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Anxiolytic Activity of Selank and Tuftsin in Generalized Anxiety Disorder: A Double-Blind, Placebo-Controlled Clinical Trial

Semenova TP, Kozlovskaya MM, Zakharova NM, Kozlovskiy VI.

Bulletin of Experimental Biology and Medicine/2010/62 participants/14 days
Key Finding

Selank (0.15 mg nasal twice daily) reduced Hamilton Anxiety Rating Scale scores by 38% versus 20% for placebo in generalized anxiety disorder, without sedation, cognitive impairment, or dependence.

Background

Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed in Russia by the Institute of Molecular Genetics as a stable analog of the immunomodulatory peptide tuftsin. It was subsequently found to have anxiolytic properties comparable to benzodiazepines but without the associated sedation, cognitive impairment, or dependence risk.

Selank is approved in Russia for generalized anxiety disorder, neurasthenia, and cognitive impairment. It has growing off-label use internationally as a nootropic and anxiolytic.

Methods

Double-blind, randomized, placebo-controlled trial at a Russian psychiatric outpatient clinic. 62 patients with DSM-IV generalized anxiety disorder. Selank 0.15% nasal drops (0.15 mg per dose, 2 doses daily) vs. placebo for 14 days.

Primary outcomes: Hamilton Anxiety Rating Scale (HAM-A), Clinical Global Impression (CGI) scale, cognitive battery (attention, memory).

Key Findings

OutcomeSelankPlacebop-value
HAM-A score reduction−38%−20%0.01
CGI improvement (“much improved”)61%28%0.003
Sedation scoreNo change
Cognitive batteryImproved or neutral
Dependence/withdrawalNone observed

Clinical Significance

Selank’s anxiolytic efficacy without sedation or dependence represents a potentially important clinical differentiation from benzodiazepines. The cognitive neutrality (or mild enhancement) is also notable — most anxiolytics produce cognitive dulling.

The HAM-A reduction (-38% vs. -20%) approaches the magnitude seen with SSRIs in 8-week trials, achieved in only 14 days — consistent with a mechanism distinct from serotonergic adaptation (likely via enkephalin/opioid peptide modulation and BDNF upregulation).

Limitations

  • Small sample (62 patients)
  • Short duration (14 days) — insufficient for remission data
  • Single center, single country; all published in Russian-language literature with limited Western peer review
  • Mechanism not fully elucidated
  • Long-term safety not established in controlled trials

Compounds Studied

Related Conditions