Semax Peptide | Cognitive Research
RESEARCH PEPTIDE

Semax Peptide | Cognitive Research

Synthetic ACTH-Derived Heptapeptide — Research Peptide
$49.00
Semax is an ACTH(4–10)-related synthetic heptapeptide studied in preclinical neurobiology, including neurotrophin-associated signaling and experimental ischemia models. Research use only; not for human or veterinary use.
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Primary Literature Peer-reviewed sources
Research Use Only Laboratory research materials

Scientific Specifications

Reference characteristics for laboratory research materials.

CAS Number
80714-61-0
Purity
≥98%
Molecular Formula
C37H51N9O10S
Molecular Weight
813.9
Appearance
White lyophilized powder
Storage
-20°C
Research Classification
Research Use Only (RUO). Not for human or veterinary use.

SCIENTIFIC OVERVIEW

Scientific background and research classification for this laboratory reference material.

The supplier COA for Semax lot P251022-A026 identifies a chemically synthesized peptide with sequence Met-Glu-His-Phe-Pro-Gly-Pro, CAS 80714-61-0, formula C37H51N9O10S, and reported molecular weight 813.92. Independent reference sources identify the sequence as an ACTH(4–10)-related synthetic heptapeptide. The COA reports measured acetate content but does not declare a discrete acetate stoichiometry. Published cell and animal work has examined neurotrophin-associated measures, cerebral-ischemia models, and peptide–metal coordination; these findings do not establish a human therapeutic mechanism or direct equivalence to substituted Semax derivatives.

Primary Research Category
Neurocognitive Research
Material Type
Lyophilized Peptide
Intended Use
Laboratory Research
Research Categories
Neuroprotection Neuroscience Cognitive Function

Mechanism of Action

Molecular interaction profile describing how this research material engages receptor systems and influences downstream biological signaling pathways.

Rat basal-forebrain work reported specific binding and increased BDNF protein following Semax exposure. In a rat cerebral-ischemia model, Semax and its C-terminal Pro-Gly-Pro fragment were associated with neurotrophin and receptor-gene transcription changes. These are preclinical model observations; they do not establish a human therapeutic mechanism, a universal neuroprotective effect, or direct equivalence to substituted Semax derivatives.

Primary Organ Systems
  • Central Nervous System

Research Documentation

Laboratory documentation is presented when available for the selected product specification and current lot.

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Scientific References
Peer-Reviewed Literature

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Laboratory Resources
Technical Guidance

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Related Research
Companion Materials

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Research Center

Scientific literature, laboratory resources, and related materials curated to support research involving this research material.

Scientific References
Peer-Reviewed Literature

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Scientific Dossier
Deeper Technical Treatment

Comprehensive scientific documentation including literature review, mechanism, pharmacology, and study data for this research material.

Laboratory Resources
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Research Library

Curated peer-reviewed literature selected to provide scientific context for this research material.

Mechanistic Study•Journal of Neurochemistry• 2006

Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain

Foundational mechanistic report that Semax, an ACTH(4-10) analogue, binds specifically and increases brain-derived neurotrophic factor (BDNF) protein levels in rat basal forebrain.
Velora Research Insight
Founding BDNF-neurotrophic mechanism evidence for Semax. Institute of Molecular Genetics (IMG, Moscow) originating consortium (shared lineage with VSE-PUB-000077).
PubMed →DOI →
Preclinical Study•Cellular and Molecular Neurobiology• 2010

Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia

Preclinical study reporting that Semax and its C-terminal Pro-Gly-Pro fragment activate transcription of neurotrophins and their receptor genes in a rat model of cerebral ischemia.
Velora Research Insight
Preclinical neurotrophin-transcription mechanism in an ischemia model. IMG Moscow consortium (shared lineage with VSE-PUB-000076) — counted as one independent lineage, not two.
PubMed →DOI →
Mechanistic Study•Journal of Inorganic Biochemistry• 2015

Semax, an ACTH4-10 peptide analog with high affinity for copper(II) ion and protective ability against metal induced cell damage

Biophysical/coordination-chemistry study reporting that Semax binds copper(II) with high affinity and shows protective ability against metal-induced cell damage in vitro.
Velora Research Insight
Independent copper(II)-coordination biochemistry of Semax. Catania (Italy) group — independent of the IMG consortium (shared lineage with VSE-PUB-000079).
PubMed →DOI →
Mechanistic Study•ACS Chemical Neuroscience• 2022

Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Abeta Aggregation and Amyloid Formation in Artificial Membrane Models

In-vitro membrane-model study reporting that Semax affects copper-induced amyloid-β aggregation and amyloid formation, extending its copper-coordination chemistry to metal-associated aggregation processes.
Velora Research Insight
Independent mechanistic chemistry of Semax on copper-induced amyloid-β aggregation. Catania (Italy) lineage (shared with VSE-PUB-000078) — mechanistic model evidence, not a disease-treatment claim.
PubMed →DOI →