Semax
A synthetic ACTH-fragment-derived heptapeptide investigated in neurotrophin, monoaminergic and neural gene-expression models.
Individually£24.99
In this set£21.74
Research Set
Neural Signalling Set
Neuropeptide signalling and neurological research: Semax and Selank.
IncludedSemax 10 mg + Selank 10 mg
Set price
£43.48£49.98
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What's Included in the Set
View Semax
Selank
A synthetic tuftsin-derived heptapeptide investigated in GABAergic, neurotransmission and neural gene-expression research.
Individually£24.99
In this set£21.74
Understanding Semax & Selank
Semax and Selank are chemically distinct synthetic peptides investigated across overlapping areas of neuropeptide research. Semax is an ACTH-fragment-derived heptapeptide whose experimental literature includes neurotrophin signalling, monoaminergic neurotransmission and neural gene-expression responses. Selank is a tuftsin-derived peptide studied through GABAergic signalling, neurotransmission-related gene expression and wider molecular responses in neural systems. These different experimental frameworks place both compounds within the broader study of neuropeptide and neural signalling.
Semax
Semax is the synthetic heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro, built from the ACTH(4–7) sequence with a C-terminal Pro-Gly-Pro extension and commonly described as an ACTH(4–10) analogue. Although structurally derived from an ACTH fragment, it was developed without the hormonal activity of full-length ACTH and has been investigated in neurotrophin, monoaminergic and neural gene-expression systems.
Semax in Research
Semax experiments span neurotrophin, neurochemical and transcriptional endpoints, with much of the mechanistic evidence coming from rodents. In rat hippocampus, a single exposure increased BDNF protein, TrkB phosphorylation and messenger RNA for BDNF and TrkB. BDNF is a neurotrophin involved in neuronal signalling and plasticity, while TrkB is one of its principal receptors; measuring both ligand expression and receptor activation helps connect a molecular response with its associated signalling system. Separate work in rat basal forebrain found specific, reversible and calcium-dependent binding of radiolabelled Semax to isolated cell membranes and a rapid increase in BDNF protein in that region, but not the cerebellum. Other rat time-course experiments reported region- and time-dependent changes in Bdnf and Ngf expression, extending the neurotrophin question beyond one transcript or brain area. A rodent neurochemical study measured tissue and extracellular monoamine parameters in the striatum. Semax altered serotonergic measurements, including 5-HIAA, but did not itself change dopamine or dopamine-metabolite concentrations. Instead, it amplified the extracellular dopamine and locomotor responses produced experimentally by amphetamine. The result therefore describes modulation of an induced dopaminergic response, not a simple increase in dopamine and serotonin. Transcriptomic studies in preclinical cerebral-ischaemia models have also reported changes across immune-, vascular- and neural-response genes. Together, these experiments connect Semax with several signalling levels, while leaving its complete mechanism unresolved and without establishing human cognitive benefit.
Selank
Selank is the synthetic heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro, derived from the tetrapeptide tuftsin by addition of a C-terminal Pro-Gly-Pro sequence. This structure places it among synthetic regulatory glyproline peptides investigated in GABAergic, neurotransmission and wider molecular-signalling models.
Selank in Research
Selank research has tested GABA-related hypotheses at gene-expression and receptor-binding levels rather than establishing the peptide as GABA itself or as a direct GABA-receptor agonist. In rat frontal cortex, investigators used real-time PCR to analyse 84 neurotransmission-related genes after Selank or GABA exposure. They reported significant expression changes in 45 genes at one hour and 22 genes at three hours, with a positive correlation between some early responses to Selank and GABA. The panel included GABA-receptor subunits, transporters, ion channels and dopamine- and serotonin-receptor genes, so the result describes a broad transcriptional response; it does not show that Selank simply increases GABA. A separate radioligand study used plasma membranes isolated from rat brain cells and measured [3H]GABA binding. Selank produced concentration- and receptor-subtype-dependent changes characterised by the authors as positive allosteric modulation. Its interactions with diazepam and olanzapine were non-cumulative and differed from either compound alone, suggesting that the relevant binding relationships were not identical. These membrane experiments support a receptor-modulation hypothesis, but do not establish Selank as an orthosteric GABA agonist. Broader cDNA-microarray work in rat hippocampus found more than twofold changes in 36 transcripts after a single exposure and 20 after repeated exposure; many encoded membrane-associated proteins. The authors proposed a connection with ion homeostasis, but that interpretation remains a mechanistic hypothesis. Overall, Selank’s molecular basis remains active research involving receptor binding, neurotransmission-related transcription and wider neural cellular responses.
Questions About the Research
How do Semax and Selank differ as research compounds?
Semax is an ACTH-fragment-derived heptapeptide investigated in neurotrophin signalling, monoaminergic neurotransmission and neural gene expression. Selank is a tuftsin-derived heptapeptide studied through GABA-related receptor binding, neurotransmission-associated transcription and broader molecular responses. Their structural origins and principal experimental questions are different.
What areas of neurological research have been studied with Semax?
Rodent experiments have measured monoaminergic neurochemistry, BDNF and TrkB expression or activation, region-dependent neurotrophin responses and transcriptional changes in neural tissue. Some gene-expression work used preclinical cerebral-ischaemia models. These studies describe experimental molecular responses and do not establish human cognitive outcomes.
Why is Selank studied in GABAergic and neurotransmission research?
Rat frontal-cortex experiments found changes across a panel of neurotransmission-related genes, with some early responses correlating with those produced by GABA. Separate rat brain-membrane experiments measured changes in radiolabelled GABA binding consistent with an allosteric-modulation hypothesis. Neither result means that Selank simply increases GABA or acts as a direct GABA agonist.
Why are Semax and Selank included in the same Research Set?
Both compounds provide access to distinct questions within neuropeptide and neural-signalling research. Semax experiments emphasise neurotrophin, monoaminergic and transcriptional responses, while Selank experiments emphasise GABAergic receptor modulation and neurotransmission-related molecular responses. The set brings these different research areas into one broader neuropeptide category.
Are Semax and Selank supplied in separate vials?
Yes. Semax and Selank are supplied as two separate vials within the Research Set. They are not combined into a single vial. Each compound retains its own strength, product identity and associated documentation.