Key takeaways
- Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) based on the ACTH(4-10) fragment.
- It keeps the neuroactive properties of ACTH fragments without the hormone's effect on the adrenal glands.
- Research centres on BDNF and TrkB signalling, hippocampal plasticity and brain ischaemia models.
In this guide
- What is Semax?
- How it's built
- BDNF and neuroplasticity
- Other mechanisms
- Research areas
- Related research
- FAQ
What is Semax?
Semax has the sequence MEHFPGP and a molecular weight of 813.93 g/mol (CAS 80714-61-0). It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences and first described in the scientific literature in 1991. It's used as a prescription medicine in Russia, but it is not approved in Canada or the United States.
How Semax is built
ACTH (adrenocorticotropic hormone) is a 39-amino-acid hormone that tells the adrenal glands to release cortisol. Researchers found that short fragments of ACTH, particularly the 4–10 region, have effects on the brain that are separate from this hormonal role.
Semax joins the ACTH(4-7) sequence (Met-Glu-His-Phe) to a Pro-Gly-Pro tripeptide. That tail protects the molecule from rapid enzymatic breakdown, and the design keeps the neuroactive properties without activating the adrenal glands.
BDNF and neuroplasticity
Much of the research on Semax centres on brain-derived neurotrophic factor (BDNF) and its receptor TrkB. BDNF supports neuron survival, the growth of new connections and synaptic plasticity, the strengthening and weakening of connections that underlies learning and memory.
In rats, Semax was reported to increase BDNF levels and TrkB expression in the hippocampus, a brain region central to memory (Dolotov et al., Brain Research, 2006).
Other mechanisms studied
- Enkephalinase inhibition: Semax was found to inhibit enzymes that break down enkephalins, the body's own opioid peptides, in human serum (Kost et al., 2001).
- Melanocortin receptor activity: as an ACTH fragment, Semax interacts with the melanocortin system.
- Brain ischaemia models: Semax has been studied in experimental models of reduced blood flow to the brain, including effects on gene expression after injury.
Key research areas
- BDNF and TrkB neurotrophic signalling
- Hippocampal plasticity, learning and memory models
- Melanocortin receptor activity
- Enkephalin-degrading enzyme inhibition
- Experimental brain ischaemia models
Semax is not approved in Canada or the United States. The research above is preclinical or from clinical use outside North America.
Related research
Semax is often compared with Selank, which was developed at the same institute using the same Pro-Gly-Pro design. See Semax vs Selank for a side-by-side comparison. Adamax is a modified Semax analogue studied in the same areas.
Frequently asked questions
What is Semax?
Semax is a synthetic seven-amino-acid peptide (Met-Glu-His-Phe-Pro-Gly-Pro) based on the ACTH(4-10) fragment of adrenocorticotropic hormone. It's studied for effects on BDNF, neuroplasticity and cognition.
Does Semax affect cortisol like ACTH?
Semax was designed to keep the neuroactive properties of ACTH fragments without the hormone's effect on the adrenal glands, which is ACTH's main hormonal role.
What is BDNF?
Brain-derived neurotrophic factor is a protein that supports neuron survival and synaptic plasticity. Semax was reported to increase BDNF and its receptor TrkB in the rat hippocampus.
Is Semax approved in Canada?
No. Semax is used as a prescription medicine in Russia but is not approved in Canada or the United States.
References
- Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006;1117(1):54–60.
- Kost NV, et al. Semax and Selank inhibit the enkephalin-degrading enzymes from human serum. Russ J Bioorg Chem. 2001;27(3):180–183.
