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Semax: sourcing, documentation and price

Semax is a synthetic ACTH(4-7) analogue heptapeptide sold for laboratory research. This page covers its identifiers, the models it has been studied in, documentation practice and catalogue pricing.

Semax is the common name for the synthetic heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro, an ACTH(4-7) analogue also referred to in the literature as ACTH(4-7)PGP and as an ACTH(4-10) analogue [2][7]. It is a research peptide, not a therapeutic product, and it is supplied as a lyophilised solid for laboratory use. The sequence given in the evidence is Met-Glu-His-Phe-Pro-Gly-Pro, and the same source describes it as a synthetic regulatory peptide with high affinity for Cu(II) ions [2].

The work on this compound centres on neuroprotective peptide signalling, with the adrenocorticotropic hormone (ACTH) framework as the structural starting point and, in separate lines of work, the mu opioid receptor gene Oprm1 as a named target [5][8].

Research Studies

Semax and amyloidosis in a transgenic Alzheimer's disease model

A study assessed the effect of Semax and a derivative on behavioural characteristics and the development of amyloidosis in transgenic animals used as an Alzheimer's disease model [1]. The paper frames the work against the broader problem that no remedies have been found that are effective in treating or significantly slowing the pathological process while being sufficiently safe, and it places natural peptide drugs within that gap [1]. The findings reported are from an animal model, not from human participants.

Semax and copper-catalysed oxidation of amyloid beta in vitro

Semax was studied in vitro for its ability to inhibit the copper-catalysed oxidation of amyloid beta [2]. The results indicate that Semax is able to extract Cu(II) from Cu(II)-amyloid beta species and to influence the redox behaviour of the complex [2]. The paper situates this against the postulate that reactive oxygen species generated in a Fenton-like reaction connected with Cu(II)/Cu(I) redox cycling of the Cu(II)-amyloid beta complex can play a key role in the molecular mechanism of neurotoxicity in Alzheimer's disease [2]. This is in vitro work; no animal or human outcome is claimed here.

Semax and gene expression in the penumbra-associated frontal cortex after tMCAO

Using RNA-Seq, differentially expressed genes associated with ACTH(4-7)PGP (Semax) and ACTH(6-9)PGP were first revealed in the penumbra-associated region of the frontal cortex of rats at 24 h after transient middle cerebral artery occlusion [5]. The peptides significantly reduced profile disturbances caused by ischemia across a large set of genes [5]. The model is rat tMCAO; the tissue is frontal cortex.

Semax and brain gene expression profile at 24 h after experimental stroke

A companion analysis examined the penumbra-associated frontal cortex of rats and the actions of the same peptides at 24 h after tMCAO using RNA-Seq [6]. The earlier work in that line had analysed the ipsilateral frontal cortex at 4.5 h after tMCAO [6]. Both timepoints are in rats; neither reports a human endpoint.

Semax and intracellular calcium dynamics in rat brain neurons

Semax was applied at 1 μM to study spontaneous fluctuations of intracellular calcium ion concentration in pyramidal neurons on hippocampal slices, and to study a proton-induced increase in intracellular calcium in cerebellar granule cells on cerebellar slices [7]. This is an ex vivo rat slice preparation.

Semax and the mu opioid receptor gene Oprm1 after spinal cord injury

Semax was studied as a synthetic heptapeptide comprising the ACTH framework in a spinal cord injury model in female mice, with the work framed around lysosomal membrane permeabilization and ubiquitination [8]. The paper reports targeting of the mu opioid receptor gene Oprm1 to promote deubiquitination and functional recovery [8]. The population is female mice.

Semax and chronic unpredictable stress in male rats

Semax and Melanotan II, both ACTH(4-10) synthetic analogues, were examined for antidepressant-like and antistress effects in male rats in a model of chronic unpredictable stress [9]. The paper notes that stressful events and hyperactivity of the hypothalamic-pituitary-adrenal axis play an important role in the pathogenesis of depression, and that HPA axis activity is itself regulated [9]. The population is male rats.

Semax and the wider therapeutic peptide literature

Semax appears within broader reviews of peptide therapeutics. A narrative review of therapeutic peptides in gerontology examined mechanisms, clinical applications, evidence base and safety profiles of peptides with demonstrated or potential applications in healthy aging and age-related conditions, drawing on PubMed, Scopus and regulatory databases [4]. A separate review of therapeutic peptides in orthopaedics describes peptides as acting on pathways including PI3K/Akt, mTOR, MAPK, TGF-beta and AMPK to influence tissue regeneration [10]. Neither review is a Semax study; they are context for how this class of molecule is documented.

Comparison of the models in which Semax has been studied

Model or preparationSpecies or systemReported focusSource
Transgenic Alzheimer's disease modelAnimalBehaviour and amyloidosis development[1]
Cu(II)-amyloid beta systemIn vitroMetal ion stripping and redox silencing[2]
tMCAO, frontal cortex, 24 hRatDifferentially expressed genes[5]
tMCAO, frontal cortex, 4.5 h and 24 hRatGene expression profile[6]
Hippocampal and cerebellar slicesRat, ex vivoIntracellular calcium dynamics[7]
Spinal cord injuryFemale miceOprm1, deubiquitination, recovery[8]
Chronic unpredictable stressMale ratsAntidepressant-like and antistress effects[9]

Sourcing and documentation

Because the evidence base for Semax is dominated by animal and in vitro work, the documentation that accompanies a research sample matters more than any single study. A catalogue entry for a research peptide should let a laboratory confirm what it has received and reconcile it against the published sequence. For Semax, the sequence Met-Glu-His-Phe-Pro-Gly-Pro is the anchor point [2].

Practical documentation points to check when sourcing:

  • Identity of the peptide as the ACTH(4-7) analogue, consistent with the sequence reported in the literature [2].
  • Whether the supplier distinguishes Semax from its derivatives, since the Alzheimer's model work assessed Semax and a derivative separately [1].
  • Whether the accompanying material states the research-use-only status of the item.
  • Whether batch-level documentation is available for the specific lot, rather than only a generic certificate.

None of the studies cited here were conducted on a commercial catalogue product, and none of them should be read as a specification for one. They describe what was observed in the stated model, in the stated species, at the stated preparation.

Price and catalogue position

Semax is listed in our catalogue as Semax at the 10 mg presentation. Price for a research peptide reflects the cost of synthesis, purification and the analytical documentation that accompanies the lot, not a clinical claim. Because the compound is supplied for laboratory work, the relevant comparison between suppliers is the documentation package rather than the headline figure alone.

Two things are worth stating plainly about the evidence base. First, the Alzheimer's-related findings come from a transgenic animal model and from in vitro chemistry; there is no human trial reported in the evidence summarised here [1][2]. Second, the stroke-related findings come from rat tMCAO tissue analysed by RNA-Seq at 4.5 h and 24 h, which is a gene-expression readout rather than a functional outcome in humans [5][6].

If you are reading this for personal health reasons

This material is sold for laboratory research only, and we do not provide dosing or medical guidance of any kind. Anyone considering a compound for themselves should speak to a licensed clinician. Nothing on this page is a recommendation for personal use.

Sources

  • [1] The Potential of the Peptide Drug Semax and Its Derivative for Correcting Pathological Impairments in the Animal Model of Alzheimer's Disease — https://europepmc.org/article/PMC/PMC12755871
  • [2] Semax, a Copper Chelator Peptide, Decreases the Cu(II)-Catalyzed ROS Production and Cytotoxicity of aβ by Metal Ion Stripping and Redox Silencing — https://europepmc.org/article/PMC/PMC12151629
  • [3] Digitally Guided Hybrid Maxillary Expansion with Supragingival Mandibular Miniplates for Class III Correction in Late Adolescents: A Pilot Clinical Study — https://europepmc.org/article/PMC/PMC13116926
  • [4] Therapeutic peptides in gerontology: mechanisms and applications for healthy aging — https://europepmc.org/article/PMC/PMC13095733
  • [5] Genes That Associated with Action of ACTH-like Peptides with Neuroprotective Potential in Rat Brain Regions with Different Degrees of Ischemic Damage — https://europepmc.org/article/PMC/PMC12249733
  • [6] ACTH-like Peptides Compensate Rat Brain Gene Expression Profile Disrupted by Ischemia a Day After Experimental Stroke — https://europepmc.org/article/PMC/PMC11673339
  • [7] The Effect of Peptide Semax, an ACTH(4-10) Analogue, on Intracellular Calcium Dynamics in Rat Brain Neurons — https://pubmed.ncbi.nlm.nih.gov/41171324/
  • [8] Semax peptide targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice — https://pubmed.ncbi.nlm.nih.gov/40692165/
  • [9] Antidepressant-like and antistress effects of the ACTH(4-10) synthetic analogs Semax and Melanotan II on male rats in a model of chronic unpredictable stress — https://pubmed.ncbi.nlm.nih.gov/39442746/
  • [10] Therapeutic Peptides in Orthopaedics: Applications, Challenges, and Future Directions — https://europepmc.org/article/PMC/PMC12753158
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