Semax Peptide (10 mg)

Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic analogue of the ACTH(4–10) fragment engineered to remove hormonal activity while preserving and enhancing its neuroactive properties. It is widely used in experimental neurobiology to investigate cognition, synaptic plasticity, neuroprotection, inflammatory signaling, and cerebrovascular regulation. Semax has demonstrated potent neuromodulatory effects in animal and human research settings, including modulation of BDNF pathways, antioxidant gene expression, and dopaminergic signaling.

Semax is stable, rapidly absorbed intranasally in research models, and capable of exerting central nervous system activity without crossing-reactivity to classical ACTH/MC2R hormonal pathways.

Specifications

Synonyms: ACTH(4–10) analogue; Met-Glu-His-Phe-Pro-Gly-Pro; Semax peptide

Sequence: MEHFPGP

Molecular formula: C₃₇H₅₁N₉O₁₀

Molecular weight: 799.86 g/mol

Class: Synthetic heptapeptide / neuroactive ACTH fragment analogue / nootropic research peptide

Mechanism of Action and Neurotrophic Signaling

Semax modulates multiple neurobiological pathways, most notably BDNF (brain-derived neurotrophic factor) and its downstream cascades:

1. BDNF Upregulation and TrkB Signaling

Experimental work has shown that Semax significantly increases BDNF mRNA expression in the hippocampus and frontal cortex, enhancing synaptic plasticity and long-term potentiation.
This is associated with activation of MAPK/ERK, PI3K/Akt, and CaMKII signaling networks.

2. Antioxidant and Stress-Response Gene Regulation

Transcriptomic studies demonstrate that Semax upregulates genes involved in:

• Antioxidant defense (SOD, catalase)

• Anti-inflammatory modulation

• Neuronal survival during hypoxic/ischemic stress

Administration in rat models led to rapid induction of neuroprotective gene clusters following cerebral ischemia.

3. Modulation of Dopaminergic and Serotonergic Systems

Semax enhances dopaminergic transmission in the nucleus accumbens and frontal cortex, contributing to its experimental cognitive and behavioral effects.

4. Neurovascular and Cerebroprotective Effects

Semax can improve cerebral microcirculation under ischemic conditions, reduce endothelial inflammation, and prevent free-radical damage in experimental stroke models.

Semax in Cognitive Research and Memory Models

Learning and Memory Enhancement

Animal studies show Semax improves:

• Spatial learning

• Memory consolidation

• Attention and task performance

This has been attributed to its modulation of neurotrophic factors and monoaminergic neurotransmission.

Attention and Executive Function

Human neuropsychological studies in controlled settings found improved attention stability, reduced mental fatigue, and enhanced resistance to cognitive overload following Semax administration.

These findings support its use as a research tool for studying cognition, neuroplasticity, and functional brain activation under stress.

Semax in Ischemia, Neurotrauma, and Inflammation Models

Cerebral Ischemia and Stroke Research

In rodent ischemia models, Semax administration:

• Reduced infarct volume

• Decreased pro-inflammatory cytokines (TNF-α, IL-1β)

• Preserved neuronal viability

• Normalized blood–brain barrier permeability

Oxidative Stress and Neuronal Protection

Semax increased expression of anti-apoptotic and antioxidant genes, limiting free-radical injury after experimental hypoxia.

Immune and Stress Response

Transcriptomic studies identified strong modulation of genes associated with:

• Immune cell activation

• Cytokine production

• Glutamatergic signaling

Other Experimental Applications

1. Pain and Analgesia Research

Semax influences nociceptive thresholds and may modulate pain transmission through interactions with melanocortin and neurotrophin signaling circuits.

2. Neurodevelopment and Plasticity

Semax has been used to study neurogenesis and synaptic remodeling, especially in models where BDNF regulation is central.

3. Stress Adaptation and Behavioral Resilience

Research indicates improved behavioral responses under acute or chronic stress, likely linked to dopaminergic and BDNF-mediated plasticity.

Research Use Only – Important Notice

This Semax (10 mg) product is supplied exclusively for laboratory research purposes.

• Not for human or veterinary use

• Not for diagnostic, therapeutic, or clinical application

• Intended solely for in vitro and controlled in vivo experimental systems

• Must be handled only by qualified laboratory professionals

All descriptions provided summarize findings from preclinical and early-stage human research and must not be interpreted as medical or clinical claims of safety or efficacy.

References

1. Inozemtseva AA et al. Semax modulates expression of genes related to neurotransmission and neurotrophic pathways. Front Pharmacol.
   https://www.frontiersin.org/articles/10.3389/fphar.2021.637995/full

2. Navolotskaya EV et al. Peptide Semax: Mechanisms of neuroprotection and neurotrophic regulation. Neurosci Behav Physiol.
   https://pubmed.ncbi.nlm.nih.gov/16465412/

3. Andreeva LA et al. Transcriptomic response to Semax after cerebral ischemia in rats. Mol Biol Reports.
   https://pubmed.ncbi.nlm.nih.gov/32914367/

4. Ashmarin IP et al. Semax and cognitive performance under high mental load. Hum Physiol.
   https://pubmed.ncbi.nlm.nih.gov/10852105/

5. Volkova TV et al. Semax-induced BDNF upregulation in hippocampal structures. Bull Exp Biol Med.
   https://pubmed.ncbi.nlm.nih.gov/15339073/

6. Andreeva LA et al. Gene networks modulated by Semax during ischemic injury. Mol Biol (Mosk).
   https://pubmed.ncbi.nlm.nih.gov/32852230/

7. Ashmarin IP et al. Analgesic properties of Semax in animal models. Bull Exp Biol Med.
   https://pubmed.ncbi.nlm.nih.gov/12564714/

8. Kolomin T et al. Neuroprotective effects of Semax in oxidative stress models. Front Neurosci.
   https://www.frontiersin.org/articles/10.3389/fnins.2020.00059/full