Semax

Peptide nootropic in nasal spray form

Analogue of adrenocorticotropic hormone 4-10 heptapeptide Semax, while not possessing hormonal activity, retains a significant part of the spectrum of nootropic effects of natural melanocortins. Semax has nootropic, neuroprotective, anxiolytic, antidepressant and analgesic effects, and is shown to affect the development of the central nervous system in animal studies. The observed effects of Semax can be mediated by an increase in the content of neurotrophic factors in the brain, as well as an increase in the functional activity of the monoaminergic system.

Many researchers have attempted to create highly effective analogs of ACTH hormone by various modifications of the primary structure of the molecule. Semax was the result of many years of those researches, an analog ACTH4-10 with the prolonged action, whose structure includes the fragment AKTH4-7 and the tripeptide Pro-Gly-Pro.

Studies of the activity of this peptide in animal experiments have shown that it improves memory and attention, has antihypoxic and antihemorrhagic effects, and helps to reduce the severity of clinical and neurophysiological manifestations of ischemic stroke. Clinical studies have shown its high effectiveness in the treatment of intellectual-amnesic disorders of various genesis.

Administration of Semax has a pronounced positive effect in the treatment of stroke. As of today, this peptide is the only neurotropic drug widely used in medicine, developed based on endogenous melanocortins. In spite of the fact that Semax has been used in clinical practice for more than 10 years, the spectrum of physiological activity of this peptide has not been determined to date, and its mechanism of action is not fully understood yet.

Studies conducted over the past 20 years have shown that Semax, like natural melanocortins, has a wide spectrum of neurotropic activity.

A study of the effect of Semax on the level of expression of neurotrophic factors showed that the administration of peptide in rats resulted in an increase in the content of brain-derived neurotrophic factor (BDNF) in the brain. The effect of Semax on the content of neurotrophins in the brain can underlie the neuroprotective and neurotrophic effects of this peptide.

The ability of neurotrophic factors to influence the growth and differentiation of nerve cells, as well as to stimulate the synthesis of various physiologically active substances, underlies the regulation of the developing brain. In addition, an increase in the level of BDNF in the hippocampus can also serve as one of the mechanisms of Semax effects.

Neurotrophic factors are involved in the regulation of conditions associated with stress, anxiety, fear, depression. Therefore, an increase in the expression of BDNF in the hippocampus may underlie the anxiolytic and antidepressant effects of Semax, since the important role of these neurotrophins in regulating the level of anxiety and depressiveness is shown in various studies.

The study of the influence of Semax on the system of biogenic brain amines has shown that the administration of this peptide leads to an increase in the serotonin and its metabolites content in the brain.

The obtained data testify to the acceleration of the turnover of this mediator, reflecting the increase in the functional activity of the serotonergic system of the brain. In addition, it is shown that Semax causes a significant increase in the content of norepinephrine in rats hypothalamus.

The anxiolytic and antidepressant effect of Semax can be associated with changes in the activity of these mediator systems. In addition, the biogenic amine system plays an important role in processes of learning and memory formation. Increase in the activity of this system, caused by intranasal administration of Semax, can provide an improvement in attention, which leads to faster learning.

Numerous experiments indicate the important role of the melanocortins system in nociception. The experiments carried out by scientists showed that peripheral administration of Semax reduces the pain sensitivity in animals.

Investigation of the mechanisms of analgesic action of semax showed that the effects of the drug partially weakened by the preliminary blockade of opioid receptors, and is also absent during the blockade of serotonin receptors. In the body, there is a descending system for controlling pain sensitivity.

Serotonin and norepinephrine are mediators of descending cerebrospinal antinociceptive impulses. Activation of these mediator systems leads to a decrease in pain sensitivity. Endogenous opioids act as internal spinal mediators, mainly for descending noradrenalinergic pathways and, to a lesser extent, serotonergic terminals in the dorsal horns of the spinal cord. Semax, by activating the serotonergic and noradrenalinergic systems, can enhance the antinociceptive downward flow and, thus, have an analgesic effect. The absence of analgesic effects of semax on the background of the blockade of serotonin receptors confirms the important role of the serotonergic system in the analgesic action of Semax.