Semax vs Selank Research

Semax vs Selank Research

Semax and Selank are both synthetic peptides with distinct pharmacological profiles and therapeutic potentials.
Semax is a heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) derived from the adrenocorticotropic hormone (ACTH) fragment (4-10). It has been extensively studied for its neuroprotective and nootropic effects. Semax has shown efficacy in enhancing cognitive functions, particularly in learning and memory, and has demonstrated neuroprotective properties in various models of brain injury, including ischemic stroke. 
The mechanism of action of Semax involves the upregulation of brain-derived neurotrophic factor (BDNF) and its receptor, trkB, which are critical for synaptic plasticity and neuronal survival. Additionally, Semax has been found to modulate the expression of genes related to the immune and vascular systems, suggesting a multifaceted role in neuroprotection. It also exhibits antidepressant-like effects by attenuating stress-induced anhedonia and modulating hippocampal BDNF levels.[1][4][5]
Selank, on the other hand, is a heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) with anxiolytic and nootropic properties. It is known for its ability to modulate the GABAergic system, acting as a positive allosteric modulator of GABA receptors, which contributes to its anxiolytic effects. Selank has been shown to affect the expression of genes involved in neurotransmission, particularly those related to the GABAergic system, which is crucial for its anxiolytic action. Unlike traditional benzodiazepines, Selank does not induce dependence or significant side effects, making it a potentially safer alternative for the treatment of anxiety disorders.[6]
In summary, while both Semax and Selank are synthetic peptides with neuroprotective and nootropic effects, their primary mechanisms and therapeutic applications differ. Semax is primarily used for its cognitive-enhancing and neuroprotective properties, particularly in conditions like ischemic stroke and depression, through the modulation of BDNF and immune-related genes. Selank, however, is primarily utilized for its anxiolytic effects, modulating the GABAergic system without the side effects associated with traditional anxiolytics.


1.Semax, an Analogue of Adrenocorticotropin (4-10), Binds Specifically and Increases Levels of Brain-Derived Neurotrophic Factor Protein in Rat Basal Forebrain.

Dolotov OV, Karpenko EA, Seredenina TS, et al. Journal of Neurochemistry. 2006;97 Suppl 1:82-6. doi:10.1111/j.1471-4159.2006.03658.x.

2. Brain Protein Expression Profile Confirms the Protective Effect of the ACTHPGP Peptide (Semax) in a Rat Model of Cerebral Ischemia-Reperfusion.

Sudarkina OY, Filippenkov IB, Stavchansky VV, et al. International Journal of Molecular Sciences. 2021;22(12):6179. doi:10.3390/ijms22126179.

3.The Peptide Semax Affects the Expression of Genes Related to the Immune and Vascular Systems in Rat Brain Focal Ischemia: Genome-Wide Transcriptional Analysis.

Medvedeva EV, Dmitrieva VG, Povarova OV, et al. BMC Genomics. 2014;15:228. doi:10.1186/1471-2164-15-228.

4. Semax, an Analog of ACTH(4-10) With Cognitive Effects, Regulates BDNF and trkB Expression in the Rat Hippocampus. Dolotov OV, Karpenko EA, Inozemtseva LS, et al. Brain Research. 2006;1117(1):54-60. doi:10.1016/j.brainres.2006.07.108.
5. 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.

Inozemtseva LS, Yatsenko KA, Glazova NY, et al. European Journal of Pharmacology. 2024;984:177068. doi:10.1016/j.ejphar.2024.177068. New Research

6.Peptide-Based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Vyunova TV, Andreeva L, Shevchenko K, Myasoedov N. Protein and Peptide Letters. 2018;25(10):914-923. doi:10.2174/0929866525666180925144642.
7. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Volkova A, Shadrina M, Kolomin T, et al. Frontiers in Pharmacology. 2016;7:31. doi:10.3389/fphar.2016.00031.
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