Selank

A 2008 study examined 62 patients with generalized anxiety disorder or neurasthenia. Thirty participants received Selank and 32 received the benzodiazepine-related medication medazepam. Researchers reported that the anxiolytic effects of the two treatments were similar on several clinical measures and also described antiasthenic and psychostimulant-type effects with Selank.

This represents legitimate human clinical evidence. However, it was a relatively small study, conducted within a narrow research setting, published primarily in Russian, and not part of a large multinational regulatory-development program. Therefore, it should be interpreted as preliminary human clinical evidence rather than definitive proof of efficacy.

A 2014 clinical study involved 60 patients with phobic-anxiety and somatoform disorders. Researchers compared Selank with phenazepam, a benzodiazepine-type anxiolytic. The study reported anxiolytic effects with Selank and described mild cognitive or “nootropic” effects as well. Researchers also reported favorable tolerability compared with phenazepam.

Again, this is relevant human evidence. But a 60-person study does not establish that Selank is equivalent or superior to established anxiety medications across broader populations.

A later study compared phenazepam alone with Selank plus phenazepam. Researchers studied 70 patients with anxiety-spectrum disorders and reported that the combination was associated with earlier improvement in some measures and fewer undesirable effects commonly associated with phenazepam, including attention and memory impairment, sedation, and asthenia.

This raises an interesting possibility that Selank may interact with pathways involved in conventional anxiolytic treatment. However, a combination study does not establish Selank as a standalone replacement for benzodiazepines or other established psychiatric medications.

GABA is the brain's major inhibitory neurotransmitter and plays an important role in anxiety regulation. Benzodiazepines reduce anxiety partly by increasing the effects of GABA at GABA-A receptors. Laboratory and animal studies suggest Selank may influence the GABAergic system through mechanisms that differ from directly binding the traditional benzodiazepine site.

A 2016 study examining rat brain tissue found that Selank altered expression of several genes involved in neurotransmission and produced changes that overlapped with those associated with GABA. Researchers proposed that one possible mechanism involves allosteric modulation of GABAergic signaling. A later molecular study also reported effects involving GABA receptor binding and suggested that Selank may act as a positive modulator of GABA-related signaling. These studies provide a plausible biological explanation for Selank's reported anxiolytic effects. They do not yet establish a complete mechanism in humans.

Selank has also been studied for its effects on enkephalins, naturally occurring opioid peptides involved in stress, pain, emotional regulation, and other neurological functions. A 2001 study found that Selank inhibited enzymes responsible for breaking down enkephalins in laboratory testing. Researchers proposed that prolonging endogenous enkephalin activity could contribute to Selank's observed anxiolytic effects.

This is an interesting mechanistic hypothesis. But it should not be interpreted to mean that Selank is itself an opioid or that it produces the same effects as opioid medications.

Selank is frequently promoted as a nootropic or cognitive-enhancing peptide. There is biological research supporting interest in this area, but most of the stronger mechanistic evidence comes from animals. Animal research has reported effects involving learning, memory consolidation, attention, serotonin metabolism, and BDNF-related signaling.

One study reported that Selank increased the stability of long-term memory traces in rats and proposed an association with serotonin and serotonin-metabolite changes. Another rat study found that Selank reduced memory and attention disturbances associated with prolonged ethanol exposure and altered BDNF levels in the hippocampus and prefrontal cortex. These findings are scientifically interesting. However, improved memory in rats does not establish Selank as an effective cognitive enhancer in healthy humans.

Brain-derived neurotrophic factor (BDNF) is involved in neuronal survival, synaptic plasticity, learning, and memory. Animal research has found that intranasal Selank can influence BDNF expression in the hippocampus.

Because BDNF is involved in many neurological and psychiatric processes, these findings have contributed to claims that Selank may support neuroplasticity, learning, memory, stress resilience, and cognitive function. But altering BDNF in an experimental animal model is not equivalent to demonstrating improved cognition or protection against neurological disease in humans.