Semax 5mg

Semax 5mg – Neuropeptide Research Compound for Cognitive and Neurological Studies

Overview

Semax’s structure is a synthetic heptapeptide analogue of the ACTH(4-7) fragment, though it’s been modified with a Pro-Gly-Pro C-terminal extension to boost its stability and activity. Its specific sequence is Met-Glu-His-Phe-Pro-Gly-Pro. It doesn’t bind to melanocortin receptors with any real affinity like native ACTH fragments do, so it won’t significantly impact cortisol or adrenal function. This makes it a much cleaner research tool for investigators looking specifically at the neurological side of ACTH-derived peptide signalling.

Researchers at the Institute of Molecular Genetics of the Russian Academy of Sciences originally developed Semax, and it’s been a fixture in preclinical models for over thirty years. It’s actually registered as a pharmaceutical in Russia and Ukraine for stroke rehabilitation, cognitive decline, and optic nerve disease, though research outside of Eastern European literature remains fairly limited. For Western research, Semax is mainly used as a nootropic peptide model to study its effects on BDNF expression, neuroprotection, and both dopaminergic and serotonergic signalling.

If you’re looking into related neuropeptides with complementary or comparative profiles, you might want to check out Selank 10mg. It is a close structural relative but features more pronounced anxiolytic properties. Another option is Pinealon 10mg, which is a different Russian-developed neuropeptide bioregulator. For research purposes only.

Research Applications

Semax’s research profile is pretty broad, spanning cognitive neuroscience, neuroprotection, stroke biology, and neurotrophic factor regulation. Most published work has been done in rodent models, though some human clinical data exists from Eastern European studies.

• BDNF upregulation studies — Semax has been shown to markedly increase BDNF and NGF expression in hippocampal and cortical tissue in rodent models
• Cognitive performance studies — learning, memory consolidation, and attention paradigms in rodent behavioural models
• Stroke and ischaemia models — neuroprotective effects in middle cerebral artery occlusion (MCAO) models and oxidative stress conditions
• Dopaminergic and serotonergic pathway research — Semax appears to modulate monoamine neurotransmitter systems relevant to attention and mood
• Neuroinflammation studies — effects on microglial activation and cytokine expression following CNS injury
• Optic nerve and retinal studies — limited but published data on neuroprotective effects in visual pathway models

Research programmes often pair Semax with DSIP 2mg to look at how sleep and cognition interact, or they’ll use NAD+ 500mg as a comparator for metabolic neuroprotection. If you’re focusing on ACTH-derived peptide biology, the wider melanocortin system’s also worth exploring via PT-141 10mg. It is a melanocortin receptor agonist with a very different research application profile.

Molecular Profile

Semax follows the Met-Glu-His-Phe-Pro-Gly-Pro sequence and stems from the ACTH(4-7)PGP parent compound. It’s got a molecular formula of C₃₇H₅₁N₉O₁₀S and a weight of 813.93 g/mol. It’s listed under CAS 80714-61-0, with purity verified at ≥98% by HPLC.

Mechanism of Action

We don’t fully understand Semax’s multifaceted mechanism of action yet, which is exactly why it’s such a compelling research subject. Its Pro-Gly-Pro C-terminal extension prevents rapid enzymatic degradation, extending the peptide’s biological half-life considerably compared to the parent ACTH(4-7) sequence. This stability tweak was central to its development as a clinically applicable compound.

The most robust finding regarding Semax’s mechanism is its ability to upregulate neurotrophic factor expression, specifically BDNF and, to a lesser degree, NGF, within the hippocampus and cortex. Researchers have demonstrated this effect in both in vitro neuronal cultures and in vivo rodent models. It’s widely thought that this upregulation underlies many of the observed cognitive effects. Since BDNF is central to synaptic plasticity, long-term potentiation, and neuronal survival, its increase is relevant to a broad spectrum of neuroscience research questions.

Semax doesn’t just regulate neurotrophic factors; it also seems to shift dopaminergic and serotonergic tone within the prefrontal and limbic regions. This likely explains why researchers see better attention spans and reduced anxiety-like behaviour in rodent models. We’ve also seen evidence of anti-inflammatory effects driven by how it modulates NFκB signalling pathways and cytokine expression, especially after an ischaemic injury. In MCAO models, it’s been shown to shrink infarct volume and boost neurological outcomes. This suggests its neuroprotective properties might translate well to clinical settings, though we’re still waiting for rigorous human trials to confirm that.

Storage and Handling

Keep lyophilised Semax at −20°C, shielded from light and humidity. It’ll stay stable for up to 24 months if stored properly. Reconstitute with bacteriostatic water or sterile saline. Once it’s reconstituted, keep it at 2–8°C and use within 4 weeks. Don’t use freeze-thaw cycles. Standard aseptic laboratory technique applies throughout. For research use only.

References

• Dolotov OV, et al. “Semax, an analogue of ACTH(4-7) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus.” Brain Research. 2006;1117(1):54–60. doi:10.1016/j.brainres.2006.08.058
• Agapova TY, et al. “Effects of the peptide nootropic drug Semax on the transcriptome of rat neocortex.” Bulletin of Experimental Biology and Medicine. 2007;144(4):525–528.
• Kupriyanova IE, Fedoseeva OB. “Neuroprotective activity of Semax in the model of focal ischemia.” Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. 1996;96:65–66.
• Inozemtseva LS, et al. “Intranasal administration of the peptide Semax regulates ACTH-receptor gene expression in the rat hippocampus.” Doklady Biological Sciences. 2008;421:241–243.
• Grivennikov IA. “Nerve growth factor and Alzheimer’s disease.” Biochemistry (Moscow). 2007;72(3):259–269.