Semax — ACTH (4–10)–Derived Heptapeptide (RUO)

Semax is a synthetic heptapeptide derived from the N-terminal fragment of Adrenocorticotropic Hormone (ACTH), specifically residues 4–10. Unlike full-length ACTH, Semax lacks hormonal activity and does not stimulate corticosteroid release. It is utilized as a molecular research probe for investigating neuropeptide signaling, neurotrophin expression, and stress-responsive gene regulation.

Compound Name:
Semax
Category:
Neurological & Cognitive
Peptide Class:
Synthetic Heptapeptide
Primary Research Focus:
Neuropeptide Signaling & Stress Response
Regulatory Status:
Research Use Only (RUO)
Verification Date:
2026-02-07
Sequence Length:
7 Amino Acids
Amino Acid Sequence:
Met–Glu–His–Phe–Pro–Gly–Pro
Chemical Formula:
C₃₉H₅₄N₁₀O₁₀S
Molecular Weight:
~855 g/mol
Store powder at +4°C (short term) or -20°C (long term). Keep desiccated.
For laboratory research use only. Reconstitute using sterile bacteriostatic water consistent with established laboratory research protocols. Preparation should be performed under aseptic conditions. Reconstituted material is not intended for long-term storage.
Chemical Formula:

Semax is widely used as a reference compound to study rapid neurotrophin upregulation in the central nervous system.

  •  BDNF & NGF mRNA: Studies demonstrate increased Brain-Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF) mRNA expression in the hippocampus and frontal cortex of rodent models.
  •  Receptor Activation: Investigation of downstream TrkB receptor signaling pathways associated with synaptic plasticity and neuronal survival.

Semax is employed in ischemic and stress-based experimental models to assess large-scale gene expression changes.

  •  Gene Cluster Regulation: Modulation of genes associated with immune response, vascular tone regulation, and cellular stress adaptation.
  •  Inflammatory Response: Evaluation of suppressed pro-inflammatory cytokine expression during acute ischemic events in experimental models.

Beyond transcriptomic effects, Semax is studied for its influence on neurotransmitter metabolism.

  • Monoamine Turnover: Analysis of dopamine and serotonin metabolic turnover in the striatum and hypothalamus.
  • Melanocortin Receptors: Investigation of peptide interaction with melanocortin receptors (MC4R/MC5R), distinguishing its non-hormonal activity from native ACTH.

Structural modification of the ACTH fragment enables Semax to serve as a stability model peptide.

  •  Pro–Gly–Pro Motif: Confirmation that the C-terminal tripeptide confers resistance to serum peptidases compared to native ACTH(4–10).
  •  Half-Life Extension: Comparative degradation kinetics measured in plasma and cerebrospinal fluid (CSF) models.

In-Vitro Extrapolation: Correlating molecular gene expression changes with behavioral outcomes remains complex.

Species Specificity: Neurotrophin signaling pathways are conserved, but receptor density varies across species.

Delivery Mechanisms: Research often utilizes intranasal or parenteral administration; stability data may not extrapolate across routes.

  • Medvedeva, E. V., et al. (2014). BMC Genomics.
  • Dolotov, O. V., et al. (2006). Brain Research.
  • Dmitrieva, V. G., et al. (2009). Neurochemical Journal.
  • Eremin, K. O., et al. (2005). Neurochemical Research.
The compound listed below is referenced in research contexts related to the mechanisms discussed in this article.
Semax is a chemical reference standard intended strictly for in-vitro and laboratory research applications (e.g., gene expression analysis, receptor binding assays). It is not a drug, dietary supplement, or nootropic and is not intended for human consumption, injection, or therapeutic use. All handling must be performed by qualified professionals in a laboratory setting.

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