# Semax References: The Cited Literature

> Semax references: the full list of peer-reviewed studies cited across this digest, with PubMed and PMC links and DOIs where available. The complete Semax source record.

Every study cited across this digest, listed with its identifiers.

## About these sources

Every quantitative claim on this site maps to a numbered study below. The list is dominated by Russian research groups, reflecting where the Semax literature actually lives, and ranges from binding and enzyme assays through genome- and proteome-wide ischemia studies to the few human EEG and clinical reports. Links go to PubMed or PubMed Central; digital object identifiers (DOIs) are given where available.

## References

[1] Dolotov OV, et al. Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. J Neurochem. 2006;97 Suppl 1:82-6. https://pubmed.ncbi.nlm.nih.gov/16635254/
[2] Agapova TY, et al. Neurotrophin gene expression in rat brain under the action of Semax, an analogue of ACTH(4-10). Neurosci Lett. 2007;417(2):201-5. https://pubmed.ncbi.nlm.nih.gov/17353092/
[3] Kost NV, et al. Semax and selank inhibit the enkephalin-degrading enzymes from human serum. Bioorg Khim (Russ J Bioorg Chem). 2001;27(3):180-183. https://pubmed.ncbi.nlm.nih.gov/11443939/
[4] Romanova GA, et al. Neuroprotective and antiamnesic effects of Semax during experimental ischemic infarction of the cerebral cortex. Bull Exp Biol Med. 2006;142(6):663-6. https://pubmed.ncbi.nlm.nih.gov/17603664/
[5] Medvedeva EV, et al. The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics. 2014;15:228. https://pubmed.ncbi.nlm.nih.gov/24661604/
[6] Shevchenko KV, et al. Kinetics of Semax penetration into the brain and blood of rats after its intranasal administration. Russ J Bioorg Chem (Bioorg Khim). 2006;32(1):57-62. https://pubmed.ncbi.nlm.nih.gov/16523722/
[7] Semax peptide targets the mu opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice. Br J Pharmacol. 2025. https://pubmed.ncbi.nlm.nih.gov/40692165/
[8] Stavchansky VV, et al. Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Cell Mol Neurobiol. 2010;30(1):71-79. https://pubmed.ncbi.nlm.nih.gov/19633950/
[9] Filippenkov IB, 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 (Basel). 2020;11(6):681. https://pmc.ncbi.nlm.nih.gov/articles/PMC7350263/
[10] Filippenkov IB, 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. Int J Mol Sci. 2021;22(12):6179. https://pubmed.ncbi.nlm.nih.gov/34201112/
[11] Filippenkov IB, et al. The Peptide Drug ACTH(4-7)PGP (Semax) Suppresses mRNA Transcripts Encoding Proinflammatory Mediators Induced by Reversible Ischemia of the Rat Brain. Dokl Biochem Biophys. 2021;498(1):152-156. https://pubmed.ncbi.nlm.nih.gov/34097675/
[12] Filippenkov IB, et al. Synthetic Adrenocorticotropic Peptides Modulate the Expression Pattern of Immune Genes in Rat Brain following the Early Post-Stroke Period. Genes (Basel). 2023;14(7):1382. https://pmc.ncbi.nlm.nih.gov/articles/PMC10379992/
[13] Agapova TY, et al. Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action. J Mol Neurosci. 2010;41(1):30-35. https://pubmed.ncbi.nlm.nih.gov/19662538/
[14] Bashkatova V, et al. Novel synthetic analogue of ACTH 4-10 (Semax) but not glycine prevents the enhanced nitric oxide generation in cerebral cortex of rats with incomplete global ischemia. Brain Res. 2001;894(1):145-149. https://pubmed.ncbi.nlm.nih.gov/11245825/
[15] Volodina MA, et al. Correction of Long-Lasting Negative Effects of Neonatal Isolation in White Rats Using Semax. Acta Naturae. 2012;4(1):86-92. https://pmc.ncbi.nlm.nih.gov/articles/PMC3372995/
[16] Shevchenko KV, et al. Stability of Semax acetyl to proteolysis in various biological media. Dokl Biol Sci. 2013;449:98-100. https://pubmed.ncbi.nlm.nih.gov/23652441/
[17] Effect of the heptapeptide Semax on the human electroencephalogram. Biull Eksp Biol Med. 1996;121(1):26-30. https://pubmed.ncbi.nlm.nih.gov/8679991/
[18] Evaluation of therapeutic effect of new Russian drug semax in optic nerve disease. Vestn Oftalmol. 2000;116(1):54-57. https://pubmed.ncbi.nlm.nih.gov/10741256/
[19] Functional Connectomic Approach to Studying Selank and Semax Effects. Dokl Biol Sci. 2020;490(1):11-14. https://pubmed.ncbi.nlm.nih.gov/32342318/
[20] Eremin KO, et al. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochem Res. 2005;30(12):1493-1500. https://pubmed.ncbi.nlm.nih.gov/16362768/

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Filed from the published record on Semax like a front-page dispatch — the rodent neuroprotection and BDNF findings set in plain ink, the Russia-and-Ukraine-only registration and the missing Western trials printed in the same column, with no clinic behind the masthead and nothing here dosed, sourced, or sold.