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Semax — Full Product Page (Detailed Version)
Product Title:
Semax — Synthetic Heptapeptide Neuropeptide Research Compound (ACTH 4–10 Fragment Analog)
Short Description:
A synthetic heptapeptide derived from the ACTH(4–10) region, investigated in preclinical neurobiology and signaling research for neurotrophin-associated transcriptional regulation, monoaminergic pathway marker analysis, systems-level neural network activity modeling, and oxidative stress biomarker investigation in controlled laboratory settings. ≥99% Purity, HPLC-Verified. Third-Party CoA Included. For in-vitro laboratory research use only.
Full Product Description:
Overview
Semax (ACTH(4–7)-PGP) is a synthetic heptapeptide derived from a defined region of adrenocorticotropic hormone (ACTH). In scientific research, Semax is employed as a molecular tool in neurobiology and signaling studies, including investigations of activity-dependent gene regulation, neurotrophin-associated transcriptional programs, monoaminergic pathway markers, and systems-level neural network activity assessed using experimental imaging and omics-based approaches.
Preclinical literature describes Semax-associated alterations in transcriptional profiles across central nervous system–relevant tissues and reports modulation of neurotrophin-related genes including BDNF and NGF in controlled animal and cell-based experimental designs.
Biochemical Characteristics
- Peptide Sequence: Met–Glu–His–Phe–Pro–Gly–Pro
- Molecular Formula: C₃₇H₅₁N₉O₁₀S
- Molecular Weight: 813.92 g/mol
- CAS Number: 80714-61-0
- Alternate Name: Pro–Gly–Pro–ACTH
Semax is a synthetic analog corresponding to amino acids 4–10 of ACTH, incorporating a C-terminal Pro–Gly–Pro motif. This structural characteristic supports its utility as a defined molecular probe in controlled neurobiology and signaling research paradigms.
Research Applications
Semax is applied in preclinical research models to examine pathway-level regulation across multiple biological domains, including:
Neurotrophin-Linked Transcriptional Regulation
Experimental readouts involving BDNF and NGF gene-expression dynamics in CNS-relevant tissue regions under defined laboratory conditions.
Systems-Level Brain Network Activity Research
Experimental neuroimaging method-based assessment of resting-state neural connectivity patterns and network behavior in controlled preclinical research paradigms.
Neurovascular & Immune-Associated Gene Program Research
Genome-wide transcriptional profiling in controlled animal models examining neurovascular and immune pathway-associated gene expression dynamics.
Learning & Memory-Related Endpoint Research
Mechanistic comparison studies of ACTH-derived peptides in controlled rodent behavioral research paradigms examining memory-related endpoint markers.
Monoaminergic Signaling Pathway Research
Serotonergic pathway measure analysis alongside neurotrophin-dependent behavioral outcome endpoints in defined preclinical research models.
Oxidative Stress Biomarker Research
Biomarker panel investigations incorporating hepatic morphofunctional measures and lipid peroxidation endpoint analysis in controlled stress-model research conditions.
Pathway & Mechanistic Context
Across published preclinical studies, Semax is evaluated primarily as a modulator of gene-expression programs and systems-level neural network activity in controlled experimental settings. Reported research outcomes include:
- Transcriptomic changes in CNS tissue samples under defined experimental conditions
- Neurotrophin-associated transcriptional dynamic alterations
- Network-level activity pattern changes measured using experimental neuroimaging platforms
- Peripheral oxidative stress marker changes and hepatic tissue endpoint readouts under defined stress-model conditions
Resting-State Network Analyses
Experimental neuroimaging studies report Semax-associated modulation of resting-state network behavior, including effects on networks classified as default-mode–related within specific analytic research frameworks. Background literature on default-mode and social-cognition network overlap is commonly referenced to contextualize these findings within neuroscience research paradigms.
Genome-Wide Transcriptional Profiling in Ischemia Models
In rodent models of focal cerebral ischemia, genome-wide expression analyses have reported Semax-associated changes across immune-related and vascular-system gene sets in brain tissue samples. These findings provide molecular context for further investigation of neurovascular and inflammatory pathway regulation within the defined model system.
Neurotrophin-Associated Gene Expression Dynamics
Rodent studies describe time-dependent transcriptional changes following Semax exposure in regions including the hippocampus and frontal cortex, including reported modulation of BDNF- and NGF-related gene-expression measures within defined study designs.
ACTH-Derived Peptides in Genetic Epilepsy Models
Preclinical work using ACTH exposure in genetic epilepsy mouse research models has reported preservation of learning- and memory-related endpoint readouts under defined experimental conditions. These findings are frequently cited to provide comparative mechanistic context for research involving ACTH-derived peptide fragments including Semax.
Monoaminergic & Neurotrophin-Linked Research Studies
Additional rodent studies examining altered hippocampal BDNF expression levels report associated behavioral and serotonergic pathway dynamic changes, supporting broader mechanistic frameworks connecting neurotrophin availability, monoaminergic signaling activity, and behavioral endpoint measurement in controlled nonclinical research paradigms.
Peripheral Oxidative Stress & Hepatic Biomarker Research
Further experimental work describes Semax-associated effects on hepatic morphofunctional parameters and lipid peroxidation markers in controlled stress-model research conditions, supporting its application in oxidative stress and metabolic research workflows.
Preclinical Research Summary
Published preclinical literature documents Semax investigation across the following primary research contexts:
- Neurotrophin-linked gene expression dynamics in CNS-relevant tissue regions
- Systems-level neural network activity assessment via experimental neuroimaging platforms
- Neurovascular and immune-associated gene program analysis via genome-wide transcriptional profiling
- Monoaminergic signaling pathway marker assessment alongside behavioral endpoint measurement
- Oxidative stress biomarker panel investigation in defined stress-model research conditions
- Hepatic morphofunctional parameter and lipid peroxidation endpoint analysis
All findings are derived exclusively from controlled preclinical research systems and do not represent clinical outcomes of any kind.
Form & Analytical Characterization
Semax is supplied as a synthetic peptide for controlled laboratory research use. Researchers typically reference sequence data, CAS numbers, and registry identifiers for internal documentation and study design purposes. Analytical characterization commonly includes:
- Chromatographic Purity Assessment (HPLC) — purity profiling and lot consistency verification
- Mass-Based Identity Confirmation (MS) — molecular identity verification consistent with standard peptide qualification practices
Purity & Quality
- ≥99% Purity — HPLC Verified
- Independently tested by accredited third-party laboratory
- Certificate of Analysis (CoA) available for every batch
Research Use Only (RUO) Notice
All products are furnished strictly for in-vitro laboratory research use only. "In-vitro" refers to studies conducted outside of a living organism in controlled laboratory conditions. These materials are not medicines or drugs and have not been evaluated or approved by the U.S. Food and Drug Administration (FDA) to diagnose, treat, cure, or prevent any disease or medical condition. Administration into humans or animals is strictly prohibited. Not for human, medical, diagnostic, or veterinary use.
