Semax: Research, Handling and Batch Documentation

Identity and research status

Also referred to as

MEHFPGP, Pro-Gly-Pro-ACTH(4-7)

Sequence

Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP)

Written Form

H-Met-Glu-His-Phe-Pro-Gly-Pro-OH (free N-terminal amine, free C-terminal carboxylate)

Parent Fragment

ACTH(4-7), with Pro-Gly-Pro replacing ACTH(8-10) Arg-Trp-Gly

Molecular Formula

C37H51N9O10S

Molecular Weight

813.93 g/mol (free acid); monoisotopic mass 813.348 Da

CAS Number

80714-61-0

PubChem CID

9811102

UNII

I5FAL2585H

InChIKey

AFEHBIGDWIGTEH-AQRCPPRCSA-N

Physical Form

White to off-white lyophilised powder

Salt Form Note

Solid-phase synthesis usually yields the acetate; each acetate equivalent adds roughly 60 g/mol to the figure above. Labels rarely state whether a quoted mass is free acid or salt.

CAS number

80714-61-0

Mechanism, in brief

The most replicated finding is that Semax raises brain-derived neurotrophic factor and the expression of its receptor. In rat hippocampus, a single intranasal application at 50 µg/kg produced a maximal 1.4-fold rise in BDNF protein, a 1.6-fold rise in TrkB tyrosine phosphorylation, a 3-fold rise in exon III BDNF mRNA and a 2-fold rise in trkB mRNA, and the treated animals produced more conditioned avoidance reactions than controls (Dolotov and colleagues, Brain Research, 2006). Those four numbers describe four different things and are frequently collapsed into a single inflated percentage elsewhere. Protein rose by 40%. Transcript rose threefold. Both statements are true and they are not the same statement.

1. Regional binding. Calcium-dependent specific binding to sites on rat basal forebrain cell membranes, KD 2.4 nM, Bmax 33.5 fmol/mg protein. The binding protein has not been identified.
2. Neurotrophin transcription. In glial cultures from newborn rat basal forebrain, BDNF mRNA rose eightfold and NGF mRNA fivefold 30 minutes after Semax exposure. In whole brain the response is region-specific and biphasic.
3. TrkB activation. TrkB tyrosine phosphorylation rose 1.6-fold in rat hippocampus alongside a 1.4-fold rise in BDNF protein, so the receptor arm moves with the ligand arm rather than lagging it.
4. Monoamine modulation. Extracellular striatal 5-HIAA rose to 180% of baseline over 1 to 4 hours after 0.15 mg/kg intraperitoneally in rats. Dopamine was unchanged alone but amphetamine-evoked release was strongly potentiated.
5. Metal handling. The free N-terminal amine plus the histidine at position 3 form a Cu(II) site. The complex is redox-silent, and Semax strips Cu(II) from amyloid-beta in membrane models.
6. No corticotropic arm. Because ACTH(8-10) is absent, the molecule lacks the region needed to drive steroidogenesis at MC2R on the adrenal cortex. This is a structural argument, not a measured cortisol result.

The full research write-up, including the findings behind each claim and the model each came from, is on the Semax 10mg 10mg page.

Vial sizes available

Every size of Semax Volta lists, in stock or not. Each is a separate catalogue page with its own batch number and specification table.

• Semax 10mg 10mgBatch #: VPSM10100
  Restocking

Purity and batch documentation

Volta's release specification is >99% (HPLC). That is a threshold we set. >99% is the specification every batch is released to. The figure on a certificate is what a laboratory measured for one lot.

No third-party certificate has been published for Semaxyet. The certificates Volta does publish, with the laboratory's own verification link on each, are in the certificate archive.

Research on Semax

Handling and stability

Regulatory context

United States

Not FDA-approved. Removed from FDA Category 2 on April 15, 2026. PCAC review scheduled July 23-24, 2026. Previously classified as Category 2, prohibiting compounding. Research chemical.

Canada

Not approved by Health Canada.

United Kingdom

Not MHRA-approved.

• the legal status of research peptides in Canada
• Health Canada's regulatory position

Primary sources

1. Dolotov OV, Karpenko EA, Inozemtseva LS, et al.. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Research (2006). doi:10.1016/j.brainres.2006.07.108
2. Dolotov OV, Karpenko EA, Seredenina TS, et al.. Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. Journal of Neurochemistry (2006). doi:10.1111/j.1471-4159.2006.03658.x
3. Shadrina MI, Dolotov OV, Grivennikov IA, et al.. Rapid induction of neurotrophin mRNAs in rat glial cell cultures by Semax, an adrenocorticotropic hormone analog. Neuroscience Letters (2001). doi:10.1016/s0304-3940(01)01994-2
4. Agapova TIu, Agniullin IaV, Silachev DN, et al.. Effect of semax on the temporary dynamics of brain-derived neurotrophic factor and nerve growth factor gene expression in the rat hippocampus and frontal cortex. Molekuliarnaia Genetika, Mikrobiologiia i Virusologiia (2008). PMID 18756821
5. Dmitrieva VG, Povarova OV, Skvortsova VI, et al.. Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Cellular and Molecular Neurobiology (2010). doi:10.1007/s10571-009-9432-0
6. Filippenkov IB, Stavchansky VV, Denisova AE, et al.. Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats. Genes (2020). doi:10.3390/genes11060681
7. Sudarkina OY, Filippenkov IB, Stavchansky VV, et al.. Brain Protein Expression Profile Confirms the Protective Effect of the ACTH(4-7)PGP Peptide (Semax) in a Rat Model of Cerebral Ischemia-Reperfusion. International Journal of Molecular Sciences (2021). doi:10.3390/ijms22126179
8. Gusev EI, Martynov MY, Kostenko EV, Petrova LV, Bobyreva SN. The efficacy of semax in the treatment of patients at different stages of ischemic stroke. Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova (2018). doi:10.17116/jnevro20181183261-68
9. Lebedeva IS, Panikratova YR, Sokolov OY, et al.. Effects of Semax on the Default Mode Network of the Brain. Bulletin of Experimental Biology and Medicine (2018). doi:10.1007/s10517-018-4234-3
10. Shevchenko KV, Nagaev IIu, Alfeeva LIu, et al.. Kinetics of Semax penetration into the brain and blood of rats after its intranasal administration. Bioorganicheskaia Khimiia (2006). doi:10.1134/s1068162006010055
11. Eremin KO, Kudrin VS, Saransaari P, et al.. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochemical Research (2005). doi:10.1007/s11064-005-8826-8
12. Sharonova IN, Bukanova YV, Myasoedov NF, Skrebitskii VG. Modulation of GABA- and Glycine-Activated Ionic Currents with Semax in Isolated Cerebral Neurons. Bulletin of Experimental Biology and Medicine (2018). doi:10.1007/s10517-018-4043-8
13. Kolbaev SN, Sharonova IN, Skrebitsky VG. The Effect of Peptide Semax, an ACTH(4-10) Analogue, on Intracellular Calcium Dynamics in Rat Brain Neurons. Bulletin of Experimental Biology and Medicine (2025). doi:10.1007/s10517-025-06501-z
14. Magri A, Tabbi G, Giuffrida A, et al.. Influence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties. Journal of Inorganic Biochemistry (2016). doi:10.1016/j.jinorgbio.2016.08.013
15. Sciacca MFM, Naletova I, Giuffrida ML, Attanasio F. Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Abeta Aggregation and Amyloid Formation in Artificial Membrane Models. ACS Chemical Neuroscience (2022). doi:10.1021/acschemneuro.1c00707
16. Inozemtseva LS, Yatsenko KA, Glazova NY, et al.. 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. European Journal of Pharmacology (2024). doi:10.1016/j.ejphar.2024.177068
17. Radchenko AI, Kuzubova EV, Apostol AA, et al.. The Potential of the Peptide Drug Semax and Its Derivative for Correcting Pathological Impairments in the Animal Model of Alzheimer's Disease. Acta Naturae (2025). doi:10.32607/actanaturae.27808
18. Liu R, Chen Y, Huang H, et al.. Semax peptide targets the mu opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice. British Journal of Pharmacology (2025). doi:10.1111/bph.70122
19. Kolomin TA, Shadrina MI, Slominsky PA, et al.. Peptides semax and selank affect the behavior of rats with 6-OHDA induced PD-like parkinsonism. Doklady Biological Sciences (2017). doi:10.1134/S0012496617030048
20. Vanhee C, Francotte A, Janvier S, Deconinck E. The occurrence of putative cognitive enhancing research peptides in seized pharmaceutical preparations: An incentive for controlling agencies to prepare for future encounters of the kind. Drug Testing and Analysis (2020). doi:10.1002/dta.2717
21. National Center for Biotechnology Information. PubChem Compound Summary for CID 9811102, Semax. PubChem (2026)
22. National Center for Biotechnology Information. PubChem Compound Summary for CID 172638603, N-acetyl semax amidate. PubChem (2026)