Study wrapper · #665
[Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia].
Editor's note
This is one of the more decision-relevant human items in this batch: a clinical comparison of the peptide anxiolytic selank (30 patients) against the benzodiazepine medazepam (32 patients) in generalized anxiety disorder and neurasthenia, with symptoms tracked by Hamilton, Zung, and CGI scales and a biological measure (leu-enkephalin activity) added. Researchers reported that the anxiolytic effects of the two drugs were similar, but that selank also had antiasthenic and psychostimulant effects. They found patients had reduced leu-enkephalin half-life correlated with illness duration and symptom severity, and that this parameter rose during selank treatment, with stronger positive correlations to anxiety, especially in GAD. The abstract does not state randomization or blinding, so I classify it as a controlled clinical comparison, not a formal RCT. Weigh it as suggestive human evidence with a plausible mechanistic marker but real design limits — small, likely open-label, single-group reporting. Evidence is best rated mixed.
Plain-language abstract
This study in people compared the peptide selank with a standard tranquilizer, medazepam, in 62 patients who had generalized anxiety disorder or neurasthenia (a condition of chronic fatigue and nervous exhaustion). Thirty patients received selank and thirty-two received medazepam. Doctors rated symptoms with standard scales and also measured an enkephalin (a natural pain- and stress-related brain chemical) in the blood. The two drugs reduced anxiety to a similar degree, but selank also appeared to counter fatigue and had a mild stimulating effect. Patients started out with a shortened lifespan of one enkephalin marker, which was linked to how long and how severe their illness was; during selank treatment, this marker increased and tracked more closely with anxiety levels, especially in the anxiety-disorder group. The report did not say patients were randomly assigned or that raters were blinded, and the study was small. It offers encouraging human evidence, and a possible biological mechanism, but not the strongest kind of proof.