Semax: what do we know about the peptide and the brain?

There are published studies in humans, but they concern patients rather than healthy people. The most concrete one included 110 people after ischemic stroke and was published in 2018 in Russian.

It measured BDNF in the blood, motor function and the Barthel Index, a measure of independence in daily life. According to the summary, those who received Semax had higher BDNF and faster motor recovery.

The comparison was made against patients who did not receive the substance, so not against placebo, and the study was carried out in the country where the substance is already used clinically. The results concern rehabilitation after stroke and cannot be transferred to claims about better memory or concentration in healthy people. Other effects are examined in animal studies, described further below.

Semax is a synthetic peptide with seven amino acids. It is based on part of the hormone ACTH, specifically the fragment ACTH(4-10), with an added tail that makes the molecule more stable.

ACTH is a hormone from the pituitary gland that controls the stress hormone cortisol. Semax, however, is designed to lack that hormonal effect and instead act directly on the nervous system.

A study in rats published in 2006 in Brain Research examined how Semax affects the expression of BDNF and its receptor trkB in the hippocampus. BDNF is a protein that helps nerve cells survive and form connections, and the hippocampus is a brain structure linked to memory.

Another study in rodents published in 2005 in Neurochemical Research described effects on the dopamine and serotonin systems, signaling substances that among other things affect motivation and mood.

Both are animal studies. They describe biological changes in laboratory animals and say nothing certain about experienced effects in humans.

There are published studies in humans. One example is a study of 110 people after ischemic stroke, published in 2018 in Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. Participants were divided according to whether rehabilitation started early or late, and each group was in turn split into a subgroup that received Semax and one that did not.

The researchers measured BDNF in the blood, motor function according to the British Medical Research Council scale, and the Barthel Index, a measure of how independent a person is in daily life. According to the summary, those who received Semax had higher BDNF levels throughout the study period, and motor recovery is described as having progressed faster.

Here is how the design should be read: the study included 110 people, the comparison was made against patients who did not receive the substance rather than against placebo, the article is published in Russian, and the work was carried out by groups in the country where the substance is already used clinically. Funding information is not stated in the English abstract.

The results therefore concern rehabilitation after stroke. They cannot be transferred to claims about better memory or concentration in healthy people. The existence of studies is not the same thing as a specific claim being proven.

Semax is not approved as a medicine in the EU or the US at the time of writing. It is used clinically in Russia. The approval status is listed in the registers of the EMA and the FDA.

The most common explanatory model is that Semax affects growth factors such as BDNF and thereby nerve cell signaling, and that it also modulates signaling substances in the brain.

This is a mechanism measured in animal models. The step from a measured change in the rat brain to a noticeable effect in humans is large and has not been demonstrated in published form.

The evidence base is uneven. A handful of internationally accessible animal studies stand against a larger body of Russian literature that is difficult to review from a distance.

Semax is a short peptide based on ACTH(4-10). Animal studies show effects on BDNF and on signaling substances in the brain.

In humans, published studies exist, including one of 110 people after stroke. Their size, comparison groups and language of publication mean they are not enough as evidence of cognitive benefit in healthy people.