- A 2008 preclinical study (Inozemtseva et al., Doklady Biological Sciences) reported that a single intranasal administration of Selank raised BDNF mRNA in the hippocampus within 3 hours and BDNF protein within 24 hours.
- A 2019 preclinical study (Kolik et al.) reported that Selank moved pathologically altered BDNF back toward normal, rather than simply raising it.
- A Russian randomised trial compared intranasal Selank with medazepam, a benzodiazepine, over 14 days in people with anxiety and reported similar effects on anxiety, without sedation.
- No study has measured Selank's effect on BDNF in people, and no study has tested whether BDNF Val66Met or any other genotype changes response to Selank.
- Selank is a registered medicine in Russia. It is not approved by the FDA for any use.
Selank is usually described as an anxiety peptide that also raises BDNF. The research behind the BDNF part is narrower than that sentence suggests: it comes from preclinical studies, from a small number of groups, and it has not been measured in people. This page sets out what those studies found, the mechanism they propose, the one comparative human trial, and where genetics does and does not fit. It is a summary of research, not a recommendation.
Time to a measurable rise in hippocampal BDNF protein after a single intranasal administration of Selank in a 2008 preclinical study (Inozemtseva et al., Doklady Biological Sciences). BDNF mRNA rose within 3 hours.
BDNF, brain-derived neurotrophic factor, is a growth factor neurons use to grow and maintain connections. Low BDNF has been associated in research with depression and cognitive decline. Exercise raises it, and so, more slowly, do some antidepressants.
Plain English: BDNF is a growth signal for nerve cells. Chronic stress hormones can suppress it. The proposed idea is that Selank calms the stress response, and BDNF recovers as a result. That idea comes from preclinical work and has not been tested in people.
How Selank is thought to raise BDNF
Selank is a synthetic seven-amino-acid analogue of tuftsin, an immune peptide the body makes. In preclinical research it has three proposed actions: it modulates GABA-A receptor sensitivity, it inhibits the enzymes that break down enkephalins (the body's own opioid peptides involved in the stress response), and it is associated with increased BDNF transcription in the hippocampus.
One proposed link between these is stress hormones. Chronic stress raises glucocorticoid levels, and glucocorticoids acting on the hippocampus can suppress BDNF gene transcription. If Selank lowers stress-axis activation, BDNF suppression would ease. That is a model drawn from preclinical work; it has not been measured in people.
The enkephalin mechanism
Selank's inhibition of enkephalin-degrading enzymes is one reason researchers have proposed that its effects differ from benzodiazepines, which do not act on enkephalins. A Russian randomised controlled trial compared intranasal Selank with oral medazepam, a benzodiazepine, over 14 days in people with anxiety. It reported similar anxiety-reducing effects, with Selank additionally associated with less fatigue and no sedation. It was a small trial run in Russia, and it has not been replicated elsewhere.
How Selank and Semax differ in the BDNF research
Both Selank and Semax have been reported to raise BDNF in preclinical studies, through different proposed mechanisms.
Proposed to raise BDNF by easing stress-related suppression. In one preclinical study, it moved abnormally altered BDNF back toward normal rather than only raising it.
Proposed to raise BDNF through direct activation of the CREB transcription pathway. Preclinical studies report a larger acute rise in BDNF.
The 2019 study by Kolik and colleagues in the Bulletin of Experimental Biology and Medicine used a preclinical model of alcohol-related brain changes in which BDNF was abnormally raised. Selank moved BDNF back toward normal rather than raising it further. The authors described this as a regulating effect rather than a one-directional boost.
"Selank corrected pathologically altered BDNF levels in both the hippocampus and prefrontal cortex..."
Kolik et al., Bulletin of Experimental Biology and Medicine, 2019
For a fuller comparison of the two peptides' research, see Semax vs. Selank.
Where BDNF genetics fits, and where it does not
BDNF Val66Met (rs6265) is one of the most studied functional variants in brain research. The Met version reduces activity-dependent BDNF release, so neurons release less BDNF in response to activity, exercise and learning. About 25 to 30% of people of European ancestry carry at least one Met copy.
Human studies have found that Met carriers show a blunted neuroplastic response to exercise compared with Val/Val carriers, including a 2016 study in Neuropsychopharmacology and a 2025 study in older adults (PMC11715055).
Because Selank is proposed to act on BDNF transcription rather than release, some have hypothesised that genotype might matter differently for it. That remains untested. No study has examined Selank in people grouped by BDNF genotype, and no study has measured Selank's effect on BDNF in people at all. A DNA report can show which version you carry and what the research on it does show; it cannot predict how anyone would respond to Selank.
COMT, the enzyme that clears dopamine from the front of the brain, also carries a well-studied common variant (Val158Met). Its links to cognition and stress have been researched widely; its interaction with Selank has not.
Regulatory status
Selank is a registered prescription medicine in Russia, authorised for generalised anxiety disorder and neurasthenia. It is not approved by the FDA for any use, and it has no EMA or MHRA marketing authorisation. Its position on FDA's compounding lists has changed during 2024 to 2026 and remains under review; FDA's current position is the authoritative source, not any website, this one included. See the Selank reference page for the full evidence summary.
Preclinical studies report that Selank raised BDNF within hours and normalised abnormally altered BDNF, with a proposed mechanism through the stress response. One Russian trial found anti-anxiety effects similar to a benzodiazepine over 14 days. No study has measured BDNF in people given Selank, and no study has tested whether any genotype changes response to it.
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Does Selank increase BDNF?
In preclinical studies, yes. A 2008 study in Doklady Biological Sciences reported that a single intranasal administration raised hippocampal BDNF mRNA within 3 hours and BDNF protein within 24 hours. A 2019 study reported that Selank moved abnormally altered BDNF back toward normal. No study has measured Selank's effect on BDNF in people.
What human evidence is there for Selank?
A Russian randomised trial compared intranasal Selank with medazepam, a benzodiazepine, over 14 days in people with anxiety and reported similar anxiety-reducing effects, with less fatigue and no sedation on Selank. It has not been replicated outside Russia.
What is the difference between Selank and Semax for BDNF?
In preclinical research, Semax is proposed to raise BDNF through direct activation of the CREB pathway, with a larger acute rise. Selank is proposed to raise BDNF by easing stress-related suppression, and in one study it normalised abnormally raised BDNF. Neither mechanism has been measured in people.
Does my BDNF gene affect how Selank works?
No study has tested it. BDNF Val66Met Met carriers show a smaller neuroplastic response to exercise in human studies, but no study has examined Selank in people grouped by BDNF genotype.
Is Selank FDA-approved?
No. Selank is a registered medicine in Russia for generalised anxiety disorder and neurasthenia, but it is not approved by the FDA for any use and has no EMA or MHRA authorisation.
This article is for informational and educational purposes only. It reports what published research found; it is not medical advice, it does not diagnose, treat, cure or prevent any disease, and nothing in it is a dose or a recommendation to use any compound. Talk to a licensed clinician about any medical decision.