transient MCAO ischemia studies (rat; growth factor genes)\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported induction of neurotrophin\/growth-factor gene expression and receptor markers in ischemia model designs.\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003eImmune-response gene regulation during ischemic injury (rat)\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported regulation of immune-response genes and inflammation-related expression patterns in controlled ischemia paradigms.\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003ctr\u003e\n\u003ctd style=\"width: 37.8136%;\"\u003eHuman clinical research contexts (acute neurological impairment; regional studies)\u003c\/td\u003e\n\u003ctd style=\"width: 62.1864%;\"\u003eReported changes in clinical scale-based recovery endpoints in study-specific settings; interpretation depends on design and comparator.\u003c\/td\u003e\n\u003c\/tr\u003e\n\u003c\/tbody\u003e\n\u003c\/table\u003e\n\u003ch2\u003eStack Suggestions\u003c\/h2\u003e\n\u003cp\u003eIn extended experimental designs, Semax is sometimes paired with:\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003eSelank (stress-response and neurotransmission-balance research contexts)\u003c\/li\u003e\n\u003cli\u003eDSIP (sleep\/stress endpoint designs, where applicable)\u003c\/li\u003e\n\u003cli\u003eNAD+ (bioenergetic and cellular resilience marker panels in broader neurobiology studies)\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eStacks discussed are for experimental design only, not safety\/efficacy guidance.\u003c\/p\u003e\n\u003ch2\u003ePossible Side Effects\u003c\/h2\u003e\n\u003cp\u003eIn research contexts, reported tolerability notes for Semax are generally described as mild and model-dependent. Where administered, observations may include transient local sensitivity or short-lived systemic effects. These notes are provided for general context only; they do not constitute medical guidance.\u003c\/p\u003e\n\u003cp\u003eLocal sensitivity: Temporary redness, swelling, or discomfort at the administration site has been reported in some settings.\u003cbr\u003eHeadache or fatigue: Transient effects have been noted anecdotally in certain protocols.\u003cbr\u003eDizziness or nausea: Occasional reports during early exposure windows in some settings.\u003cbr\u003eSensitivity reactions: Rare hypersensitivity-like responses are possible and warrant caution.\u003c\/p\u003e\n\u003ch2\u003eScientific References\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/16635254\/\"\u003eSemax, an analogue of adrenocorticotropin (4–10), binds neurotrophin-related pathways and stimulates BDNF synthesis in astrocyte systems\u003c\/a\u003e — In vitro \/ mechanistic\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/14556513\/\"\u003eThe heptapeptide Semax stimulates BDNF expression in different areas of the rat brain in vivo\u003c\/a\u003e — Animal\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/16996037\/\"\u003eSemax affects cognitive brain functions by modulating the hippocampal BDNF\/TrkB system\u003c\/a\u003e — Preclinical \/ mechanistic\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/24661604\/\"\u003eSemax affects expression of genes related to immune and vascular system function during rat brain focal ischemia\u003c\/a\u003e — Animal \/ transcriptomics\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC3987924\/\"\u003eSemax affects expression of genes related to immune and vascular system function during rat brain focal ischemia (full text)\u003c\/a\u003e — Animal \/ transcriptomics (PMC)\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/19024553\/\"\u003eEffect of Semax and the C-terminal peptide PGP on growth factor gene expression and receptors in experimental cerebral ischemia\u003c\/a\u003e — Animal\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC11498467\/\"\u003eSemax and Pro-Gly-Pro activate transcription of neurotrophins and receptors after cerebral ischemia (full text)\u003c\/a\u003e — Animal \/ gene expression (PMC)\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/28255762\/\"\u003eSemax regulates expression of immune response genes during ischemic brain injury in rats\u003c\/a\u003e — Animal \/ gene expression\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11517472\/\"\u003eEffectiveness of Semax in the acute period of hemispheric ischemic stroke (clinical study context)\u003c\/a\u003e — Human clinical study\u003c\/li\u003e\n\u003cli\u003e\n\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/30255741\/\"\u003eThe molecular aspects of Semax biological activity\u003c\/a\u003e — Review\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003ch2\u003eCautions\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003eFor educational and scientific context only; not intended to diagnose, treat, cure, or prevent any disease.\u003c\/li\u003e\n\u003cli\u003eIf you are pregnant, nursing, have a medical condition, or use prescription medication, consult a qualified professional.\u003c\/li\u003e\n\u003cli\u003eDiscontinue use if sensitivity occurs.\u003c\/li\u003e\n\u003c\/ul\u003e","brand":"Peptoora","offers":[{"title":"Default Title","offer_id":61559767859530,"sku":"PE-NT-PEN-003","price":349.0,"currency_code":"EUR","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0887\/1139\/7706\/files\/AC-Semax-NH230mg.png?v=1775829277","url":"https:\/\/peptoora.com\/fr\/products\/semax-ac-semax-nh2-5-10mg-pen-test","provider":"Peptoora LTD","version":"1.0","type":"link"}