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RUO Report

Semax

Also: Semax, ACTH(4-10) analog, Met-Glu-His-Phe-Pro-Gly-Pro, MEHFPGP

NeuropeptideLimitedSynthetic ACTH(4-10)-fragment analog (heptapeptide) studied predominantly in preclinical animal and in-vitro models, with a limited and largely Russian-language clinical literature. Not an FDA-approved drug in the United States. Characterized here for research and educational reference only; not for human or veterinary use.

This profile summarizes research context only. It is not medical advice and does not describe how to use this compound in humans or animals — no dosing, administration, or protocols. Learn more

This entry is a draft pending editorial and source verification. It is excluded from search indexing until reviewed.

Semax is a synthetic heptapeptide described in the research literature as an analog of a short fragment of adrenocorticotropic hormone (ACTH(4-10)), with the C-terminal Pro-Gly-Pro motif reported to slow enzymatic breakdown. It originated in Russian neuropharmacology research and has been examined mainly in preclinical (animal and in-vitro) models, alongside a limited and largely Russian-language clinical literature. It is discussed in the research literature as a neuropeptide that has been studied in relation to neurotrophic and neuromodulatory signaling, but the available evidence is limited and requires careful interpretation due to study design and translation constraints. This profile is research-use-only and makes no claim that Semax is safe, effective, or suitable for any human or animal use.

Mechanism as described in the literature

Semax is described in the research literature as an analog of the ACTH(4-10) fragment, commonly represented by the sequence Met-Glu-His-Phe-Pro-Gly-Pro. The added C-terminal Pro-Gly-Pro is reported in mechanistic studies to reduce susceptibility to enzymatic degradation relative to the native fragment. Unlike full-length ACTH, the molecule is generally characterized in preclinical work as lacking corticotropic (hormone-releasing) activity.

Mechanisms discussed in preclinical and in-vitro models include modulation of neurotrophic signaling (for example, reported changes in BDNF and associated receptor pathways), and possible interaction with monoaminergic and other neuromodulatory systems. These mechanistic descriptions come predominantly from rodent and cell-based experiments; how, or whether, they translate to humans remains uncertain and is not established.

Research areas

  • Neurotrophic signaling pathways (e.g., BDNF-related) examined in preclinical models
  • Neuroprotection-related endpoints studied in animal ischemia/hypoxia models
  • Cognitive and behavioral endpoints in rodent studies
  • Peptide stability and metabolism (enzymatic degradation kinetics) examined in vitro
  • Monoaminergic and neuromodulatory system interactions discussed in preclinical research

Documentation notes

References

References for this entry are pending editorial verification. We do not publish citations we have not confirmed.

Frequently asked questions

What is Semax?+

Semax is a synthetic heptapeptide described in the research literature as an analog of a short fragment of ACTH (ACTH(4-10)), studied mainly in preclinical neuroscience research. It is presented here for research and educational reference only, with no claim of safety or benefit.

What does the research on Semax show?+

Most published work is preclinical (animal and in-vitro), describing mechanisms such as modulation of neurotrophic signaling, alongside a limited and largely Russian-language clinical literature. This evidence is limited and requires careful interpretation, and it does not establish any human outcome.

Is Semax approved or proven safe and effective?+

No. Semax is not an FDA-approved drug in the United States, and the available literature does not establish that it is safe or effective for any use. This profile does not recommend it for any human or animal application.