GlamCO Semax
99%+ Purity
Verified by HPLC
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Semax

$60.00
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Semax lyophilized heptapeptide for in vitro research. Met-Glu-His-Phe-Pro-Gly-Pro (ACTH(4-10)-PGP analog) studied in neuroprotection and neurotrophin pathway models.

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Sterility & Endotoxins PASSED
Net Content & Purity PASSED
Third-Party Lab Verified

Independently Tested. Verifiably Pure.

Every batch of Semax is sent to an accredited independent laboratory before it ships. Here is exactly what we screen for - and the certificate that proves it.

What We Test Every Batch For

HPLC Purity Analysis
Confirms the peptide is ≥99% pure
Mass Spectrometry
Verifies the exact molecular identity
Heavy Metals Screening
Lead, arsenic, cadmium & mercury - Pass
Endotoxins (LPS)
Bacterial endotoxin levels - Pass
Sterility Testing
No microbial contamination - Pass
TFA Content
Residual trifluoroacetic acid - Not Detected
Net Peptide Content
Actual peptide mass per vial verified
📄
100+
Published Studies
ACTH(4-10)-derived peptide research
🧬
7
Amino Acids
Met-Glu-His-Phe-Pro-Gly-Pro
🧠
~813
Molecular Weight
~813.94 Da · C37H51N9O10S
🛡️
99%+
Purity Verified
HPLC tested, COA included
Preclinical Mechanism

How Semax Works

ACTH(4-10) fragment-derived signaling studied across neurotrophin, monoaminergic, and neuroprotection research models

BDNF / NGF Pathway

BDNF / NGF Upregulation Research

Preclinical studies report Semax rapidly upregulates Bdnf and Ngf transcripts and protein levels in rat hippocampus and frontal cortex. Shadrina et al. (PMID 19662538) and Dolotov et al. (PMID 16635254) describe specific BDNF binding and neurotrophin induction following ACTH(4-10)-PGP exposure.

  • Induces Bdnf and Ngf mRNA in hippocampus and frontal cortex
  • Elevates mature BDNF protein in basal forebrain models
  • Activates downstream TrkB signaling pathway research
Neuroprotection

Neuroprotection & Anti-Oxidative Pathway

In vitro work by Storozhevykh et al. (PMID 17760984) shows Semax protects cultured rat hippocampal neurons against glutamate-induced calcium overload and oxidative injury. The peptide reduces ROS generation and stabilizes mitochondrial function in cortical neuron models.

  • Attenuates glutamate excitotoxicity in hippocampal cultures
  • Reduces ROS and stabilizes mitochondrial membrane potential
  • Modulates inflammatory cytokine expression in ischemia models
Monoaminergic

Monoaminergic & Cognitive Pathway Modulation

Eremin et al. and Medvedeva (2018 review, PMID 30201095) describe Semax modulation of dopaminergic, serotonergic, and enkephalinergic systems. The peptide enhances enkephalin tone via inhibition of peptidase degradation and influences learning and memory consolidation models.

  • Modulates dopamine and serotonin turnover in rat brain
  • Inhibits enkephalin-degrading enzymes, raising endogenous opioid tone
  • Enhances acquisition and retention in passive-avoidance learning models
Preclinical Outcomes

What Research Has Shown

Key findings from peer-reviewed Semax publications (rodent and in vitro models)

Hippocampal Bdnf mRNA Increase (Shadrina 2010) ~3x
BDNF Protein, Rat Basal Forebrain (Dolotov 2006) ~2x
Glutamate-Induced Neuronal Death Reduction (Storozhevykh 2007) ~40%
Neurotrophin Pathway Activation Confirmed
Investigational Fields

Research Applications

Primary areas of Semax preclinical investigation

Neuroprotection

Neuroprotection Preclinical Models

In vitro and rodent studies investigate Semax against glutamate excitotoxicity, oxidative stress, and ischemia-reperfusion injury. Cultured hippocampal neurons show reduced calcium dysregulation and ROS following ACTH(4-10)-PGP exposure.

Storozhevykh et al. 2007 ↗
Neurotrophins

BDNF / NGF Pathway Research

Temporal expression studies of Bdnf and Ngf transcripts in rat hippocampus, frontal cortex, and retina show rapid Semax-induced upregulation. Mature BDNF protein is also elevated in basal forebrain models, supporting neurotrophin pathway research.

Shadrina et al. 2010 ↗
Cognition

Cognitive / Learning Preclinical Studies

Rodent behavioral models report improved acquisition and retention in passive-avoidance and conditioned-reflex paradigms following Semax administration. Effects are linked to neurotrophin induction and monoaminergic modulation in cortical and limbic regions.

Medvedeva et al. 2018 ↗
ACTH Pharmacology

ACTH-Fragment Pharmacology

Semax serves as a stable, non-corticotropic ACTH(4-10) analog for studying melanocortin and proteolytic-stability pharmacology. The C-terminal Pro-Gly-Pro extension blocks rapid degradation while preserving central nervous system activity.

Medvedeva et al. 2018 ↗
Technical Specifications

Compound Information

Technical specifications and analytical profile

Chemical Name
Methionyl-glutamyl-histidyl-phenylalanyl-prolyl-glycyl-proline (ACTH(4-10)-PGP analog)
Sequence
Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP, 7 amino acids)
Molecular Weight
~813.94 Da
Molecular Formula
C37H51N9O10S
CAS Number
80714-61-0
Form
Lyophilized powder
Purity
≥99% (HPLC verified)
Testing
Third-party HPLC, Mass Spec, Endotoxin
Storage (lyophilized)
-20°C for long-term stability
Storage (reconstituted)
2-8°C, use within 14 days
Solubility
Bacteriostatic water for reconstitution
COA
Included with every order
Common Inquiries

Frequently Asked Questions

Common questions about Semax research parameters

Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP). It is derived from the ACTH(4-10) fragment with an added C-terminal Pro-Gly-Pro extension that confers proteolytic stability. It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences and is supplied for in vitro research use only.
Semax is structurally derived from the 4-10 fragment of adrenocorticotropic hormone (ACTH) but lacks the corticotropic activity of full-length ACTH. Preclinical literature describes it as a non-corticotropic ACTH analog with retained central nervous system effects, often studied as a melanocortin-pathway-adjacent research tool.
Multiple rodent studies report Semax rapidly upregulates Bdnf and Ngf mRNA in the hippocampus and frontal cortex, with elevated mature BDNF protein in basal forebrain. Shadrina et al. (2010, PMID 19662538) and Dolotov et al. (2006, PMID 16635254) are key references for the neurotrophin pathway findings.
Semax has been investigated in cultured hippocampal neurons against glutamate excitotoxicity (Storozhevykh 2007, PMID 17760984), in rodent middle cerebral artery occlusion models of ischemia, and in oxidative-stress paradigms. It is reported to reduce ROS, attenuate calcium dysregulation, and modulate inflammatory gene expression in preclinical settings.
Lyophilized Semax should be stored at -20°C for long-term stability. Once reconstituted with bacteriostatic water, it should be refrigerated at 2-8°C and used within 14 days. Avoid repeated freeze-thaw cycles and protect from light. For in vitro research use only — not for human or veterinary administration.
The C-terminal Pro-Gly-Pro tripeptide is added to the natural ACTH(4-10) sequence to dramatically slow enzymatic degradation by aminopeptidases and endopeptidases. This proteolytic stability extends the duration of CNS activity in preclinical models compared to the parent ACTH(4-10) fragment alone.
Academic Literature

Sources & References

Peer-reviewed PubMed-indexed publications

PUBMED

Semax, an analogue of ACTH(4-10), binds specifically and increases levels of BDNF protein in rat basal forebrain

2006 · Dolotov OV et al. · PMID 16635254
View Source ↗
PUBMED

Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action

2010 · Shadrina MI et al. · PMID 19662538
View Source ↗
PUBMED

Heptapeptide Semax prevents glutamate-induced calcium dysregulation and ROS generation in cultured rat hippocampal neurons

2007 · Storozhevykh TP et al. · PMID 17760984
View Source ↗
PUBMED

Semax — an analog of ACTH(4-10): a review of pharmacological and neurotrophin-pathway research

2018 · Medvedeva EV et al. · PMID 30201095
View Source ↗