Semax

Semax Peptide (MEHFPGP) – BDNF, Neuroplasticity & Neuroprotection Research

ACTH-Derived Synthetic Heptapeptide for BDNF/TrkB Signaling, Experimental Cerebral Ischemia, Neuronal Gene Expression & Cognitive Neuroscience

Semax is a synthetic linear heptapeptide consisting of seven amino acids: methionine, glutamic acid, histidine, phenylalanine, proline, glycine and proline.

Its sequence is Met–Glu–His–Phe–Pro–Gly–Pro, abbreviated MEHFPGP.

Semax was developed as an analogue of a region of adrenocorticotropic hormone (ACTH), with a C-terminal Pro–Gly–Pro extension. It has been investigated in experimental neuroscience, particularly for its effects on neurotrophin expression, neuronal signaling, cerebral ischemia-associated responses and behavioral outcomes.

Its principal research areas include:

• Brain-derived neurotrophic factor (BDNF) expression

• Tropomyosin receptor kinase B (TrkB) signaling

• Nerve growth factor (NGF) research

• Experimental cerebral ischemia

• Neuronal gene expression

• Synaptic plasticity and hippocampal biology

• Learning and memory-associated animal models

• Neuroimmune and inflammatory signaling

• Vascular and cellular stress responses

• ACTH-derived peptide structure–activity relationships

• Pro–Gly–Pro peptide metabolism

• Analytical peptide characterization

Semax has a history of clinical use in Russia, where specific pharmaceutical formulations have been used for certain neurological indications.

However, the human evidence base remains concentrated in regional publications, and large, independently replicated clinical trials meeting contemporary international regulatory standards are lacking.

Semax is not an FDA-approved medicine and does not have EMA centralized marketing authorization.

ICAME Pharmacy Semax is intended exclusively for laboratory research.

FOR RESEARCH USE ONLY — NOT FOR HUMAN OR VETERINARY USE.

What Is Semax?

Semax is a synthetic neuroactive research peptide containing seven amino acids.

It was developed from research into fragments of ACTH, a peptide hormone produced by the anterior pituitary.

Although Semax is frequently described as an ACTH(4–10) analogue, its precise structure is more accurately represented as:

ACTH(4–7)–Pro–Gly–Pro

This distinction is important.

The first four residues of Semax correspond to positions 4–7 of ACTH:

Met–Glu–His–Phe

The remaining three residues are:

Pro–Gly–Pro

These replace the original ACTH residues that would otherwise follow phenylalanine.

Consequently, Semax is not simply an unchanged seven-residue fragment of ACTH.

Its modified structure is relevant to research on peptide stability, neurochemical activity and structure–function relationships.

Semax Molecular Structure

Semax is a linear heptapeptide joined by six peptide bonds.

It contains no disulfide bridge and is not a cyclic peptide.

Molecular Characteristics

These values refer to the unmodified Semax free peptide.

Trifluoroacetate, acetate and other salt or formulation forms can have different overall compositions and molecular masses.

Semax Amino Acid Sequence

The complete sequence of Semax is:

H-Met-Glu-His-Phe-Pro-Gly-Pro-OH

The N-terminal portion is derived from an ACTH-related sequence.

The C-terminal Pro–Gly–Pro region is a distinctive feature of Semax.

The peptide contains a sulfur-bearing methionine residue, which is relevant to oxidative stability research.

Semax and ACTH: Understanding the Structural Relationship

ACTH is a 39-amino-acid peptide hormone involved in adrenal steroid hormone regulation.

It interacts with the melanocortin 2 receptor (MC2R) as part of the hypothalamic–pituitary–adrenal axis.

Semax was developed from a modified ACTH-derived peptide sequence.

Structural Comparison

ACTH(4–7):

Met–Glu–His–Phe

ACTH(4–10):

Met–Glu–His–Phe–Arg–Trp–Gly

Semax:

Met–Glu–His–Phe–Pro–Gly–Pro

Semax therefore preserves the first four residues of ACTH(4–10) but replaces the following three residues.

This modification distinguishes Semax from the original hormone fragment.

Semax should not be assumed to possess the endocrine activity of full-length ACTH.

Why Is the Pro–Gly–Pro Sequence Important?

The C-terminal Pro–Gly–Pro motif is central to Semax's chemical design.

Proline-rich peptide regions can influence enzymatic degradation and molecular conformation.

Pro–Gly–Pro has also been investigated independently in experimental neurobiology.

Research Areas

Peptide stability

Proteolytic degradation

Enzyme–substrate interactions

Structure–activity relationships

Peptide metabolites

Neurotrophic gene expression

Comparative peptide pharmacology

Some experiments have compared Semax with Pro–Gly–Pro alone.

These studies found partially overlapping but distinct gene-expression responses.

This suggests that the complete Semax molecule and its C-terminal fragment should be investigated separately.

Scientific Background of Semax

Semax was developed through Russian research programs involving regulatory peptides and ACTH-derived analogues.

Its development was associated with investigations into neuroprotection, neurological recovery and peptide pharmacology.

Research has included cell-based experiments, animal models and human clinical observations.

A substantial portion of the clinical literature concerns cerebrovascular disorders.

Experimental studies have examined whether Semax influences neurotrophic signaling and cellular responses following brain injury.

The compound remains scientifically interesting because it connects peptide chemistry with multiple aspects of nervous system biology.

However, the existence of mechanistic findings does not establish clinical efficacy.

How Does Semax Work?

Semax does not have one fully established molecular mechanism explaining all reported biological effects.

Its proposed activity involves several interconnected processes.

These include:

Changes in neurotrophin gene expression

BDNF-associated signaling

TrkB receptor-associated responses

NGF-related signaling

Neuronal transcriptional regulation

Inflammatory and vascular gene-expression changes

Experimental responses to cerebral ischemia

Simplified Research Framework

Semax (MEHFPGP)

↓

Exposure in Experimental Neural Models

↓

Changes in Selected Neurotrophin and Signaling-Related Genes

↓

BDNF / NGF / Trk-Associated Molecular Responses

↓

Neuronal and Cellular Signaling Changes

↓

Measured Outcomes in Experimental Models

This framework represents research observations and hypotheses.

It does not establish a universal receptor-mediated mechanism or a clinically validated therapeutic effect.

Semax and BDNF Research

Brain-derived neurotrophic factor, or BDNF, is a protein involved in neuronal development, survival and synaptic function.

BDNF signaling is an important area of neuroscience research.

Semax has been investigated for its effects on BDNF gene expression and protein-associated signaling.

A 2006 study in Brain Research examined Semax in rat hippocampal tissue.

The investigators reported increases in BDNF-related molecular measurements, including BDNF protein levels and TrkB phosphorylation.

The study also examined learning-associated behavioral outcomes.

These findings support the investigation of Semax in neurotrophic signaling research.

However, they do not establish that Semax reliably increases BDNF or improves cognition in humans.

What Is BDNF?

BDNF belongs to the neurotrophin family.

It participates in several neuronal processes.

Principal Research Areas

Neuronal survival

Synaptic plasticity

Neuronal differentiation

Hippocampal signaling

Activity-dependent gene expression

Learning-associated neural adaptations

Neural circuit function

BDNF commonly signals through the TrkB receptor.

However, BDNF-related pathways are complex and depend on tissue and physiological context.

Semax and TrkB Signaling

TrkB is a receptor tyrosine kinase encoded by the NTRK2 gene.

It is a principal receptor for BDNF.

BDNF binding can activate intracellular signaling pathways including:

PI3K–AKT

RAS–RAF–MEK–ERK

PLCγ-associated signaling

These pathways influence neuronal functions in experimental systems.

Important Distinction

Semax should not be described as a proven direct TrkB receptor agonist.

Research has reported changes in BDNF expression and TrkB-associated signaling after Semax exposure.

These findings do not establish direct receptor binding by Semax.

Simplified BDNF/TrkB Signaling Pathway

BDNF

↓

TrkB Receptor Activation

↓

Intracellular Signaling

↓

PI3K–AKT / MAPK–ERK / PLCγ

↓

Context-Dependent Neuronal Responses

Semax has been investigated for its ability to influence components of this system.

The pathway shown above describes established BDNF biology, not a confirmed direct binding mechanism for Semax.

Semax and Nerve Growth Factor Research

Nerve growth factor, or NGF, is another member of the neurotrophin family.

It participates in neuronal development and maintenance.

A 2007 study investigated the effects of Semax on neurotrophin gene expression in rat brain regions.

The researchers reported region-specific changes in BDNF and NGF gene expression.

Research Areas

NGF transcription

Regional gene expression

Neurotrophic signaling

Neuronal stress responses

Growth-factor receptor biology

Neural tissue regulation

Importantly, the direction of gene-expression changes differed between brain regions.

Therefore, Semax should not be described as uniformly increasing all neurotrophins throughout the brain.

Semax and Region-Specific Gene Expression

The effects of a neuroactive compound can differ between brain regions.

Semax research has examined:

Hippocampus

Frontal cortex

Brainstem

Cerebellum

Cerebral cortex following ischemia

Some experiments reported increases in neurotrophin-related genes in certain regions and decreases in others.

This highlights the complexity of neural regulation.

Changes in messenger RNA do not necessarily correspond to proportional changes in protein concentration or biological function.

Semax and Neuroplasticity Research

Neuroplasticity refers to the nervous system's ability to change in response to activity, experience and injury.

BDNF-associated signaling plays a role in synaptic plasticity.

Because Semax has been investigated in BDNF-related pathways, it has attracted interest in neuroplasticity research.

Experimental Research Areas

Synaptic signaling

Hippocampal function

Neurotrophin expression

Neuronal adaptation

Activity-dependent responses

Learning-associated behavior

Neuronal survival

However, a change in BDNF expression is not sufficient to establish clinically meaningful neuroplasticity enhancement.

Semax and Synaptic Plasticity

Synaptic plasticity involves changes in communication between neurons.

Researchers study processes such as:

Long-term potentiation

Long-term depression

Synaptic protein expression

Neurotransmitter signaling

Dendritic morphology

Activity-dependent transcription

Semax-related neurotrophin findings provide a rationale for further investigation.

However, direct evidence supporting broad human synaptic enhancement remains insufficient.

Semax and Hippocampal Research

The hippocampus is involved in learning, memory and spatial processing.

Several Semax studies have focused on hippocampal tissue.

Experimental findings have included changes in:

BDNF expression

TrkB-associated signaling

NGF-related pathways

Neurotransmission-associated genes

Learning-related animal behavior

These results contribute to understanding potential peptide effects in neural tissue.

They do not establish that Semax improves memory in healthy humans.

Semax and Cognitive Research

Semax is frequently discussed as a nootropic research peptide.

The term nootropic is commonly used for compounds investigated or promoted for cognitive effects.

However, this designation does not establish efficacy.

Cognitive Research Areas

Learning-related behavior

Memory-associated processes

Attention

Neurotrophic signaling

Stress and cognition interactions

Neuronal gene expression

Experimental behavioral pharmacology

Some animal studies reported changes in learning-associated behavioral tasks.

Human cognitive enhancement claims remain insufficiently supported by large, independently replicated clinical trials.

Semax and Memory Research

Memory involves coordinated activity across multiple neural systems.

Semax has been investigated in experimental models involving hippocampal function and conditioned learning.

Some studies reported changes in behavioral outcomes.

However, the available evidence does not establish reliable improvements in human memory.

Semax should not be marketed as a clinically proven memory-enhancing treatment.

Semax and Attention Research

Attention involves several interacting neurotransmitter and neural network systems.

Semax has been discussed in connection with attention-related research.

Some regional clinical publications have examined neurological and cognitive outcomes.

However, strong international clinical evidence establishing Semax as an effective treatment for attention disorders is lacking.

Its effects should not be equated with those of approved attention-related medicines.

Semax and Cerebral Ischemia Research

Cerebral ischemia occurs when blood supply to brain tissue becomes insufficient.

It can lead to oxygen deprivation, metabolic disruption and neuronal injury.

Semax has been investigated in animal models of cerebral ischemia.

A frequently used experimental model is middle cerebral artery occlusion.

Research Areas

Ischemia-associated gene expression

Neurotrophin signaling

Inflammatory responses

Vascular-associated genes

Neuronal stress

Cell survival

Tissue injury responses

Recovery-associated molecular pathways

These models help researchers study biological mechanisms.

However, findings in rodents cannot establish efficacy in human stroke treatment.

Semax and Middle Cerebral Artery Occlusion Models

Middle cerebral artery occlusion, or MCAO, is a commonly used animal model of focal cerebral ischemia.

Researchers have investigated how Semax influences gene expression following experimental arterial occlusion.

A 2009 study reported that Semax and Pro–Gly–Pro altered transcription of neurotrophins and their receptors in rat cerebral cortex after permanent MCAO.

The observed effects varied across time points.

Research Topics

BDNF expression

NGF expression

Trk receptor-associated genes

Time-dependent transcription

Ischemia-associated stress responses

Comparative Semax and PGP effects

These results provide evidence of experimental molecular activity.

They do not demonstrate a clinically validated stroke treatment.

Semax and Neuroinflammation Research

Neuroinflammation involves interactions among neurons, glial cells and immune-associated signaling systems.

Cerebral ischemia can activate inflammatory pathways.

Semax has been investigated for its effects on gene-expression networks associated with inflammation.

Experimental Research Areas

Cytokine-associated signaling

Immune-response genes

Glial-associated processes

Inflammatory pathway regulation

Cellular stress responses

Post-ischemic tissue changes

Some transcriptomic studies have reported changes in inflammation-associated gene expression following Semax exposure.

However, the direction and biological significance of these changes depend on the experimental model.

Semax is not established as a clinically effective anti-inflammatory treatment.

Semax and Neuroimmune Communication

The nervous and immune systems interact through complex signaling pathways.

Neural injury can alter immune-associated gene expression.

Semax has been studied in experimental systems involving these interactions.

Potential endpoints include:

Immune-associated transcription

Neural cell responses

Cytokine signaling

Vascular regulation

Inflammatory pathway activity

Tissue stress responses

These findings are relevant to systems-level neuroscience.

However, experimental transcriptomic changes do not establish immune-enhancing or disease-modifying effects in humans.

Semax and Vascular Research

Cerebral blood flow and vascular regulation are important aspects of brain physiology.

Experimental ischemia can influence vascular-associated gene networks.

Semax-related studies have examined changes in genes involved in vascular and immune-associated processes.

Research Areas

Vascular gene expression

Ischemic tissue responses

Endothelial-associated signaling

Cellular stress

Neurovascular interactions

Post-injury molecular adaptation

However, Semax has not been established as a clinically effective treatment for vascular disease.

Semax and Neuroprotection Research

Neuroprotection refers to experimental strategies intended to reduce or prevent neuronal injury.

Semax has been investigated in preclinical neuroprotection models.

Some studies have reported favorable changes in molecular or behavioral endpoints.

Research Areas

Neuronal survival

Ischemia-associated stress

Neurotrophin signaling

Inflammatory gene expression

Cellular stress responses

Experimental tissue injury

Behavioral recovery measures

However, neuroprotective effects reported in animal models do not establish human clinical efficacy.

Semax and Oxidative Stress Research

Oxidative stress is relevant to neuronal injury and ischemia.

It involves an imbalance between reactive species and antioxidant defenses.

Semax-related research has investigated cellular stress responses in experimental neurological models.

Potential Research Endpoints

Reactive oxygen species

Oxidative injury markers

Cell viability

Stress-associated gene expression

Mitochondrial-associated processes

Neuronal signaling

However, Semax should not be described as a clinically proven antioxidant treatment.

Semax and Neuronal Gene Expression

One of the most important areas of Semax research involves changes in gene expression.

Modern transcriptomic methods allow researchers to measure thousands of messenger RNA species simultaneously.

Semax has been investigated in studies examining gene-expression patterns after experimental brain injury.

Research Areas

RNA sequencing

Differential gene expression

Neurotrophin-associated transcripts

Inflammatory pathways

Vascular-associated genes

Neuronal signaling networks

Time-dependent responses

These studies provide insight into the complexity of experimental peptide activity.

However, gene-expression changes do not necessarily demonstrate improved clinical outcomes.

Semax and Transcriptomic Research

Transcriptomics examines RNA expression across a biological sample.

Semax studies have used gene-expression methods to investigate responses following experimental cerebral ischemia.

Researchers have identified changes in multiple biological pathways.

Important Interpretation

A transcriptomic result is not equivalent to a demonstrated therapeutic benefit.

The direction and significance of gene-expression changes require validation through protein, functional and physiological measurements.

Semax and Dopaminergic Research

Dopamine is involved in movement, motivation and reward-associated signaling.

Semax has been investigated in neurochemical and behavioral research involving monoamine systems.

Research Topics

Dopamine-associated signaling

Neurotransmitter metabolism

Behavioral responses

Neural circuit activity

Neurochemical adaptation

However, Semax has not been established as a clinically reliable dopamine enhancer.

Claims that it consistently increases motivation or treats dopamine-related disorders are unproven.

Semax and Serotonergic Research

Serotonin participates in mood-associated, sensory and physiological processes.

Some Semax-related research has explored broader neurotransmitter interactions.

Potential research areas include:

Serotonin-associated signaling

Neurochemical regulation

Stress-related responses

Behavioral pharmacology

Neural adaptation

However, Semax is not an established selective serotonin reuptake inhibitor or clinically validated serotonergic treatment.

Semax and Melanocortin Research

Semax is structurally related to an ACTH-derived sequence.

ACTH belongs to the melanocortin peptide family.

Melanocortin receptors participate in diverse physiological functions.

However, the structural relationship between Semax and ACTH does not establish identical receptor pharmacology.

Research Questions

Does Semax interact directly with melanocortin receptors?

Which molecular targets mediate its experimental effects?

Does its modified C-terminal sequence change receptor interactions?

Are observed effects receptor-dependent or indirect?

How does Semax differ from full-length ACTH?

These questions require direct receptor-binding and functional assays.

Semax should not be described as a confirmed universal melanocortin receptor agonist.

Semax and the HPA Axis

The hypothalamic–pituitary–adrenal axis regulates stress-associated endocrine signaling.

Full-length ACTH stimulates adrenal corticosteroid production.

Semax is a modified ACTH-derived peptide.

However, it is not equivalent to full-length ACTH.

Its experimental neurological effects should not be interpreted as proof of conventional ACTH-like adrenal stimulation.

The endocrine pharmacology of Semax requires product- and model-specific evaluation.

Semax and Learning-Related Animal Models

Behavioral neuroscience uses animal models to study learning-associated processes.

Semax has been investigated in selected learning and conditioning experiments.

Some studies reported changes in conditioned behavioral responses.

Research Areas

Conditioned avoidance

Hippocampal-associated learning

Behavioral adaptation

Neurotrophin expression

Stress-associated performance

Experimental memory tasks

However, animal behavioral findings cannot establish improved learning performance in humans.

Semax and Brain Injury Research

Experimental brain injury involves complex processes.

These include:

Metabolic stress

Inflammation

Neuronal dysfunction

Vascular responses

Oxidative injury

Cell death

Tissue remodeling

Semax-related studies have examined some of these processes.

However, Semax has not been established as an FDA- or EMA-approved treatment for traumatic brain injury, stroke or other neurological injuries.

Semax and Neurodegenerative Disease Research

Neurodegenerative diseases involve progressive changes in neuronal function and survival.

BDNF-associated signaling and neuroinflammation are relevant to several neurodegenerative research fields.

Because Semax has been investigated in these pathways, it may be of exploratory interest.

Potential Research Areas

Neurotrophic signaling

Neuronal survival

Synaptic dysfunction

Oxidative stress

Inflammatory signaling

Neural network adaptation

However, Semax has not been demonstrated to prevent or treat Alzheimer's disease, Parkinson's disease or other neurodegenerative disorders in rigorous human clinical trials.

Semax and Alzheimer's Disease Research

Alzheimer's disease involves complex molecular and cellular pathology.

BDNF and synaptic dysfunction are relevant research topics.

Semax's reported effects on neurotrophin-associated pathways provide a rationale for exploratory investigation.

However, this does not establish a disease-modifying effect.

Semax is not an established treatment for Alzheimer's disease.

Semax and Parkinson's Disease Research

Parkinson's disease involves degeneration of specific neuronal populations and complex neurochemical changes.

Neurotrophic signaling has been investigated in Parkinson's disease research.

However, Semax has not been clinically established to prevent or reverse dopaminergic neuronal degeneration.

Claims of therapeutic benefit require stronger evidence.

Semax and Peptide Stability

Semax is a short linear peptide.

Its chemical stability can be influenced by environmental conditions and formulation.

Potential degradation processes include:

Oxidation

Peptide bond hydrolysis

Enzymatic cleavage

Chemical modification

Aggregation or adsorption

Temperature-dependent degradation

pH-dependent reactions

The methionine residue is relevant to oxidation-associated stability research.

Product-specific analytical data are necessary to establish validated storage conditions.

Semax and Proteolytic Degradation

Proteolytic enzymes can break peptide bonds.

The Pro–Gly–Pro extension has been investigated in relation to peptide metabolism and biological activity.

Research Topics

Protease susceptibility

Peptide fragments

Enzymatic degradation

Metabolite identification

Peptide stability

Structure–activity relationships

The presence of a Pro–Gly–Pro motif does not establish a universal biological half-life.

Semax vs. Selank

Semax and Selank are both synthetic linear heptapeptides.

They have different structural origins and research backgrounds.

Although they share a C-terminal motif, Semax and Selank are distinct compounds.

Their reported effects should not be treated as interchangeable.

Semax vs. N-Acetyl Semax Amidate

N-Acetyl Semax Amidate is a chemically modified derivative of Semax.

It differs from standard Semax in terminal chemistry.

Standard Semax

H-Met-Glu-His-Phe-Pro-Gly-Pro-OH

N-Acetyl Semax Amidate

Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH₂

The N-terminal acetylation and C-terminal amidation change molecular composition and potentially influence chemical and biological properties.

However, claims of superior stability, potency or brain penetration require direct experimental evidence.

Data from standard Semax cannot automatically establish the effects of N-Acetyl Semax Amidate.

Semax vs. ACTH

ACTH is an endogenous 39-amino-acid peptide hormone.

Semax is a synthetic seven-amino-acid analogue of a modified ACTH-derived region.

Semax should not be classified as full-length ACTH.

Semax vs. Pinealon

Semax and Pinealon are distinct research peptides.

Semax: Met–Glu–His–Phe–Pro–Gly–Pro

Pinealon: Glu–Asp–Arg

Research results from one compound cannot be assumed to apply to the other.

Semax vs. Oxytocin

Oxytocin is an endogenous cyclic nonapeptide hormone.

Semax is a synthetic linear heptapeptide.

The two peptides are not interchangeable.

Semax vs. KPV

KPV is a tripeptide associated with α-MSH-derived research.

Semax is a heptapeptide associated with ACTH-derived research.

Both are structurally related to different regions of the melanocortin peptide family.

However, their sequences and research areas differ.

Semax Human Clinical Research

Semax has been studied in humans, particularly in Russia.

Published investigations have examined neurological outcomes in conditions including cerebrovascular disorders.

Some studies reported favorable outcomes.

However, important limitations remain.

Major Limitations

Regional concentration of clinical research

Limited independent international replication

Variable study designs

Incomplete methodological reporting in some publications

Small or moderate participant groups

Limited long-term safety data

Insufficient high-quality confirmatory trials

Uncertain generalizability

The existence of clinical studies does not establish approval or efficacy under FDA or EMA standards.

Semax Regulatory Status

United States

Semax is not an FDA-approved human therapeutic drug.

European Union

Semax does not have EMA centralized marketing authorization.

Russia

Semax has a history of regional pharmaceutical development and clinical use.

Research-Grade Products

Research-grade Semax is not equivalent to an approved pharmaceutical formulation.

Regional pharmaceutical use does not authorize human administration of research-grade material.

Semax Safety Considerations

The human safety profile of Semax remains incompletely characterized.

Unknown Long-Term Safety

Large, independently replicated long-term studies are lacking.

Incomplete Human Pharmacokinetics

Absorption, distribution, metabolism and elimination are not comprehensively characterized across formulations.

Potential Neurological Effects

Experimental changes in neurochemical signaling require further investigation.

Unknown Drug Interactions

Interactions with neurological or psychiatric medicines have not been adequately characterized.

Formulation Differences

Research-grade products may differ in purity, peptide content and manufacturing controls.

Peptide Degradation

Chemical instability or degradation may affect product identity and experimental reproducibility.

Unproven Clinical Benefits

Claims involving memory enhancement, attention, stroke recovery or neurodegenerative disease treatment require stronger clinical evidence.

Research Product Limitations

Research-grade Semax is not automatically sterile, pharmaceutical-grade or suitable for human administration.

Research-grade Semax must not be used as a substitute for evidence-based neurological or psychiatric treatment.

Semax Analytical Characterization

Accurate molecular identification is essential for peptide research.

Important Specifications

Verified amino acid sequence

Molecular identity

Terminal chemistry

Peptide purity

Peptide content

Counterion composition

Impurity profile

Residual reagents

Oxidation-related degradation products

Batch-specific documentation

High-Performance Liquid Chromatography

HPLC can help evaluate peptide purity and detect chromatographic impurities.

A high purity percentage does not establish pharmaceutical quality or clinical efficacy.

Liquid Chromatography–Mass Spectrometry

LC-MS can support molecular identity verification.

For standard unmodified Semax, the expected molecular mass is approximately 813.9 g/mol.

The analytical result should be consistent with the specified molecular form.

Methionine Oxidation Analysis

Semax contains methionine, a sulfur-containing amino acid.

Methionine can undergo oxidation under certain conditions.

Analytical testing may be used to assess oxidation-related degradation.

Such testing is relevant to peptide stability and research reproducibility.

Peptide Content Analysis

Peptide content analysis helps distinguish the quantity of actual peptide from the total mass of supplied material.

This is particularly relevant when counterions, water or other formulation components are present.

Certificate of Analysis

A batch-specific COA should provide relevant analytical information.

Important data may include:

• Product identity

• Batch or lot number

• Analytical methods

• Peptide purity

• Peptide content

• Molecular identity

• Counterion information

• Impurity profile

• Stability documentation

A COA does not establish therapeutic efficacy or authorization for human use.

Scientific Evidence and Research Limitations

Established Molecular Facts

• Semax is a synthetic linear heptapeptide.

• Its amino acid sequence is MEHFPGP.

• Its molecular formula is C₃₇H₅₁N₉O₁₀S.

• Its molecular weight is approximately 813.9 g/mol.

• Its CAS number is 80714-61-0.

• It contains a modified ACTH-derived sequence.

• Its C-terminal region contains Pro–Gly–Pro.

• Animal studies have reported changes in BDNF-related signaling.

• Experimental ischemia studies have reported neurotrophin gene-expression changes.

• Semax has been investigated in human clinical research, primarily in Russia.

Important Limitations

• A complete molecular mechanism has not been established.

• Direct receptor interactions remain incompletely characterized.

• Large, independently replicated international clinical trials are lacking.

• FDA approval has not been granted.

• EMA centralized authorization has not been granted.

• Long-term human safety is insufficiently characterized.

• Reliable cognitive enhancement in healthy humans is not established.

• Human stroke-treatment efficacy has not been established under FDA/EMA regulatory standards.

• Neurodegenerative disease treatment benefits are unproven.

• Findings from standard Semax cannot automatically be applied to modified derivatives.

• Research-grade preparations are not approved pharmaceutical products.

Potential Semax Research Applications

Semax may be relevant to appropriately controlled laboratory investigations involving:

• ACTH-derived peptide chemistry

• Neurotrophin gene expression

• BDNF signaling

• TrkB-associated pathways

• NGF expression

• Trk receptor research

• Hippocampal neurobiology

• Synaptic plasticity

• Learning-associated animal models

• Experimental cerebral ischemia

• Middle cerebral artery occlusion models

• Post-ischemic gene expression

• Neuroimmune signaling

• Inflammatory pathway research

• Vascular-associated gene expression

• Neuronal stress responses

• Neurotransmission

• Transcriptomic research

• Pro–Gly–Pro peptide metabolism

• Peptide stability

• Methionine oxidation

• Structure–activity relationships

• Analytical method development

These are scientific research applications, not established therapeutic benefits.

Semax Research Overview

Compound Name: Semax

Alternative Names: MEHFPGP / ACTH(4–7)PGP

Classification: Synthetic Linear Heptapeptide

Amino Acid Length: 7

Sequence: H-Met-Glu-His-Phe-Pro-Gly-Pro-OH

One-Letter Sequence: MEHFPGP

Molecular Formula: C₃₇H₅₁N₉O₁₀S

Molecular Weight: Approximately 813.9 g/mol

CAS Number: 80714-61-0

PubChem CID: 9811102

Structural Origin: Modified ACTH-Derived Peptide

Principal Research Areas: BDNF / TrkB Signaling / Experimental Neuroprotection / Cerebral Ischemia

Established Single Molecular Receptor: Not Conclusively Identified

Human Clinical Evidence: Limited Regional Studies

FDA/EMA Approval: No

Intended Research Use: Laboratory Research Only

ICAME Pharmacy Product Information

Product Name: Semax

Alternative Name: MEHFPGP

Brand: ICAME Pharmacy

Product Category: Research Peptide

Research Classification: Synthetic ACTH-Derived Heptapeptide

Research Areas: Neurobiology / BDNF Signaling / Cerebral Ischemia / Peptide Pharmacology

Intended Use: Laboratory Research & Development Only

Product identity and specifications should be verified using batch-specific analytical documentation.

Relevant quality information includes:

• Verified amino acid sequence

• Molecular identity

• Peptide purity

• Peptide content

• Counterion composition

• Impurity profile

• Analytical methodology

• Certificate of Analysis (COA)

• Batch or lot identification

• Validated stability and storage conditions

No claims of pharmaceutical quality, sterility, injectable suitability or clinical efficacy should be made without appropriate supporting documentation.

Important Research Use Notice

FOR RESEARCH USE ONLY (RUO)

This ICAME Pharmacy product is intended exclusively for legitimate laboratory, analytical and scientific research purposes.

Not for human or veterinary use. Not for diagnostic, therapeutic, cognitive enhancement, neurological recovery, stroke treatment, performance-enhancing or other clinical purposes. Not for direct administration to humans or animals.

Semax is a synthetic heptapeptide investigated in experimental neuroscience and limited regional clinical studies.

Its precise molecular mechanism, human pharmacokinetics, long-term safety and broad clinical efficacy have not been adequately established.

Experimental findings involving BDNF expression, TrkB-associated signaling or cerebral ischemia do not establish therapeutic benefits in humans.

Regional pharmaceutical use of Semax does not establish the suitability of research-grade products for clinical administration.

Information presented on this page is intended solely for scientific and educational purposes and does not constitute medical advice, prescribing information, dosage guidance or instructions for human use.

About ICAME Pharmacy

ICAME Pharmacy provides specialized research products for professional laboratory and scientific applications.

Our portfolio focuses on compounds relevant to peptide science, neurobiology, molecular signaling, neurotrophic research and analytical chemistry.

We emphasize accurate product identification, responsible research use, scientific transparency and clear communication of evidence limitations.

For batch-specific analytical documentation and product inquiries, please contact ICAME Pharmacy.

Frequently Asked Questions About Semax

What is Semax?

Semax is a synthetic seven-amino-acid peptide developed from a modified ACTH-derived sequence.

What is the amino acid sequence of Semax?

Met–Glu–His–Phe–Pro–Gly–Pro.

What is the one-letter sequence of Semax?

MEHFPGP.

How many amino acids does Semax contain?

Seven amino acids.

What is the molecular formula of Semax?

C₃₇H₅₁N₉O₁₀S.

What is the molecular weight of Semax?

Approximately 813.9 g/mol.

What is the CAS number of Semax?

80714-61-0.

Is Semax a cyclic peptide?

No. Semax is a linear heptapeptide.

Is Semax derived from ACTH?

Yes. Semax contains the ACTH(4–7) sequence followed by Pro–Gly–Pro.

Is Semax identical to ACTH(4–10)?

No. Semax is a modified analogue rather than the unchanged ACTH(4–10) sequence.

What is the mechanism of action of Semax?

Its complete mechanism is not established. Research has investigated neurotrophin expression, BDNF/TrkB-associated signaling and other neuronal gene-expression pathways.

Does Semax increase BDNF?

Some rat studies reported increases in BDNF-associated measurements, but reliable clinical effects in humans have not been established.

Does Semax activate TrkB?

Experimental studies have reported changes in TrkB-associated signaling. Direct agonism of the TrkB receptor by Semax has not been conclusively established.

Has Semax been studied in stroke research?

Yes. Semax has been investigated in experimental cerebral ischemia models and regional human clinical studies.

Does Semax treat stroke?

Its efficacy has not been established through the large, independently replicated clinical trials required for FDA or EMA authorization.

Does Semax improve memory?

Some animal studies reported learning-related effects, but reliable human memory enhancement has not been established.

Does Semax improve attention?

Strong international clinical evidence establishing attention-related benefits is lacking.

Is Semax the same as Selank?

No. Semax is MEHFPGP, while Selank is TKPRPGP.

Is Semax the same as N-Acetyl Semax Amidate?

No. N-Acetyl Semax Amidate is a chemically modified derivative.

Does Semax have ACTH-like hormonal activity?

Semax is structurally related to an ACTH fragment but should not be assumed to reproduce the endocrine activity of full-length ACTH.

Is Semax approved by the FDA?

No. Semax is not an FDA-approved human therapeutic drug.

Is Semax approved by the EMA?

Semax does not have EMA centralized marketing authorization.

Is Semax used as a medicine in Russia?

Yes. Semax has a history of regional pharmaceutical use in Russia.

Is Semax safe for human use?

Its human safety profile, particularly for research-grade preparations, has not been adequately established.

Is ICAME Pharmacy Semax intended for human use?

No. ICAME Pharmacy Semax is intended strictly for laboratory research and development purposes.