Selank

Ten papers are cited, published between 2014 and 2022. One is clinical: a comparison of selank with phenazepam in patients with anxiety disorders, assessing anxiolytic effect and tolerability. The other nine are preclinical. Five used rats, in models of morphine withdrawal, chronic restraint stress, chronic foot-shock stress and ethanol-induced memory impairment. One measured cytokines under 'social' stress, one compared two routes of administration in two mouse strains, and two examined the peptide's relationship with GABA signalling, one of them in IMR-32 cells.

The rat studies reported that selank weakened aversive signs of morphine withdrawal, as diazepam also did; lowered corticosterone and reduced stress-related tissue changes in the large intestine; returned the nucleus-to-cytoplasm ratio of liver cells towards normal after foot-shock stress; and restored colonic microbiota disturbed by restraint stress. The ethanol study measured BDNF in the hippocampus and prefrontal cortex and tied its memory findings to that neurotrophin. Under social stress, IL-1β, IL-6, TNF-α and TGF-β1 fell to near control values. At the molecular level, one paper proposed subtype-selective, concentration-dependent allosteric modulation of GABA receptors, and the IMR-32 study partly supported an effect on how GABA interacts with GABA-A receptors. The mouse study attributed the different pharmacological profiles of the two routes to pharmacokinetics and biotransformation.

Almost all of this evidence comes from animals and cultured cells. The single human study is a comparison with phenazepam, and no other human data are cited. Five of the ten papers appeared in the same journal, three of the five rat studies measured tissue, hormone or microbiota changes rather than behaviour, and most models appear in a single paper. The GABA and BDNF mechanisms were proposed from cell and animal work and have not been tested in people in the studies cited here.